Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology > Renal > Flashcards

Renal Flashcards

1
Q

Elevation of blood urea nitrogen and creatinine levels with dec GFR

A

Azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hypoperfusion of kidneys
Dec GFR
No parenchymal damage

A

Prerenal azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Obstruction of urine flow below kidney

Relief of obstruction followed by azotemia

A

Postrenal azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Azotemia with clinical symptoms and biochem abnormalities

A

Uremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q 
Glomerular injury 
acute onset of visible hematuria
proteinuria
azotemia
edema 
hypertension
A

Nephritis

Poststreptococcal glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Heavy proteinuria >3.5g per day, hypoalbuminemia
severe edema
hyperlipidemia
lipiduria

A

Nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Crucial to maintenance of glomerular barrier function as diffusion barrier

A

Podocyte

Also synthesize GBM components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

transmembrane glycoprotein of the slit diaphragms between adjacent foot processes

A

Nephrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Maintains selective permeability of filtration barrier along with nephrin

A

Podocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Systemic and immunologically mediated diseases affecting glomerules

(SLE, Alport, DM, HUS)

A

Secondary glomerular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Two forms of antibody assoc injury in glomerulonephritis:

A

1 deposition of soluble circulating antigen-antibody complex in glomerulus
2 antibodies reacting in situ within glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pathogens that incite GN

A

1 streptococcal
2 Hepatitis B
3 Plasmodium falciparum malaria
4 Spirochetal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Antigen-antibody complex producing injury through activation of complement and recruitment of leukocyte

A

Glomerulonephritis by immune complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Electron microscopy of GN show immune complexes on (4)

A 
Mesangium 
Subendothelial (bet endothelial and GBM)
Subepithelial (bet outer GBM and podocyte)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Complexes in endothelium and subendothelium elicit

A

Inflammatory reaction from infiltration of leukocyte and proliferation of glomerular cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Antibodies directed at subepithelial region of glomerulus produce

A

Noninflammatory lesions similar to Heymann nephritis or membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Antibodies directed fixed antigen in GBM
LINEAR pattern of staining
Conformational change in alpha3 chain of type IV collagen in GBM

A

Anti-glomerular basement membrane Antibody-mediated crescentic Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Complication/sequelae of Anti-GBM Antibody-mediated GN with antibodies also cross reacting with basement membrane of lung alveoli

A

Goodpasture syndrome

simultaneous lung and kidney lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Immune injury on Glomerulus pathophy

A

Complement activation via classical pathway:
Chemotactic agents C5a for neutrophil and monocyte
Protease release from neutrophils causing GBM degradation
O2 radical generation causing damage
Arachidonic acid metab causing dec GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Antibody mediated GN show this type of pattern desposition

A

Granular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Immune complex antibodies cause injury by

A

1 complement activation

2 leukocyte recruitment with mediator release sometimes damaging podocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nephrotic syndrome clinical complex (4)

A

1 massive proteinuria >3.5g/day
2 hypoalbuminemia <3g/dL
3 Generalized edema
4 hyperlipidemia and lipiduria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hyperlipidemia in nephrotic syndrome is caused by

A

Inc release of lipoproteins in liver or

Loss of lipoprotein synthesis inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Most common cause of primary glomerular disease nephrotic in children

A

Minimal-change disease 65%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Most common cause of primary glomerular disease nephrotic in adults

A

Focal segmental glomerulosclerosis 35%

Membranous nephropathy 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Primary nephrotic renal disease occurs

A

95% in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

In adults, primary nephrotic disease is caused by

A

Renal manifestation of systemic disease 40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Glomeruli have normal appearance by light microscopy but show uniform diffuse effacement of podocyte foot processes on EM
Common at ages 1-7

A

Minimal change disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

90% of children respond to a short course of corticosteroid therapy

A

MCD

2/3 will have recurrence of proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

FSGS may be secondary attributed to (5)

A 
HIV
Heroin
IgA nephropathy 2 event
Maladaptation to nephron loss
Mutation in cytoskeletal proteins and podocin for integrity of podocyte and variant in apolopoprotein L1 gene APOL1 on chromosome 22
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Injury to podocyte as initiating event
First affects some of glomeruli of JM
Lesions occuring in some tufts within a glomerulus and sparing of others
Inc mesangial matrix, obliterated capillary lumina, deposition of hyaline masses and lipid droplets

A

Focal segmental glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Collapse of glomerular tuft and podocyte hyperplasia

Poor prognosis

A

Collapsing glomerulopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hematuria
Hypertension
Non selective proteinuria
Poor response to corticosteroid

A

Focal segmental glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Subepithelial IgG deposit along GBM
Diffuse thickening of capillary wall
Chronic immune complex GN by antibodies against glomerular Ag.
Without inflammation

A

Membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Antigen most commonly recognized by causative antibodies in MN

A

Phospholipase A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Spike and dome pattern

with granular deposits

A

Membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

MN may be caused by inciting events such as (5)

