Kidney Flashcards
(286 cards)
0
Q
average wt adult of kidney
A
150 g
1
Q
lower urinary tract division
A
pelvicalcyceal system
ureters
bladder
urethra
2
Q
cortical thickness of normal kidney
A
1-1.5 c,
3
Q
elevation of BUN and creatinine levels
decreased GFR
A
azotemia
4
Q
prerenal azotemia
A
hypoperfusion of kidneys that impairs renal fxn without parenchymal damage
5
Q
postrenal azotemia
A
obstruction beyond the level of the kidney
6
Q
failure of renal excretory function
metabolic and endocrine alterations resulting from renal damage
A
uremia
7
Q
classic presentation of acute poststreptococcal GN
A
nephritic syndrome
8
Q
nephritic syndrome signs
A
acute onset of grossly visible hematuria mild to mod proteinuria azotemia oliguria edema hytpertension
9
Q
nephritic syndrome with rapid decline - hours to days
A
RPGN
10
Q
nephrotic syndrome signs
A
heavy proteinuria >3.5 g/day hypoalbuminemia severe edema hyperlipidemia lipiduria
11
Q
acute renal failure
A
oliguria or anuria
recent onset of azotemia- acute tubular necrosis
12
Q
renal tubular defects
A
polyuria
nocturia
electrolyte dsorders
13
Q
renal tubular defect cause
A
dse that directly affect tubular structure
or
cause defects in tubular functions
14
Q
urinary tract infection
A
bacteriuria
pyuria
symptomatic or not
15
Q
kidney uti
A
pyelonephritis
16
Q
bladder uti
A
cystitis
17
Q
nephrolothiasis
A
severe spasms of pain
hematuria
recurrent stone formation
18
Q
end result of all renal parenchymal diseases
A
chronic renal failure
19
Q
cause of chronic renal failure
A
azotemia -> uremia
chronic
20
Q
stage 1
DIMINISHED RENAL RESERVE
A
GFR 50%
normal serum BUN and creatine
asymptomatic
susceptible to azotemia with additional renal insult
21
Q
stage 2
RENAL INSUFFICIENCY
A
GFR 20-50% azotemia anemia hypertension polyuria nocturia uremia precepitated by stress
22
Q
stage 3
CHRONIC RENAL FAILURE
A
<20-25% GFR edema metabolic acidosis hyperkalemia overt uremia dneuroooig GI CV complications
23
Q
stage 4
END STAGE RENAL DISEASE
A
<5% GFR
terminal stage of uremia
24
systemic manifestations:
| FLUID AND ELECTROLYTES
metabolic acidosis
edema
hyperkalemia
dehydration
25
systemic manifestations:
CALCIUM
PHOSPHATE
BONE
hyperphosphatemia
secondary hyperparathyroidism
hypocalcemia
renal osteodystrophy
26
systemic manifestations:
| HEMATOLOGIC
anemia
| bleeding diathesis
27
systemic manifestations:
| CARDIOPULMONARY
```
cardiomyopathy
congestive heart failure
hypertension
uremic pericarditis
pulmonary edema
```
28
gastrointestinal manifestations
```
bleeding
esophagitis
gastritis
colitis
nausea
vomiting
```
29
systemic manifestations
| NEUROMUSCULAR
peripheral neuropathy
encephalopathy
myopathy
30
systemic manifestations
| DERMATOLOGIC
pruritus
sallow color
dermatitis
31
cavity in which plasma filtrate collects first
urinary space
32
supporting network of the interconnecting capillary lumen
mesangium
33
glomerulus fxn
maintain the integrity of the glomerular filtration barrier
34
glomerular filtration barrier composition
fenestrated endothelial cells
basement membrane
epithelial podocytes layer or visceral layer
35
factors that determine filtration
size of the molecule
| charge of the barrier
36
MW of molecules that can pass through the filter
<70 kilodalton
37
responsible for the slit like diaphragm
podocytes or visceral epithelium
38
charge of the barrier
anionic
39
charge of the substance
cationic
40
coats the membranes of endothelial and epithelial together with the basement membrane
responsible for the negative charge of the barrier
proteoglycans
| sialoglycans
41
increase in number of cells in the glomerular tufts
hypercellularity
42
hypercellulariy characteristics
cellular proliferation of mesangial, endothelial, epithelial cells
leukocytic infiltration of neutrophils, monocytes, lymphocytes
crescents
43
composition of crescents
parietal epithelial cells
| leukocytes
44
elicits crescenteric response
fibrin
45
basement membrane thickening is due to deposition of
immune complexes on the endothelial and epithelial side of the basement membrane or within GBM itself
46
hyalinosis denotes accumulation of
plasma proteins as a consequence of capijllary or endothelial wall injury
47
sclerosis is accumulations of
