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Pathology > Kidney > Flashcards

Kidney Flashcards

0
Q

average wt adult of kidney

A

150 g

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1
Q

lower urinary tract division

A

pelvicalcyceal system
ureters
bladder
urethra

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2
Q

cortical thickness of normal kidney

A

1-1.5 c,

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3
Q

elevation of BUN and creatinine levels

decreased GFR

A

azotemia

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4
Q

prerenal azotemia

A

hypoperfusion of kidneys that impairs renal fxn without parenchymal damage

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5
Q

postrenal azotemia

A

obstruction beyond the level of the kidney

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6
Q

failure of renal excretory function

metabolic and endocrine alterations resulting from renal damage

A

uremia

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7
Q

classic presentation of acute poststreptococcal GN

A

nephritic syndrome

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8
Q

nephritic syndrome signs

A 
acute onset of grossly visible hematuria
mild to mod proteinuria
azotemia
oliguria
edema
hytpertension
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9
Q

nephritic syndrome with rapid decline - hours to days

A

RPGN

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10
Q

nephrotic syndrome signs

A 
heavy proteinuria >3.5 g/day
hypoalbuminemia
severe edema
hyperlipidemia
lipiduria
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11
Q

acute renal failure

A

oliguria or anuria

recent onset of azotemia- acute tubular necrosis

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12
Q

renal tubular defects

A

polyuria
nocturia
electrolyte dsorders

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13
Q

renal tubular defect cause

A

dse that directly affect tubular structure
or
cause defects in tubular functions

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14
Q

urinary tract infection

A

bacteriuria
pyuria
symptomatic or not

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15
Q

kidney uti

A

pyelonephritis

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16
Q

bladder uti

A

cystitis

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17
Q

nephrolothiasis

A

severe spasms of pain
hematuria
recurrent stone formation

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18
Q

end result of all renal parenchymal diseases

A

chronic renal failure

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19
Q

cause of chronic renal failure

A

azotemia -> uremia

chronic

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20
Q

stage 1

DIMINISHED RENAL RESERVE

A

GFR 50%
normal serum BUN and creatine
asymptomatic
susceptible to azotemia with additional renal insult

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21
Q

stage 2

RENAL INSUFFICIENCY

A 
GFR 20-50%
azotemia 
anemia
hypertension
polyuria
nocturia
uremia precepitated by stress
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22
Q

stage 3

CHRONIC RENAL FAILURE

A 
<20-25% GFR
edema
metabolic acidosis
hyperkalemia
overt uremia
dneuroooig GI CV complications
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23
Q

stage 4

END STAGE RENAL DISEASE

A

<5% GFR

terminal stage of uremia

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24
Q

systemic manifestations:

FLUID AND ELECTROLYTES

A

metabolic acidosis
edema
hyperkalemia
dehydration

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25
Q

systemic manifestations:
CALCIUM
PHOSPHATE
BONE

A

hyperphosphatemia
secondary hyperparathyroidism
hypocalcemia
renal osteodystrophy

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26
Q

systemic manifestations:

HEMATOLOGIC

A

anemia

bleeding diathesis

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27
Q

systemic manifestations:

CARDIOPULMONARY

A 
cardiomyopathy
congestive heart failure
hypertension
uremic pericarditis
pulmonary edema
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28
Q

gastrointestinal manifestations

A 
bleeding
esophagitis
gastritis 
colitis
nausea 
vomiting
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29
Q

systemic manifestations

NEUROMUSCULAR

A

peripheral neuropathy
encephalopathy
myopathy

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30
Q

systemic manifestations

DERMATOLOGIC

A

pruritus
sallow color
dermatitis

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31
Q

cavity in which plasma filtrate collects first

A

urinary space

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32
Q

supporting network of the interconnecting capillary lumen

A

mesangium

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33
Q

glomerulus fxn

A

maintain the integrity of the glomerular filtration barrier

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34
Q

glomerular filtration barrier composition

A

fenestrated endothelial cells
basement membrane
epithelial podocytes layer or visceral layer

