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Lecom pathology year 2 > Kidney-chapter 20 > Flashcards

Kidney-chapter 20 Flashcards

1
Q

What is the most common mediator/cause of glomerular diseases

A

Immunologically mediated

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2
Q

What are most tubular and interstitial disorders disorders frequently caused by

A

Toxic or infectious agents

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3
Q

What is defined as increased BUN and creatinine, usually related to decreased GFR

A

Azotemia

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4
Q

When is prerenal azotemia encountered

A

When there is hypoperfusion of the kidneys that impairs renal function in the absence of parenchyma damage

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5
Q

What is the term for azotemia plus other metabolic and endocrine alterations resulting from renal damage

A

Uremia

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6
Q

What disorder is a nephritic syndrome with rapid decline (hours to days) in GFR

A

Rapidly progressive glomerulonephritis

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7
Q

What is the definition of acute kidney injury

A

Rapid decline in GFR, increased BUN, creatinine, most severe- oliguria and anuria

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8
Q

What is the definition of end-stage renal disease

A

GFR less than 5% of normal

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9
Q

What domain of the GBM is important for helix formation and for assembly of collagen monomers into the basement suprastructure

A

NC1

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10
Q

What denotes the accumulation of material that is homogenous and eosinophilia by light microscopy

A

Hyalinosis

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11
Q

What is a common end result of various forms of glomerular damage

A

Hyalinosis

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12
Q

What is sclerosis characterized by

A

Deposition of extracellular collagenous matrix

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13
Q

What are the manifestations of fluid and electrolyte balance in chronic renal failure

A

Dehydration, Edema, hyperkalemia, metabolic acidosis

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14
Q

What are the cardiopulmonary manifestations of chronic renal failure

A

HTN, CHF, cardiomyopathy, pulmonary edema, uremia pericarditis

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15
Q

What disease is induced by immunizing rats with an antigen (megalin) that is present in epithelial cell foot processes

A

Heymann nephritis

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16
Q

What is the antigen that underlies most cases of primary human membranous nephropathy

A

M type PLA2R

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17
Q

What is heymann nephritis characterized by

A

Presence of numerous discrete subepithelial electron dense deposits

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18
Q

What is the pattern in IF of heymann nephritis

A

Granular

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19
Q

What is the GBM antigen responsible for classic anti-GBM antibody induced glomerulonephritis and goodpasture syndrome

A

Component of the NC1 of the alpha3 chain of type 4 collagen

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20
Q

What complement pathway is activated in dense deposit disease

A

Activation of alternative complement pathway

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21
Q

What disease is defined as progressive fibrosis involving portions of some glomeruli developing after many types of renal injury and leads to proteinuria and increased functional impairment

A

Focal segmental glomerulosclerosis

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22
Q

What disease is defined as tubulointerstitial injury, manifested by tubular damage and interstitial inflammation

A

Tubulointerstitial fibrosis

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23
Q

What disease is often characterized in the glomeruli, usually presenting with hematuria, red cell casts in the urine, azotemia, oliguira, and mild to moderate HTN

A

Nephritic syndrome

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24
Q

What is acute proliferative glomerulonephritis defined as

A

Cluster of diseases characterized by diffuse proliferation of glomerular cells associated with influx of leukocyte

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25
Q

How long after strep infection does acute proliferative glomerulonephritis typically develop

A

1-4 weeks after infection

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26
Q

Who is acute proliferative glomerulonephritis most common in

A

Kids age 6-10

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27
Q

How do adults with acute proliferative glomerulonephritis typically present

A

With sudden HTN and/or edema and elevated BUN

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28
Q

What is the characteristic EM finding in acute postrreptococcal glomerulonephritis

A

Humps appearance (discrete, amorphous, electron-dense deposits on the epithelial side of the membrane)

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29
Q

What is the lab finding in poststreptococcal glomerulonephritis

A

Elevated antistreptococcal antibody titers and decline in serum concentration of C3

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30
Q

What disease is rapid and progressive loss of renal function associated with severe oliguria

A

Rapidly progressive (crescentic) GN

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31
Q

What is an example of a type 1 rapidly progressive crescentic GN

A

Goodpasture syndrome

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32
Q

What is an example of type III pauci-immune nephritic disease

A

ANCA, granulomatosis with polyangiitis

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33
Q

Describe the kidneys in RPGN

A

Enlarged and pale, often with petechial hemorrhages on cortical surfaces

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34
Q

What is the histology picture of RPGN dominated by

A

Distinctive crescents

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35
Q

What type of fluorescence does goodpasture syndrome show

A

Linear GBM

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36
Q

What are the clinical findings of RPGN

A

Hematuria with RBC casts in urine, moderate proteinuria, variable HTN and edema

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37
Q

What is nephrotic syndrome caused by

A

Derangement in glomerular capillary walls resulting in increased permeability to plasma proteins