extracellular collagenous matrix in mesangial areas and or capillary loops
48
common feature of focal segmental glomerulosclerosis
hyalinosis
49
capillary lumen obliteration by sclerosis could lead to formation of
fibrous adhesions between the sclerotic portions of the glomeruli and the nearby parietal epithelium
50
hyalinosis and sclerosis are manifestations of
end stage irreversible injury
51
numerous discrete electron-dense deposits along the subepithelial aspect of the basement membrane
granular pattern
Heymann Nephritis
52
Heymann antigen with homology to LDL receptor
megalin
53
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
antibodies against planted antigens
54
antibodies are directed against intrinsic fixed antigens that are normal components of the GBM
diffuse linear pattern
anti GBM antibody induced GN
55
anti GBM cross react to lung alveoli, a feature of
Goodpasture Syndrome
56
GBM antigen responsible for classic anti GBM GN and Goodpature syndrome is a component of
NC1 of the alpha 3 chain of collagen type 4
57
fxn of NC1 of the alpha 3 chain of collagen type 4
maintenance of GBM suprastructure
58
anti GBM GN are characterized by ---- and the clinical syndrome of -----
severe cresenteric glomerular damage
| RPGN
59
caused by trapping of circulating ag ab complex
granular
circulating immune complex GN
60
endogenous origin of antigens that trigger circulating immune complexes
SLE
61
exogenous origin of antigens that trigger circulating immune complexes
hepa b, c
treponema
plasmodium
tumor
62
continuous cycles of immune complex formation as seen in SLE and viral hepatitis may lead to
membranous or membranoproliferative type of GN
63
alternative complement pathway activation occurs in
dense deposit disease
MPGN type 2
-may occur in some proliferative GN
64
epithelial cell injury is seen in
minimal change disease
| focal segmental glomerulosclerosis
65
Primary glomerular diseases under acute nephritis
acute diffuse GN
| rapid progressive/crescentic GN
66
Primary glomerular diseases under nephrotic presentation
minimal change disease
focal segemental glomerulosclerosis
membranous GN
membranoproliferative GN
67
Primary glomerular diseases under primary hematuria
IgA nephropathy or Berger's dse
68
prototype of acute diffuse glomerulonephritis
Poststrep GN
69
histologic alterations in acute diffuse GN
hypercellularity
70
features of acute diffuse GN
```
1-4 weeks after strep infection
6-10 years old
hematuria, edema, HTN
can be endogenous or exogenous
GRANULAR
```
71
etiologic agent of acute diffuse GN
nephritogenic strains of group A- beta hemolytic strep types 12,14,1
72
pathogenesis of acute diffuse GN
circulating ab-ag complexes➡️entrapped in glomeruli➡️glomerular injury by activation of complement by immune complexes
73
deposited in the GBM and mesangium in acute diffuse GN
IgG
IgM
C3
74
electron microscopy feature of acute diffuse Gn
discrete amorphous electron dense deposit on the epithelial side of the membrane
HUMPS
75
clinical course of acute diffuse GN
good prognosis
| young child develops malaise, fever, nausea, oliguria, hematuria
76
other postinfectious GN
```
staphylococcal endocarditis
pneumococcal pneumonia
meningococcemia
hep b,c
varicella
hiv
infectious mononucleosis
malaria
toxoplasmosis
```
77
severe proliferation that obliterates the glomerular tuft resulting to rapid and progressive decline
rapid progressive GN
78
manifestation of RPGN
severe olioguria
nephritis
crescent formation
79
3 groups based on immuno mechanism RPGN
1: anti GBM antibody induced ( renal limited)
2: immune complex mediates
3: pauci-immune type
80
syndrome associated with type 1 RPGN
Goodpasture syndrome
81
pattern of IgG and C3 deposition
linear
82
complication of post infectious GN, lupus nephritis, henoch-schonlein purpura
granular pattern
type 2 immune complex mediated
83
has circulating ANCAs which attacks visceral epithelial cells
type 3: pauci immune type
84
RPGN gross morphology
enlarged, pale, with cortical petechial hemorrhage
85
RPGN light microscopy features
crescent formation by proliferation of parietal epithelial cells
obliterated bowman's space
WBC migration and some fibrin strands between crescent layers
86