A 
Infection Hep B, syphilis, schistosomiasis, malaria
Malignancy CA of Lung, colon melanoma
SLE
Inorganic salt gold and mercury exposure
Drugs (Penicillamine, captopril, NSAID)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Full blown nephrotic syndrome without antecedent illness
Non-selective proteinuria
Not responsive to corticosteroid
Protein in 60%

A

Membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Caused by circulating immune complex or planted antigen with in situ complex
Assoc with Hepa B and C antigen, SLE, AV shunt

A

MPGN Type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Excess compliment activation against C3 convertase or nephritic factor that lead to uncontrolled activation of alternative complement

A

MPGN Type II

Dense deposit disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

MPGN Type II is associated with mutations in gene encoding complent regulatory factor protein

A

factor H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Hypocomplementemia is marked in MPGN Type II due to

A

excessive consumption of C3 and reduced synthesis by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Glomeruli with lobular appearance, proliferation of mesangial and endothelial cell and infiltrating leukocytes
GBM thickening

A

MPGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Tram track or double contour capillary wall

Splitting of GBM

A

MPGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

subendothelial electron dense immune deposit

C3 in irregular pattern

A

Type I MPGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Irregular, ribbon-like lamina densa and subendothelial space from unknown composition
C3 present in irregular chunky segmental linear foci
Complement dysregulation

A

Dense deposit disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Poor prognosis recurring in transplant patients

A

MPGN type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Underlying mechanism of proteinuria from immune and nonimmune causes

A

Podocyte injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Nephritic syndrome complex

A

1 hematuria
2 oliguria and azotemia
3 hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Glomerular deposition of immune complexes resulting in proliferation and damage to glomerular cells and infiltration of leukocytes esp neutrophils

A

Acute Postinfectious Poststreptococcal Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Others pathogens in Postinfectious GN

A 
Pneumococcal
Staph
Mumps
Measles
Varicella
Hep B, C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Inciting agent in Acute Postinfectious GN

A

Group A Beta Hemolytic Strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Immune complex disease by complement activation of classical pathway
Hypocomplementemia
Granular deposits of IgG and complement on GBM

A

Poststrep GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Antigen implicated in PSGN

A

Streptococcal exotoxin B (Spe B)

Streptococcal GAPDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Increased cellularity of glomerular tuft (diffuse)
Infiltrating neutrophils and monocytes
Subendothelial, intramem or subepithelial humps of immune complexes against GBM
Granular deposits of IgG and complement cleared over 2 months

A

APSGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q 
Smoky brown gross hematuria
Oliguria/Azotemia
HTN
Low complement
Inc anti-streptolysin O
A

PSGN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Gross hematuria within 1-2d of URTI

Most common cause of recurrent microscopic or gross hematuria

A

IgA Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Most common nephritic glomerular disease revealed by renal biopsy

A

Iga Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Deposition of IgA in IgA nepropathy occurs in

A

mesangium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Systemic syndrome involving skin, GI, joints and kidneys with IgA deposition in mesangium

A

Henoch-Schonlein Purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Abnormality (inc) in IgA production and clearance

Antibodies against abnormally glycosylated IgA depositing in mesangium activating alternative complement pathway

A

IgA Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Secondary IgA nephropathy occurs in

A

Celiac disease

Liver disease defective hepatobiliary clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Immunoflorescence shows mesangial deposition of IgA with C3 either focal, diffuse or over crescentic

A

IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

IgA Nephropathy dx

65
Q

Hereditary disorders caused by mutation in genes encoding GBM proteins
Nerve deafness
Lens dislocation, Posterior cataracts, Corneal dystrophy

A

Hereditary nephritis

Alport Syndrome

66
Q

Foam cells with fat and mucopolysaccharide accumulation in interstitial cells
Thin basement membrane of glomeruli
Basketweave appearance of lamina densa

A

Hereditary nephritis

Alport syndrome

67
Q

X linked heterogenous mutation of gene encoding a5 type IV collagen
M>F, Renal failure
Persistent hematuria

A

Hereditary nephritis

Alport syndrome

68
Q 
Immunologically mediated
12% anti-GBM antibody mediated crescentic GN with or without lung involvement
44% immune complex GN with crescent
44% pauciimmune 
Severe glomerulus
A

Rapidly Progressive Glomerulonephritis

69
Q

Linear IgG

C3 on GBM sometimes on alveolar capillary producing hemoptysis and renal failure

A

Goodpasture Syndrome

Anti-GBM Antibody-Mediated Crescentic Glomerulonephritis

70
Q

Tx for goodpasture

A

Plasmapharesis

71
Q

Enlarged pale kidneys with petechial hemorrhage on cortex

Crescents of parietal cell and mac into Bowman’s space

A

Anti-GBM Antibody-Mediated Crescentic GN

72
Q

Lumpy bumpy pattern of staining for IgG/complement but does not respond to plasmapheresis

A

Immune-Complex Mediated Crescentic GN

73
Q

Segmental necrosis and GBM break with crescent formation

Granular pattern of immune complex

A

Immune-Complex Mediated Crescentic Glomerulonephritis

74
Q

Lack of anti-GBM antibodies or immune deposition
+ ANCA in serum
Sometimes part of microscopic polyangiitis, wegener granulomatosis