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38
Q

What are the common clinical findings with nephrotic syndrome

A

Massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia and lipiduria

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39
Q

How does lipid appear in the urine in nephrotic syndrome

A

Oval fat bodies

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40
Q

What is the most frequent cause of nephrotic syndrome in kids

A

Minimal change disease

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41
Q

Describe the IF of minimal change disease

A

Negative

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42
Q

Describe the principle lesion in minimal change disease

A

In visceral epithelial cells; sometimes termed fusion of foot processes

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43
Q

What nephrotic disease is known to have good response to corticosteroids

A

Minimal change disease

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44
Q

Describe the basement membrane in membranous nephropathy

A

Basement membrane material is laid down between deposits, appearing as irregular spikes protruding from GBM

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45
Q

What is the most common form of nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis

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46
Q

Describe the hallmark epithelial damage/change in focal segmental glomerulosclerosis

A

Hyalinosis and sclerosis stem from entrapment of plasma proteins in extremely hyperpermeable foci and increased ECM deposition

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47
Q

What does the NPHS1 gene involved is FSGS encode

A

Protein nephrin

48
Q

What do mutations of NPHS1 give rise to

A

Congenital nephrotic syndrome of Finnish type

49
Q

What does NPHS2 encode (involved in FSGS)

A

Podocin

50
Q

What does mutation in NPHS2 result in

A

Syndrome of steroid-resistant nephrotic syndrome of childhood onset

51
Q

What disease is associated with double contour or tram track appearance

A

Membranoproliferative GN

52
Q

Who does membranoproliferative GN typically occur in

A

Young adults or adolescence

53
Q

Describe the issues in the complement pathway with dense deposit disease

A

Decreased C3 but normal C1 and C4; decreased factor B and proper sin

54
Q

What is the predominant pattern of injury in dense deposit disease

A

Mesangial proliferative pattern

55
Q

What immunoglobulin is typically absent on IM in dense deposit disease

A

IgG

56
Q

What is another name for IgA nephropathy

A

Berger disease

57
Q

What is the major characteristic of Berger disease

A

IgA deposits in the mesangial regions

58
Q

What defect is believed to be associated with Berger disease

A

Defect in O-linked glycans

59
Q

What can occur in individuals with Berger disease that are children

A

Henoch-schonlein purpura

60
Q

What is the abnormality in Alport syndrome

A

Alpha chains in type 4 collagen

61
Q

Describe the morphology of Alport syndrome

A

Basket-weave apperance; GBM shows irregular foci with thickening alternating with attenuation and pronounced splitting and lamination of the lamina densa

62
Q

What is the most common presenting sign of Alport syndrome

A

Hematuria

63
Q

When do symptoms of Alport syndrome typically appear

A

Age 5-20

64
Q

Describe the kidneys in chronic glomerulonephritis

A

Symmetrically contracted and have diffusely granular cortical surfaces

65
Q

What portions of the kidney are especially vulnerable to acute tubular injury/necrosis

A

Straight portion of proximal tubule and ascending thick limb

66
Q

What causes marked ballooning and hydrophobic or vacuolar degeneration of proximal convoluted tubules

A

Ethylene glycol

67
Q

What does acute pyelonephritis usually present with

A

Sudden onset pain at the CVA and systemic evidence of infection (fever, malaise)

68
Q

What does reflux nephropathy occur as a result of in early childhood

A

Result of superimposition of urinary infection on congenital vesicoureteral reflux and nitrate all reflux

69
Q

What type of pyenolonephritis is sometimes confused with renal carcinoma

A

Xathnogranulomatous pyelonephritis

70
Q

Describe lab findings with bile cast nephropathy

A

Serum bilirubin markedly elevated, with bile cast formation in distal nephron segment

71
Q

What is the consequence of narrowing with benign nephrosclerosis

A

Patchy ischemic atrophy

72
Q

What is a common pathological finding with malignant nephrosclerosis

A

Fibrinoid necrosis and onion-skinning

73
Q

What in the plasma is markedly elevated in patients with malignant HTN

A

Renin

74
Q

What disease has flea-bitten appearance on cortical surface

A

Malignant nephrosclerosis

75
Q

What is the most common cause of renal artery stenosis

A

Atherosclerosis

76
Q

What is the Pentad for TTP

A

Fever, neuro symptoms, microangiopathic hemolytic anemia, thrombocytopenia, renal failure