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35
Q

factors that determine filtration

A

size of the molecule

charge of the barrier

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36
Q

MW of molecules that can pass through the filter

A

<70 kilodalton

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37
Q

responsible for the slit like diaphragm

A

podocytes or visceral epithelium

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38
Q

charge of the barrier

A

anionic

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39
Q

charge of the substance

A

cationic

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40
Q

coats the membranes of endothelial and epithelial together with the basement membrane
responsible for the negative charge of the barrier

A

proteoglycans

sialoglycans

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41
Q

increase in number of cells in the glomerular tufts

A

hypercellularity

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42
Q

hypercellulariy characteristics

A

cellular proliferation of mesangial, endothelial, epithelial cells
leukocytic infiltration of neutrophils, monocytes, lymphocytes
crescents

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43
Q

composition of crescents

A

parietal epithelial cells

leukocytes

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44
Q

elicits crescenteric response

A

fibrin

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45
Q

basement membrane thickening is due to deposition of

A

immune complexes on the endothelial and epithelial side of the basement membrane or within GBM itself

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46
Q

hyalinosis denotes accumulation of

A

plasma proteins as a consequence of capijllary or endothelial wall injury

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47
Q

sclerosis is accumulations of

A

extracellular collagenous matrix in mesangial areas and or capillary loops

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48
Q

common feature of focal segmental glomerulosclerosis

A

hyalinosis

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49
Q

capillary lumen obliteration by sclerosis could lead to formation of

A

fibrous adhesions between the sclerotic portions of the glomeruli and the nearby parietal epithelium

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50
Q

hyalinosis and sclerosis are manifestations of

A

end stage irreversible injury

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51
Q

numerous discrete electron-dense deposits along the subepithelial aspect of the basement membrane

granular pattern

A

Heymann Nephritis

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52
Q

Heymann antigen with homology to LDL receptor

A

megalin

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53
Q

immune mechanism which includes cationic molecules that bind to anionic components of the glomerulus
DNA, nucleosomes, and other nuclear proteins, bacterial products, etc

granular pattern

A

antibodies against planted antigens

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54
Q

antibodies are directed against intrinsic fixed antigens that are normal components of the GBM

diffuse linear pattern

A

anti GBM antibody induced GN

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55
Q

anti GBM cross react to lung alveoli, a feature of

A

Goodpasture Syndrome

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56
Q

GBM antigen responsible for classic anti GBM GN and Goodpature syndrome is a component of

A

NC1 of the alpha 3 chain of collagen type 4

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57
Q

fxn of NC1 of the alpha 3 chain of collagen type 4

A

maintenance of GBM suprastructure

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58
Q

anti GBM GN are characterized by —- and the clinical syndrome of —–

A

severe cresenteric glomerular damage

RPGN

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59
Q

caused by trapping of circulating ag ab complex

granular

A

circulating immune complex GN

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60
Q

endogenous origin of antigens that trigger circulating immune complexes

A

SLE

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61
Q

exogenous origin of antigens that trigger circulating immune complexes

A

hepa b, c
treponema
plasmodium
tumor

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62
Q

continuous cycles of immune complex formation as seen in SLE and viral hepatitis may lead to

A

membranous or membranoproliferative type of GN

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63
Q

alternative complement pathway activation occurs in

A

dense deposit disease
MPGN type 2

-may occur in some proliferative GN

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64
Q

epithelial cell injury is seen in

A

minimal change disease

focal segmental glomerulosclerosis

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65
Q

Primary glomerular diseases under acute nephritis

A

acute diffuse GN

rapid progressive/crescentic GN

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66
Q

Primary glomerular diseases under nephrotic presentation

A

minimal change disease
focal segemental glomerulosclerosis
membranous GN
membranoproliferative GN

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67
Q

Primary glomerular diseases under primary hematuria

A

IgA nephropathy or Berger’s dse

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68
Q

prototype of acute diffuse glomerulonephritis

A

Poststrep GN

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69
Q

histologic alterations in acute diffuse GN

A

hypercellularity

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70
Q

features of acute diffuse GN

A 
1-4 weeks after strep infection
6-10 years old
hematuria, edema, HTN
can be endogenous or exogenous
GRANULAR
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71
Q

etiologic agent of acute diffuse GN

A

nephritogenic strains of group A- beta hemolytic strep types 12,14,1

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72
Q

pathogenesis of acute diffuse GN

A

circulating ab-ag complexes➡️entrapped in glomeruli➡️glomerular injury by activation of complement by immune complexes