electron microscopy RPGN features
subepithelial deposits and rupture of the GBM
| cause fibrin to escape the glomerulus and settle in space
87
manifestations of nephrotic syndrome
```
massive proteinuria
hypoalbuminemia
generalized edema
hyperlipidemia
lipiduria
```
88
most important primary glomerular dse
primary: children: lipoid nephrosis
secondary: adults: membranous GN
all ages: focal segmental GS
89
may occur with lipiduria in patients susceptible to infection
globinuria
90
loss of anticoagulant glycoprotein factors in patients with nephrotic syndrome may lead to
thrombotic or thromboembolic complications
91
most common nephrotic syndrome in adults
membranous GN
92
membranous GN histological features
uniform diffuse thickening of capillary walls
irregular SPIKES of silver staining matrix
effaced foot processes
93
pathogenesis of membranous GN
direct action of c5-c9 which activates the glomerular mesangial and epithelial cells ➡️liberates proteases and oXidants➡️capillary wall injury➡️increased protein leakage
94
most common type of membranous GN 85%
idioipathic or primary
95
2ary membranous GN etiologies
hep b, c
penicillamine, captopril, gold therapy, NSAIDs
lung ca, colon, melanomas
SLE 15%
96
clinical course of membranous GN
```
40% of cases can proceed to renal failure
adults
nonselective proteinuria
poor response to corticosteroid therapy
sudden presentation, minimal hematuria
```
97
most frequent cause of nephrotic syndrome in children
minimal change disease or lipoid nephrosis
98
most characteristic feature of minimal change disease
good response to corticosteroid therapy
99
pathogenesis of minimal change disease
abscence of immune complexes
elaboration of cytokine (t cell derived)like circulating substance leads to proteinuria
proteinuria selective to albumin only
100
light microscopy feature of minimal change disease
normal
101
immunofluorescence feature of minimal change dse
normal, no deposits
102
electron microscopy feature of minimal change disease
uniform and diffuse foot processes replaced by a rim of cytoplasm often showing vacuolization, swelling, and hyperplasia of villi
103
MCD in adults is associated with
Hodgkin's lymphoma
104
secondary MCD may follow
NSAID therapy
| associated with acute interstitial nephritis
105
most common form of glomerulosclerosis in adults
focal segmental GS
106
hallmark of FSFGS
epithelial damage
107
pathogenesis of FSGS
epithelial damage
hyalinosis
sclerosis
108
on LM, FSGS initially involves only
juxtamedullary glomeruli
109
immunoflorEscence features of FSGS
deposition of IgM and c3 in sclerotic areas and or mesangium
110
FSGS may lead to
global glomerulosclerosis with pronouced tubular atrophy and interstitial fibrosis
111
morphologic variant of FSGs
collapsing glomerulopathy
112
cause of collapsing glomerulopathy
idiopathic but is the most characteristic lesion of HIV associated nephropathy
113
clinical course of FSGS
poor corticosteroid response
114
clincal presentation: nephrotic or mixed nephrotic/nephritic with low c3
MPGN or mesangiocapillary GN
115
idiopathic type 1 MPGN
immune complexes in the glomerulus
| activation of both classic and alternative pathways
116
type 2 MPGN or dense deposit dse
activation of alternative complement pathway
consistently decreased serum c3 but normal c4 and c1
low factor b and properdin
no IgG deposition
C3NeF
117
secondary MPGN
SLE, hep b,c
alpha 1-antitrypsin deficiency
CLL, lymphoma
hereditary deficiency of complement regulatory proteins
118
MPGN morphology
```
segmental basement membrane thickening
proliferation
enlarged glomeruli
leukcytic infiltration
double track or SPLITTING in pas or silver stain
```
119
GBM thickening of MPGN is at
peripheral capillary loops
120
type 1 MPGN
subendothelial electron dense deposits
c3 deposited in GRANULAR pattern
IgG and early complement proteins(c1q and 4)
121
type 2 MPGN
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
frequent cause of recurrent gross hematuria and mild proteinuria
immunoflorEscence microscopy detection only
IgA nephropathy or Berger disease
123
IgAN epidemiology
most common form of GN except among African americans
124
bad prognosis in IgAN
>1g/day
| HTN
125
pathogenesis of IgAN