77
Q

What are the most common abnormalities with sickle cell nephropathy

A

Hematuria and diminished concentration ability (hyposthenuria)

78
Q

What are the Defects in with adult polycystic kidney disease

A

Defects in mechanosensing, calcium flux, and signal transduction

79
Q

What gene is commonly knocked ou with adult polycystic kidney disease

A

PKD1

80
Q

What are most cases of childhood polycystic kidney disease due to mutation of

A

PKHD1

81
Q

What does PKHD1 encode

A

Fibrocystin

82
Q

Describe the morphology with childhood polycystic kidney disease

A

Enlarged and have smooth external surface; spongelike appearance

83
Q

How does nephronopthisis often present in kids

A

Polyuria and polydipsia’ sodium wasting and tubular acidosis often present

84
Q

What is the most common characteristic with multicystic renal hyperplasia

A

Presence of islands of undifferentiated mesenchyme

85
Q

What do the cysts commmonly contain with acquired (dialysis associated) cystic disease

A

Calcium oxalate crystals

86
Q

Describe the appearance of renal papillary adenoma

A

Small, invariable within cortex and appear grossly as yellow-gray, discreet well circumscribed nodules

87
Q

What is the tubular sclerosis associated with angiomyolipoma characterized by

A

Lesions of the cerebral cortex

88
Q

What are oncocytomas composed of

A

Large eosinophilia cells having small, round benign=appearing nuclei that have large nucleoli; tan or mahogany brown

89
Q

What is the buzz word for collecting duct carcinoma

A

Hobnail pattern

90
Q

What are chromophone renal carcinoma cells

A

Pale eosinophilic cells

91
Q

What are the classic clinical features with renal cell carcinomas

A

Costovertebral pain, palpable mass, hematuria

92
Q

what congenital kidney issue is defined as conjoined kidney usually connected at lower pole

A

horseshoe kidney

93
Q

what is included in potter sequence

A

lung hypoplasia, flat face with lowset ears, development of defects in extremities

94
Q

what is the non-inherited congenital malformation of renal parenchyma characterized by cysts and abnormal tissue

A

dysplastic kidney

95
Q

what is the inherited defect of the kidney presenting as bilateral enlarged kidneys with cysts in renal cortex and medulla

A

PKD

96
Q

how does autosomal recessive PKD present

A

in infants, worsening renal failure and HTN

97
Q

how does autosomal dominant PKD present

A

in adults as HTN, hematuria, worsening renal failure

98
Q

what is the often cause of death in autosomal dominant PKD

A

berry aneurysms

99
Q

describe the result of medullar cystic kidney disease

A

inherited autosomal dominant defect that the parenchymal fibrosis results in shrunken kidneys and worsening renal failure

100
Q

what is sen in the urine with acute tubular necrosis

A

brown granular casts

101
Q

what is the major hallmark of nephrotic syndrome

A

proteinuria

102
Q

what does the hypoalbuminemia of nephrotic syndrome lead to

A

decrease oncotic pressure, leading to edema

103
Q

what is the most common cause of nephrotic syndrome in african americans and hispanics

A

FSGS

104
Q

what is the hallmark of nephritic syndrome

A

glomerular inflammation and bleeding

105
Q

how does alport syndrome clinically present

A

thinning and splitting of glomerular basement membrane; presents as isolated hematuria, sensory hearing loss, ocular disturbances

106
Q

describe the presentation of a patient with nephrolithiasis

A

colicky pain with hematuria and unilateral flank tenderness

107
Q

what renal neoplasma is defined as hamartoma comprised of blood vessels, smooth muscle, and adipose tissue; increased frequency in tuberous sclerosis

A

angiomyolipoma

108
Q

what is the clinical triad associated with renal cell carcinoma

A

hematuria, palpable mass, flank pain

109
Q

what does von hippel-lindua disease increase the risk for

A

hemangioblastoma of cerebellum and renal cell carcinoma

110
Q

what is von hippel lindua disease caused by

A

autosomal dominant inactivation of VHL gene

111
Q

what is wilms tumor comprised of

A

blastoma, primitive glomeruli and tubules, stroll cells

112
Q

who is wilms tumor most common in

A

kids

113
Q

how does someone with a wilms tumor typically present clinically

A

large unilateral flank mass with hematuria and HTN

114
Q

what does WAGR syndrome stand for

A

wilms tumor, aniridia, genital abnormalities, mental/motor retardation

115
Q

where does urothelial carcinoma typically occur

A

bladder

116
Q

what is the major risk factor for urothelial carcinoma

A

cigarette smoke

117
Q

what is the classic presentation of urothelial carcinoma in older adults

A

painless hematuria

Lecom pathology year 2 (18 decks)

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