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73
Q

deposited in the GBM and mesangium in acute diffuse GN

A

IgG
IgM
C3

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74
Q

electron microscopy feature of acute diffuse Gn

A

discrete amorphous electron dense deposit on the epithelial side of the membrane
HUMPS

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75
Q

clinical course of acute diffuse GN

A

good prognosis

young child develops malaise, fever, nausea, oliguria, hematuria

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76
Q

other postinfectious GN

A 
staphylococcal endocarditis
pneumococcal pneumonia
meningococcemia
hep b,c 
varicella
hiv
infectious mononucleosis
malaria
toxoplasmosis
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77
Q

severe proliferation that obliterates the glomerular tuft resulting to rapid and progressive decline

A

rapid progressive GN

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78
Q

manifestation of RPGN

A

severe olioguria
nephritis
crescent formation

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79
Q

3 groups based on immuno mechanism RPGN

A

1: anti GBM antibody induced ( renal limited)
2: immune complex mediates
3: pauci-immune type

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80
Q

syndrome associated with type 1 RPGN

A

Goodpasture syndrome

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81
Q

pattern of IgG and C3 deposition

A

linear

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82
Q

complication of post infectious GN, lupus nephritis, henoch-schonlein purpura
granular pattern

A

type 2 immune complex mediated

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83
Q

has circulating ANCAs which attacks visceral epithelial cells

A

type 3: pauci immune type

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84
Q

RPGN gross morphology

A

enlarged, pale, with cortical petechial hemorrhage

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85
Q

RPGN light microscopy features

A

crescent formation by proliferation of parietal epithelial cells
obliterated bowman’s space
WBC migration and some fibrin strands between crescent layers

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86
Q

electron microscopy RPGN features

A

subepithelial deposits and rupture of the GBM

cause fibrin to escape the glomerulus and settle in space

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87
Q

manifestations of nephrotic syndrome

A 
massive proteinuria
hypoalbuminemia
generalized edema
hyperlipidemia
lipiduria
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88
Q

most important primary glomerular dse

A

primary: children: lipoid nephrosis
secondary: adults: membranous GN
all ages: focal segmental GS

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89
Q

may occur with lipiduria in patients susceptible to infection

A

globinuria

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90
Q

loss of anticoagulant glycoprotein factors in patients with nephrotic syndrome may lead to

A

thrombotic or thromboembolic complications

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91
Q

most common nephrotic syndrome in adults

A

membranous GN

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92
Q

membranous GN histological features

A

uniform diffuse thickening of capillary walls
irregular SPIKES of silver staining matrix
effaced foot processes

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93
Q

pathogenesis of membranous GN

A

direct action of c5-c9 which activates the glomerular mesangial and epithelial cells ➡️liberates proteases and oXidants➡️capillary wall injury➡️increased protein leakage

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94
Q

most common type of membranous GN 85%

A

idioipathic or primary

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95
Q

2ary membranous GN etiologies

A

hep b, c
penicillamine, captopril, gold therapy, NSAIDs
lung ca, colon, melanomas
SLE 15%

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96
Q

clinical course of membranous GN

A 
40% of cases can proceed to renal failure
adults
nonselective proteinuria
poor response to corticosteroid therapy
sudden presentation, minimal hematuria
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97
Q

most frequent cause of nephrotic syndrome in children

A

minimal change disease or lipoid nephrosis

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98
Q

most characteristic feature of minimal change disease

A

good response to corticosteroid therapy

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99
Q

pathogenesis of minimal change disease

A

abscence of immune complexes
elaboration of cytokine (t cell derived)like circulating substance leads to proteinuria
proteinuria selective to albumin only

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100
Q

light microscopy feature of minimal change disease

A

normal

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101
Q

immunofluorescence feature of minimal change dse

A

normal, no deposits

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102
Q

electron microscopy feature of minimal change disease

A

uniform and diffuse foot processes replaced by a rim of cytoplasm often showing vacuolization, swelling, and hyperplasia of villi