IgA links with antigen and is carried into circulation➡️deposition in mesangium➡️activates complement➡️injury
126
morphology of IgAN
mesangial deposition of IgA with c3, properdin and lesser amts of IgG and IgM
c1q, 4 absent
127
treatment for IgAN
ACE inh
ARBs
renal transplantation for recurrent cases
128
2 hereditary nephritis
alport syndrome
| thin basement membrane dse
129
clinical features of aliport syndrome
hematuria progressing to renal failure
nerve deafness
various eye disorders
130
mode of inheritance of Alport syndrome
X linked
131
pathogenesis of alport syndrome
mutation of gene encoding TYPE 4 collagen
| - GBM, lens of the eye, cochlea
132
morphology of alport syndrome
basket weave appearance
- irregular foci of thickening and alternating with attenuation (thinning)
- pronounced splitting and lamination of the lamina densa
133
aka BENIGN FAMILIAR HYPERPLASIA
thin membrane disease
134
clinical manifestation of TBMD
familial asymptomatic hematuria discovered on urine urinalysis
135
GBM is thinned frm 300-400mm normal to
150-250mm
136
mode of inheritance of TBMD
heterozygous
137
pathogenesis of TBMD
defective genes encoding alpha 3 or alpha 4 chains of type 4 collagen
138
gross Chronic GN
symmetrically contracted
diffusely granular cortical surface
thinned out cortex
increased pelvic fat
139
progression sign in chronic GN
obliteration of glomeruli➡️acellular eosinophilic masses
140
potential etiologic factors of SLE
EBV
estrogen
HLA b???
procainamide
141
seen in 5%'SLE patients
class 1 minimal or no detectable abnormality
142
seen in 10-25% SLE patients
granular mesangial deposits of IG and complement
class 2 mesangial lupus glomerulonephritis
143
20-25% of SLE patients
class 3 focal proliferative glomerulonephritis
144
most serious form of Lupus nephritis
class 4 diffuse proliferative GN
145
wire loop due to capillary basement membrane thickening
diffuse proliferativ GN
146
similar to idipathic GN
class 5 membranous GN
147
one of the most common cause of end stage renal failure
diabetic nephropathy
148
diabetes can affect the kidney in 3 forms
complications of diabetic vasculature
diabetic glomerular damage
increased susceptibility to infection and papillary necrosis
149
contributors to renal tissue injury
hyperglycemia
non enzymatic glycosylation of proteins
hemodynamic changes
150
morphologic changes in diabetic nephropathy
capillary BM thickening
diffuse messangial sclerosis
nodular sclerosis- Kimmelstiel Wilson disease
151
purpuric skin lesions affecting the extensor surface of arms, legs, buttocks
abdominal manifestation
urinary abnormalities
poor prognosisi for adults
henodch schonlein
152
renal manifestations of HS
gross or microscopic hematuria
proteinuria
nephrotic syndrome
153
documents amyloidosis
congo red stain
154
amyloid deposition in kidneys
GBM
| mesangium
155
resemble amyloid fibrils but does not stain with Congo red
Fibrillary GN
156
deposits are microtubular in structure and 30-50 nm in width
immunotactoid GN
157
main causes of tubular injury
ischemia
158
aka acute tubular necrosis
acute tubular injury
159
most common cause of acute renal failure
acute kidney injury
160
mechanism of AKI
failure to maintain fluid and electrolyte, and acid base balance manifesting as oliguria or urine flow to less than 400mL within 24 hours
161
part most susceptible to ischemia
proximal convoluted tubule
162
toxic substances to tubules
```
gentamycin
radiocontrast dyes
myoglobin
hemoglobin
radiation
```
163
2 patterns of AKI based on process involved
ishemic
| nephrotoxic
164
two events in AKI
disturbance in blood flow
injury to tubuloepithelial cell
165
acute tubular necrosis morphology
karyolytic necrotic tubular cells
focal, patchy
coagulative necrosis
separation of cells from BM- tuborerrhexis
166
AKI initiation phase
- 36 hours
slight decrease in urine output
rise in BUN / creatinine
167
AKI maintenance phase
```
sustained decrease in urine output (40-400ml a day
rising BUN and creatinine
hyperkalemia
metabolic acidosis
uremia
```
168
recovery phase of aki
Increae urine output to 3L per day with water
sodium and potassium losses
renal tubule function restored
hypokalemia becomes a concern
169
distinguished from glomerular diseases by the absence of the hallmarks of nephritic or nephrotic syndrome
tubuluinterstitial nephritis
170
most common cause of tubulointerstitial nephritis
infections
171
metabolic causes of interstitial nephritis
urates
calcium
oxalates
172
acute form of tubulointerstitial nephritis
neutrophils and eosinophils
| edema of the interstitium
173
chronic form of tubulointerstitial nephritis
lymphocytes, plasma cells
interstitial fibrosis
tubular atrophy
174
pyelonephritis affects
tubules
interstitium
renal pelvis
175
dominant etiologic agents of pyelonephritis
E.coli
Proteus
Klebsiella
Enterobacter
176
viral etiologic agents of pyelonephritis
polyoma virus
cmv
adenovirus
177
2 routes in pyelonephritis
ascending
| hematogenous
178
hematogenous route results from seeding bacteria from
septicemia
| infective endocarditis
179
type of inflammation in actue pyelonephritis
diffuse suppurative
180
acute pyelonephritis complication seen in diabetics and bilateral ut obstruction
papilary necrosis
181
complication of acute pyelonephritis due to total or almost complete obstruction high in the urinary tract
pyonephrosis
182
complication of acute pyelonephritis
| extension into the renal capsule and perinephric tissue
perinephric abscess
183
classic symptoms of acute pyelonephritis
```
fever
costovertebral lumbar tenderness
pain
dysuria
pyuria
```
184
gross hallmark of chronic pyelonephritis
pitting geographic scars
185
most common mechanism in acquiring chronic pyelonephritis
reflux due to anatomic defect in the valve
186
reflux leads to
reflux nephropathy
187
in this mechanism the pressure is reflected backwards causing dilatation to the helices
obstructive
188
in reflux nephropathy, injury is at the
upper and lower poles of kidney
189
in chronic obstructive nephropathy, injury is
distributed in all areas
190
chronic pyelonephritis microscopic features
mononuclear inflammation
interstitial fibrosis
tubular atrophy- flattened epithelium
thyroidization
191
three ways in which drugs or toxins produce renal injury
intersitial immunological reaction
acute renal failure
cumulative injury
192
acute drug induced interstitial nephritis is associated with
```
penicillins
rifampin
diuretics
nsaids
allopurinol
cimetidine
```
sulfonamide
193
acute drug induced interstitial nephritis begins
after 2 weeks of exposure
194
mechanism of acute drug induced interstitial nephritis
type 1 hypersensitivity reaction because of eosinophilia and elevated serum IgE levels
195
chronic disorder due to excessive intake of
aspirin
tylenol
nsaids
analgesic nephropathy
196
analgesics contain this substance which depletes tubular cells of glutathione and then induce the formation of oxidative metabollites
phenacetin
197
morphological characteristics of analgesic nephropathy
| q
papillary necrosis
| chronic tubulointerstital nephritis
198
clinical features of acute drug induced interstitial nephritis
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
precipitiation of urate crystals in the tubules like
low pH
200
3 clinical forms of urate nephropathy
acute urate nephropathy
chronic urate or gouty nephropathy
urate nephrolithiasis
201
usually seen in patients with leukemias and lymphomas
acute urate nephropathy
202
genetic disposition of the individual to hyperuricemia
chronic urate nephropathy
203
uric acid in kidney is in its ionized form which precipitates in the tubules especially in acidic environment
urate nephrolithiasis
204
caused by complications of nonrenal malignant tumors of hematopoietic origin and therapy
multiple myeloma
light-chain cast nephropathy
205
causes direct toxicity to tubules and forms a cast giving rise to tubular obstruction
bence jonce protein
206
aka arteriolar nephrosclerosis
benign nephrosclerosis
207
benigh NS affects
renal arterioles and small arteries
208
benign NS is associated with
low grade essential HTN
| DM
209
at risk groups of developin renal insufficiency in benign NS
african descent
more severe BP elevations
second underlying disease
210
gross feature of benign NS
grain leather appearance
| loss of mass
211
histologic features of bening NS
arteriolar thickening and hyalinization
| fibroplastic hyperplasia of interlobular and arcuate aa.