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103
Q

MCD in adults is associated with

A

Hodgkin’s lymphoma

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104
Q

secondary MCD may follow

A

NSAID therapy

associated with acute interstitial nephritis

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105
Q

most common form of glomerulosclerosis in adults

A

focal segmental GS

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106
Q

hallmark of FSFGS

A

epithelial damage

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107
Q

pathogenesis of FSGS

A

epithelial damage
hyalinosis
sclerosis

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108
Q

on LM, FSGS initially involves only

A

juxtamedullary glomeruli

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109
Q

immunoflorEscence features of FSGS

A

deposition of IgM and c3 in sclerotic areas and or mesangium

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110
Q

FSGS may lead to

A

global glomerulosclerosis with pronouced tubular atrophy and interstitial fibrosis

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111
Q

morphologic variant of FSGs

A

collapsing glomerulopathy

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112
Q

cause of collapsing glomerulopathy

A

idiopathic but is the most characteristic lesion of HIV associated nephropathy

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113
Q

clinical course of FSGS

A

poor corticosteroid response

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114
Q

clincal presentation: nephrotic or mixed nephrotic/nephritic with low c3

A

MPGN or mesangiocapillary GN

115
Q

idiopathic type 1 MPGN

A

immune complexes in the glomerulus

activation of both classic and alternative pathways

116
Q

type 2 MPGN or dense deposit dse

A

activation of alternative complement pathway
consistently decreased serum c3 but normal c4 and c1
low factor b and properdin
no IgG deposition
C3NeF

117
Q

secondary MPGN

A

SLE, hep b,c
alpha 1-antitrypsin deficiency
CLL, lymphoma
hereditary deficiency of complement regulatory proteins

118
Q

MPGN morphology

A 
segmental basement membrane thickening
proliferation
enlarged glomeruli
leukcytic infiltration
double track or SPLITTING in pas or silver stain
119
Q

GBM thickening of MPGN is at

A

peripheral capillary loops

120
Q

type 1 MPGN

A

subendothelial electron dense deposits
c3 deposited in GRANULAR pattern
IgG and early complement proteins(c1q and 4)

121
Q

type 2 MPGN

A

lamina densa becomes irregular, ribbonlike
c3 in irregular granular or linear foci in BM on either side
c3 in mesangium : MESANGIAL rings
no IgG

122
Q

frequent cause of recurrent gross hematuria and mild proteinuria
immunoflorEscence microscopy detection only

A

IgA nephropathy or Berger disease

123
Q

IgAN epidemiology

A

most common form of GN except among African americans

124
Q

bad prognosis in IgAN

A

> 1g/day

HTN

125
Q

pathogenesis of IgAN

A

IgA links with antigen and is carried into circulation➡️deposition in mesangium➡️activates complement➡️injury

126
Q

morphology of IgAN

A

mesangial deposition of IgA with c3, properdin and lesser amts of IgG and IgM
c1q, 4 absent

127
Q

treatment for IgAN

A

ACE inh
ARBs
renal transplantation for recurrent cases

128
Q

2 hereditary nephritis

A

alport syndrome

thin basement membrane dse

129
Q

clinical features of aliport syndrome

A

hematuria progressing to renal failure
nerve deafness
various eye disorders

130
Q

mode of inheritance of Alport syndrome

A

X linked

131
Q

pathogenesis of alport syndrome

A

mutation of gene encoding TYPE 4 collagen

- GBM, lens of the eye, cochlea

132
Q

morphology of alport syndrome

A

basket weave appearance

  • irregular foci of thickening and alternating with attenuation (thinning)
  • pronounced splitting and lamination of the lamina densa
133
Q

aka BENIGN FAMILIAR HYPERPLASIA

A

thin membrane disease

134
Q

clinical manifestation of TBMD

A

familial asymptomatic hematuria discovered on urine urinalysis

135
Q

GBM is thinned frm 300-400mm normal to

A

150-250mm

136
Q

mode of inheritance of TBMD

A

heterozygous

137
Q

pathogenesis of TBMD

A

defective genes encoding alpha 3 or alpha 4 chains of type 4 collagen

138
Q

gross Chronic GN

A

symmetrically contracted
diffusely granular cortical surface
thinned out cortex
increased pelvic fat

139
Q

progression sign in chronic GN

A

obliteration of glomeruli➡️acellular eosinophilic masses

140
Q

potential etiologic factors of SLE

A

EBV
estrogen
HLA b???
procainamide

141
Q

seen in 5%’SLE patients

A

class 1 minimal or no detectable abnormality

142
Q

seen in 10-25% SLE patients

granular mesangial deposits of IG and complement

A

class 2 mesangial lupus glomerulonephritis

143
Q

20-25% of SLE patients

A

class 3 focal proliferative glomerulonephritis

144
Q

most serious form of Lupus nephritis

A

class 4 diffuse proliferative GN

145
Q

wire loop due to capillary basement membrane thickening

A

diffuse proliferativ GN

146
Q

similar to idipathic GN

A

class 5 membranous GN

147
Q

one of the most common cause of end stage renal failure

A

diabetic nephropathy

148
Q

diabetes can affect the kidney in 3 forms

A

complications of diabetic vasculature
diabetic glomerular damage
increased susceptibility to infection and papillary necrosis

149
Q

contributors to renal tissue injury

A

hyperglycemia
non enzymatic glycosylation of proteins
hemodynamic changes

150
Q

morphologic changes in diabetic nephropathy

A

capillary BM thickening
diffuse messangial sclerosis
nodular sclerosis- Kimmelstiel Wilson disease

151
Q

purpuric skin lesions affecting the extensor surface of arms, legs, buttocks
abdominal manifestation
urinary abnormalities
poor prognosisi for adults

A

henodch schonlein

152
Q

renal manifestations of HS

A

gross or microscopic hematuria
proteinuria
nephrotic syndrome

153
Q

documents amyloidosis

A

congo red stain

154
Q

amyloid deposition in kidneys

A

GBM

mesangium

155
Q

resemble amyloid fibrils but does not stain with Congo red

A

Fibrillary GN

156
Q

deposits are microtubular in structure and 30-50 nm in width

A

immunotactoid GN

157
Q

main causes of tubular injury

A

ischemia

158
Q

aka acute tubular necrosis

A

acute tubular injury

159
Q

most common cause of acute renal failure

A

acute kidney injury

160
Q

mechanism of AKI

A

failure to maintain fluid and electrolyte, and acid base balance manifesting as oliguria or urine flow to less than 400mL within 24 hours

161
Q

part most susceptible to ischemia

A

proximal convoluted tubule

162
Q

toxic substances to tubules

A 
gentamycin
radiocontrast dyes
myoglobin
hemoglobin
radiation
163
Q

2 patterns of AKI based on process involved

A

ishemic

nephrotoxic

164
Q

two events in AKI

A

disturbance in blood flow

injury to tubuloepithelial cell

165
Q

acute tubular necrosis morphology

A

karyolytic necrotic tubular cells
focal, patchy
coagulative necrosis
separation of cells from BM- tuborerrhexis

166
Q

AKI initiation phase

A
  • 36 hours

slight decrease in urine output
rise in BUN / creatinine

167
Q

AKI maintenance phase

A 
sustained decrease in urine output (40-400ml a day
rising BUN and creatinine
hyperkalemia
metabolic acidosis
uremia
168
Q

recovery phase of aki

A

Increae urine output to 3L per day with water
sodium and potassium losses
renal tubule function restored
hypokalemia becomes a concern

169
Q

distinguished from glomerular diseases by the absence of the hallmarks of nephritic or nephrotic syndrome