212
associated with rapidly progressive or accelerated HTN
malignant NS
213
gross features of malignant NS
kidney size depends on the duration and severity
| small pinpoint petechial hemorrhages on cortical surface
214
histologic features of malignant ns
```
vascular damage
fibrinoid necrosis
onion skinning
ischemia
significant luminal narrowing
```
215
rare cause of kidney hypertension caused by renin secretion by cells of the JG apparatus
renal artery stenosis
216
pathologic lesions of renal artery stenosis
atheromatous plaque
| fibromuscular dysplasia type
217
more common cause of renal artery stenosis
atheromatous plaque
218
fibromuscular, dysplasia type of lesion in renal artery stenosis is seen in
women and younger age groups
219
constriction in fibromuscular lesion of renal stenosis is usually at
middle or distal portion of the renal artery
220
fibroproliferation or nonatherosclerotic hyperplasia is most common in
medial hyperplasia
221
clinical features of renal artery stenosis
essential HTN similarities
bruit on auscultation of kidneys
arteriography required
222
special stain in fibromuscular dysplasia renal stenosis
elastin stain
223
characterized clinically by microangiopathic hemolytic anemia, thrombocytopenia, renal failure
thrombotic microangiopathies
224
important clue in the diagnosis of TMA
schistocutes
225
morphological lesion in TMA
thrombotic lesions in capillaries and arterioles
226
hemolytic uremic syndrome is largely due to
endothelial injury
227
TTP is largely due to
platelet activation
228
typical HUS
epidemic, classic, diarrhea postive
229
Typical HUS is associated with infection of
E coli strains O157:H7
| producing shiga-like toxin
230
atypical HUS is associated with inherited deficiency or mutation of complement regulatory proteins
atypical, nonepidemic, diarrhea negative HUS
231
c3 regulatory proteins function
inactivates c3 convertase in order to oppose the action od rhe alternative complement pathway
232
acquired causes of endothelial injury in atypical HUs
```
antiphospholipid antibodies
pregnancy complications
oral contraceptives
vascular renal diseases such as scleroderma and hypertensions
chemo and immunosup drugs
radiation
```
233
deficiency in TTP
ADAMTS13
234
ADAMTS13 function
metalloprotease the regulates the function of the vWF
235
gross features of thrombotic microangiopathy
patchy or diffuse cortical necrosis and subcapsular petechiae
236
histologic feature of TMA
occluded glomerulal capillaries by platelets and fibrin
| thickened capillary walls due to swelling and subendothelial deposits
237
chronic TMA is confined to patients with
atypical HUS and TTP
238
gross features of chronic TMA
various degrees of scarring
239
histologic features of chronic TMA
tam tracks
onion skinning
hypoperfusion
ischemic atrophy
240
unilateral renal artery stenosis can lead to
hypertension
241
bilateral renal artery disease leads to
chronic ischemia with renal insufficiency sometimes in the absence of HTN
242
atheroembolic renal disease can be recognized by
rhomboid clefts or cholesterol crystals in the lumens and walls of arcuate and intralobular arteries
243
most common clincal and functional abnormalities in sickle cell nephropathy
hematuria
| hyposthenuria
244
major source of emobli in renal artery infarct
mural thrombosis in the left atrium and ventricle as a result of MI
245
gross features of renal infarct
```
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
ischemic coagulative necrosis in renal infarcts present with
intense eosinophilic staining
247
autosommal recessive renal cystic dses
childhood polycystic
| familial juvenile nephrophthisis