A

tubuluinterstitial nephritis

170
Q

most common cause of tubulointerstitial nephritis

A

infections

171
Q

metabolic causes of interstitial nephritis

A

urates
calcium
oxalates

172
Q

acute form of tubulointerstitial nephritis

A

neutrophils and eosinophils

edema of the interstitium

173
Q

chronic form of tubulointerstitial nephritis

A

lymphocytes, plasma cells
interstitial fibrosis
tubular atrophy

174
Q

pyelonephritis affects

A

tubules
interstitium
renal pelvis

175
Q

dominant etiologic agents of pyelonephritis

A

E.coli
Proteus
Klebsiella
Enterobacter

176
Q

viral etiologic agents of pyelonephritis

A

polyoma virus
cmv
adenovirus

177
Q

2 routes in pyelonephritis

A

ascending

hematogenous

178
Q

hematogenous route results from seeding bacteria from

A

septicemia

infective endocarditis

179
Q

type of inflammation in actue pyelonephritis

A

diffuse suppurative

180
Q

acute pyelonephritis complication seen in diabetics and bilateral ut obstruction

A

papilary necrosis

181
Q

complication of acute pyelonephritis due to total or almost complete obstruction high in the urinary tract

A

pyonephrosis

182
Q

complication of acute pyelonephritis

extension into the renal capsule and perinephric tissue

A

perinephric abscess

183
Q

classic symptoms of acute pyelonephritis

A 
fever
costovertebral lumbar tenderness
pain
dysuria
pyuria
184
Q

gross hallmark of chronic pyelonephritis

A

pitting geographic scars

185
Q

most common mechanism in acquiring chronic pyelonephritis

A

reflux due to anatomic defect in the valve

186
Q

reflux leads to

A

reflux nephropathy

187
Q

in this mechanism the pressure is reflected backwards causing dilatation to the helices

A

obstructive

188
Q

in reflux nephropathy, injury is at the

A

upper and lower poles of kidney

189
Q

in chronic obstructive nephropathy, injury is

A

distributed in all areas

190
Q

chronic pyelonephritis microscopic features

A

mononuclear inflammation
interstitial fibrosis
tubular atrophy- flattened epithelium
thyroidization

191
Q

three ways in which drugs or toxins produce renal injury

A

intersitial immunological reaction
acute renal failure
cumulative injury

192
Q

acute drug induced interstitial nephritis is associated with

A 
penicillins
rifampin
diuretics
nsaids 
allopurinol
cimetidine

sulfonamide

193
Q

acute drug induced interstitial nephritis begins

A

after 2 weeks of exposure

194
Q

mechanism of acute drug induced interstitial nephritis

A

type 1 hypersensitivity reaction because of eosinophilia and elevated serum IgE levels

195
Q

chronic disorder due to excessive intake of
aspirin
tylenol
nsaids

A

analgesic nephropathy

196
Q

analgesics contain this substance which depletes tubular cells of glutathione and then induce the formation of oxidative metabollites

A

phenacetin

197
Q

morphological characteristics of analgesic nephropathy

q

A

papillary necrosis

chronic tubulointerstital nephritis

198
Q

clinical features of acute drug induced interstitial nephritis

A

women
those with recurrent headache, muscle pain, psychoneurotic patients and factory workers
UTI complicatesn50% of cases
small % pose a risk in developing transitional carcinoma of the renal pelvis

199
Q

precipitiation of urate crystals in the tubules like

A

low pH

200
Q

3 clinical forms of urate nephropathy

A

acute urate nephropathy
chronic urate or gouty nephropathy
urate nephrolithiasis

201
Q

usually seen in patients with leukemias and lymphomas

A

acute urate nephropathy

202
Q

genetic disposition of the individual to hyperuricemia

A

chronic urate nephropathy

203
Q

uric acid in kidney is in its ionized form which precipitates in the tubules especially in acidic environment

A

urate nephrolithiasis

204
Q

caused by complications of nonrenal malignant tumors of hematopoietic origin and therapy
multiple myeloma

A

light-chain cast nephropathy

205
Q

causes direct toxicity to tubules and forms a cast giving rise to tubular obstruction

A

bence jonce protein

206
Q

aka arteriolar nephrosclerosis

A

benign nephrosclerosis

207
Q

benigh NS affects

A

renal arterioles and small arteries

208
Q

benign NS is associated with

A

low grade essential HTN

DM

209
Q

at risk groups of developin renal insufficiency in benign NS

A

african descent
more severe BP elevations
second underlying disease

210
Q

gross feature of benign NS

A

grain leather appearance

loss of mass

211
Q

histologic features of bening NS

A

arteriolar thickening and hyalinization

fibroplastic hyperplasia of interlobular and arcuate aa.

212
Q

associated with rapidly progressive or accelerated HTN

A

malignant NS

213
Q

gross features of malignant NS

A

kidney size depends on the duration and severity

small pinpoint petechial hemorrhages on cortical surface

214
Q

histologic features of malignant ns

A 
vascular damage
fibrinoid necrosis
onion skinning
ischemia
significant luminal narrowing
215
Q

rare cause of kidney hypertension caused by renin secretion by cells of the JG apparatus

A

renal artery stenosis

216
Q

pathologic lesions of renal artery stenosis

A

atheromatous plaque

fibromuscular dysplasia type

217
Q

more common cause of renal artery stenosis

A

atheromatous plaque

218
Q

fibromuscular, dysplasia type of lesion in renal artery stenosis is seen in

A

women and younger age groups

219
Q

constriction in fibromuscular lesion of renal stenosis is usually at

A

middle or distal portion of the renal artery

220
Q

fibroproliferation or nonatherosclerotic hyperplasia is most common in

A

medial hyperplasia

221
Q

clinical features of renal artery stenosis

A

essential HTN similarities
bruit on auscultation of kidneys
arteriography required

222
Q

special stain in fibromuscular dysplasia renal stenosis

A

elastin stain

223
Q

characterized clinically by microangiopathic hemolytic anemia, thrombocytopenia, renal failure

A

thrombotic microangiopathies

224
Q

important clue in the diagnosis of TMA

A

schistocutes

225
Q

morphological lesion in TMA

A

thrombotic lesions in capillaries and arterioles

226
Q

hemolytic uremic syndrome is largely due to

A

endothelial injury

227
Q

TTP is largely due to

A

platelet activation

228
Q

typical HUS

A

epidemic, classic, diarrhea postive

229
Q

Typical HUS is associated with infection of

A

E coli strains O157:H7

producing shiga-like toxin

230
Q

atypical HUS is associated with inherited deficiency or mutation of complement regulatory proteins

A

atypical, nonepidemic, diarrhea negative HUS

231
Q

c3 regulatory proteins function

A

inactivates c3 convertase in order to oppose the action od rhe alternative complement pathway

232
Q

acquired causes of endothelial injury in atypical HUs

A 
antiphospholipid antibodies
pregnancy complications
oral contraceptives
vascular renal diseases such as scleroderma and hypertensions
chemo and immunosup drugs
radiation
233
Q

deficiency in TTP

A

ADAMTS13

234
Q

ADAMTS13 function

A

metalloprotease the regulates the function of the vWF

235
Q

gross features of thrombotic microangiopathy

A

patchy or diffuse cortical necrosis and subcapsular petechiae

236
Q

histologic feature of TMA

A

occluded glomerulal capillaries by platelets and fibrin

thickened capillary walls due to swelling and subendothelial deposits

237
Q

chronic TMA is confined to patients with

A

atypical HUS and TTP

238
Q

gross features of chronic TMA

A

various degrees of scarring

239
Q

histologic features of chronic TMA

A

tam tracks
onion skinning
hypoperfusion
ischemic atrophy

240
Q

unilateral renal artery stenosis can lead to

A

hypertension

241
Q

bilateral renal artery disease leads to

A

chronic ischemia with renal insufficiency sometimes in the absence of HTN

242
Q

atheroembolic renal disease can be recognized by

A

rhomboid clefts or cholesterol crystals in the lumens and walls of arcuate and intralobular arteries

243
Q

most common clincal and functional abnormalities in sickle cell nephropathy

A

hematuria

hyposthenuria

244
Q

major source of emobli in renal artery infarct

A

mural thrombosis in the left atrium and ventricle as a result of MI

245
Q

gross features of renal infarct

A 
multiple or bilateral
base is along the surface of the kidNey, apex at area of occlusion
wedge shaped
well delineated 
white infarct
heal with a scar
246
Q