248
autosommal dominant renal cystic dses
adult polycystic kidney dse
| adult onset medullary cystic dse
249
familial juvenile nephrophthisis and adult onset cystic dse present as
corticomedullary cysts
| shrunken kidneys
250
complications of adult polycystic renal disease
```
hematuria
flank pain
urinary tract infection
renal stones
hypertension
```
251
complication of childhood polycystic kidney dse
hepatic fibrosis
252
typical outcome of childhood polycystic disease
variable
| death in infancy or childhood
253
benign renal cystic dses
medullary sponge disease
| simple cysts
254
unrelieved obstruction leads to
hydronephrosis or obstructive uropathy
255
common causes of urinary tract obstruction
```
urolithiasis
congenital strictures
prostate enlargement
tumors
sloughed clots, papillae
pregnancy
neurogenic
```
256
gross feature of urinary tract obstruction
dilatation of renal pelvis extending to calyxes
loss or atrophy of renal tissue
thinning of parenchma
257
urolithiasis peak age of onset
20-30 usually in men
258
causes of urolithiasis
calcium oxalate or phosphate
magnesium ammonium phosphate
uric acid
259
infections due to proteus present as
staghorn calculi of magnesium phosphate stones
260
benign renal cell neoplasms
papillary adenoma
angiomyolipoma
oncocytoma
261
disease associated with angiomyolipoma
tuberous sclerosis
262
loss of function mutation in tuberous sclerosis
TSC1 or TSC2
263
large neoplastic cells with vesicular nuclei
| abundant eosinophilic granular cytoplasm
oncocytoma
264
most common primary tumor of the kidney
| 3% of visceral cancers
adenocarcinoma of the kidney
265
renal cancer is mostly sporadic but autosomal dominant forms occur in young individuals
von Hippel-lindau syndrome
hereditary (familial) clear cell carcinoma
hereditary papillary carcinoma
266
genetic features of clear cell RCC
3p-/VHL mutations, inactivations,losses
267
papillary RCC genetic features
7+/ cnet mutations, 17+, other losses or gains
268
chromophobe RCC genetic features
...10-,13-,17-,21-
269
collecting duct carcinoma genetic features
deletion 1q32, 1-32.2,1-,14-,15-,22-
270
epidemiology of RCC
```
male
6th-7th decade of life
tobacco
obesity in women
htn
unoppesed estrogen therapy
exposure to asbestos, petroleum pdTs, heavy metals
```
271
most common classification of RCC
clear cell variant
272
mutation in RCC
3p25
| loss of sequences in the short arm of chromosome 3
273
gross features of RCC clear cell variant
golden yellow mass with irregular borders distorting the outline of the kidney
274
histologic features of RCC clear cell variant
acinar or tubular growth pattern with clear cell cytoplasm
275
most common type of RCC in patients who develop dialysis associated cystic disease
papillary tumor RCC
276
papillary tumor variant RCC arises form the
DCT
277
papillary tumor variant RCC is not associated with ch 3p deletions but in
chromosome 7
278
gross features of papillary tumor RCC
multifocal
bilateral
hemorrhagic
brownish discoloration
279
histologic features of papillary RCC
papillary
cuboidal or low columnar neoplastic cells
abundant histiocytes within the papillary core
psamomma bodies
stroma scanty but highly vascularized
280
most reliable symptom of RCC
hematuria
281
other features of RCC
costovertebral pain
palpable mass
tendency to metastasize
282
poor prognosis of RCC
when the tumor encroaches the renal pelvis at the insertion or entrance of the renal vein or artery
283
transitional CA usually arise from
renal pelvis-hilum
284
tumor stage at the renal vein, vena cava or regional lymph nodes
stage 3
285
tumor beyod gerota's fascia
stage 4