ischemic coagulative necrosis in renal infarcts present with

A

intense eosinophilic staining

247
Q

autosommal recessive renal cystic dses

A

childhood polycystic

familial juvenile nephrophthisis

248
Q

autosommal dominant renal cystic dses

A

adult polycystic kidney dse

adult onset medullary cystic dse

249
Q

familial juvenile nephrophthisis and adult onset cystic dse present as

A

corticomedullary cysts

shrunken kidneys

250
Q

complications of adult polycystic renal disease

A 
hematuria
flank pain
urinary tract infection
renal stones
hypertension
251
Q

complication of childhood polycystic kidney dse

A

hepatic fibrosis

252
Q

typical outcome of childhood polycystic disease

A

variable

death in infancy or childhood

253
Q

benign renal cystic dses

A

medullary sponge disease

simple cysts

254
Q

unrelieved obstruction leads to

A

hydronephrosis or obstructive uropathy

255
Q

common causes of urinary tract obstruction

A 
urolithiasis
congenital strictures
prostate enlargement
tumors
sloughed clots, papillae
pregnancy 
neurogenic
256
Q

gross feature of urinary tract obstruction

A

dilatation of renal pelvis extending to calyxes
loss or atrophy of renal tissue
thinning of parenchma

257
Q

urolithiasis peak age of onset

A

20-30 usually in men

258
Q

causes of urolithiasis

A

calcium oxalate or phosphate
magnesium ammonium phosphate
uric acid

259
Q

infections due to proteus present as

A

staghorn calculi of magnesium phosphate stones

260
Q

benign renal cell neoplasms

A

papillary adenoma
angiomyolipoma
oncocytoma

261
Q

disease associated with angiomyolipoma

A

tuberous sclerosis

262
Q

loss of function mutation in tuberous sclerosis

A

TSC1 or TSC2

263
Q

large neoplastic cells with vesicular nuclei

abundant eosinophilic granular cytoplasm

A

oncocytoma

264
Q

most common primary tumor of the kidney

3% of visceral cancers

A

adenocarcinoma of the kidney

265
Q

renal cancer is mostly sporadic but autosomal dominant forms occur in young individuals

A

von Hippel-lindau syndrome
hereditary (familial) clear cell carcinoma
hereditary papillary carcinoma

266
Q

genetic features of clear cell RCC

A

3p-/VHL mutations, inactivations,losses

267
Q

papillary RCC genetic features

A

7+/ cnet mutations, 17+, other losses or gains

268
Q

chromophobe RCC genetic features

A

…10-,13-,17-,21-

269
Q

collecting duct carcinoma genetic features

A

deletion 1q32, 1-32.2,1-,14-,15-,22-

270
Q

epidemiology of RCC

A 
male
6th-7th decade of life
tobacco
obesity in women
htn
unoppesed estrogen therapy 
exposure to asbestos, petroleum pdTs, heavy metals
271
Q

most common classification of RCC

A

clear cell variant

272
Q

mutation in RCC

A

3p25

loss of sequences in the short arm of chromosome 3

273
Q

gross features of RCC clear cell variant

A

golden yellow mass with irregular borders distorting the outline of the kidney

274
Q

histologic features of RCC clear cell variant

A

acinar or tubular growth pattern with clear cell cytoplasm

275
Q

most common type of RCC in patients who develop dialysis associated cystic disease

A

papillary tumor RCC

276
Q

papillary tumor variant RCC arises form the

A

DCT

277
Q

papillary tumor variant RCC is not associated with ch 3p deletions but in

A

chromosome 7

278
Q

gross features of papillary tumor RCC

A

multifocal
bilateral
hemorrhagic
brownish discoloration

279
Q

histologic features of papillary RCC

A

papillary
cuboidal or low columnar neoplastic cells
abundant histiocytes within the papillary core
psamomma bodies
stroma scanty but highly vascularized

280
Q

most reliable symptom of RCC

A

hematuria

281
Q

other features of RCC

A

costovertebral pain
palpable mass
tendency to metastasize

282
Q

poor prognosis of RCC

A

when the tumor encroaches the renal pelvis at the insertion or entrance of the renal vein or artery

283
Q

transitional CA usually arise from

A

renal pelvis-hilum

284
Q

tumor stage at the renal vein, vena cava or regional lymph nodes

A

stage 3

285
Q

tumor beyod gerota’s fascia

A

stage 4

Pathology (5 decks)

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