A

Pauci-immune Crescentic GN

75
Q

Segmental necrosis and GBM break with crescent formation

No deposits

A

Pauciimmune Crescentic GN

76
Q

Nephritic syndrome with rapid loss of renal fxn

77
Q

severe glomerular injury with necrosis and GBM breaks and proliferation of crescent

78
Q

Principal causative organism in acute pyelonephritis

A 
Enteric gram neg
E coli - mc
Proteus
Klebsiella
Enterobacter
Pseudomonas
79
Q

Most important and common route of bacterial infection in kidney

A

Ascending LUTI

also hematogenous at times

80
Q

Important cause of ascending infection allowing bacteria to ascend to pelvis

A

vesicoureteral reflux

20-40% in young children bec of congenital defect

81
Q

Open duct at tip of papilla where urine can be propelled up

A

Intrarenal reflux

82
Q

Discrete yellow raised abscess grossly apparent on renal surface
Liquefactive necrosis with abscess within parenchyma
Non affectation of glomeruli but of the rest

A

Acute Pyelonephritis

83
Q

Necrosis of papilla from DM, obstruction and analgesia

ischemic and suppurative of tips of renal pyramid
Gray white necrosis of 2/3 of pyramids
Coagulative necrosis

A

Papillary necrosis

84
Q

Uneven scarring
Scarring involving pelvis of calyxes
Calyceal deformity

A

chronic pyelonephritis

85
Q

Thyroidization with neutrophils
Chronic inflammation
Arteriolosclerosis
Glomerulosclerosis

A

Chronic Pyelonephritis

86
Q

Edema infiltration by mac and lymhpocytes

A

Drug induced nephritis

Methicillin, thiazide, rifampin - interstitial non-necrotizing granuloma with giant cell

NSAIDs- podocyte foot process effacement

87
Q 
Fever
Eosinophilia
Rash
Renal abnormality
15 days after drug intake
A

Drug induced Interstitial nephritis

88
Q

ATI by AKI

A

oliguria (<400mL/day)

89
Q

Proteinaceous cast in distal tubule and duct along with hemoglobin in ischemic ATI

A

Tam-horsfall protein

90
Q

Thickening and sclerosis of arterial wall and renal changes assoc with benign hypertension

A

Arterionephrosclerosis

Hyaline arteriosclerosis

91
Q

Arterionephrosclerosis implicate mutations in

A

apolipoprotein L1 gene as in FSGS

92
Q

Mutation in apolipoprotein L1 confers protection against

A

tyrpanosomal disease

93
Q

Symmetric atrophy
Diffuse fine granularity like grain leather
Hyaline arteriosclerosis
Fibroelastic hyperplasia of media

A

Arterionephrosclerosis

94
Q

BP >200/120

A

Malignant hypertension

95
Q

Malignant hypertension

A

Kidney vessel injury
Inc permeability to proteins, endothelial injury and platelet with fibrinoid necrosis of arterioles and small arteries
PDGF and intimal hyperplasia lead to hyperplastic arteriolosclerosis
Angiotensin II -> vasoconstriction
Inc Aldosterone

96
Q

Pinpoint petechial hemorrhage on cortical surface
Flea-bitten appearance
Fibrinoid necrosis of small vessel
Onion skin appearance (Hyperplastic arteriolosclerosis)

A

Malignant hypertension

97
Q

Malignant hypertension deaths 90% caused by

98
Q

Widespread thrombosis in microcirculation

Microangiopathic hemolytic anemia, thrombocytopenia, renal failure

A

Thrombotic microangiopathies

99
Q

Cause of thromoangiopathy

A 
Child HUS
Adult HUS
TTP
Drugs
Malignant hypertension scleroderma
100
Q

Thrombotic microangiopathy pathogenesis

A

Endothelial activation (HUS)
Platelet activation and aggregation (TTP)
Small vessel thrombosis

101
Q

75-% of cases following intestinal infection of Shiga toxin producing E coli or Shigella dysenteriae Type I targetting glomerular endothelial cell
Damage leads to thrombosis

A

Thrombotic microangiopathy

102
Q

Acquired defect in proteolytic cleavage of von Willebrand factor due to autoantibody or inherited defect

103
Q

Autoantibodies are directed against this disintegrin and metalloprotease with thrombospondin like motifs in TTP

A

ADAMST 13

autoantibody binding leads to loss of function and inc large vWF multimers

aggregation and thrombosis

104
Q

25% of children with HUS will develop this consequence secondary to scarring after 25 years

A

Renal insufficiency

CNS involvement
TTP>HUS

Kidney
HUS>TTP

105
Q

Progressive chronic renal damage assoc with HTN

Hyaline arteriosclerosis and narrowing of lumina with cortical atrophy

A

Arterionephrosclerosis

106
Q

Severe elevation of BP
Fibrinoid necrosis and hyperplasia of smooth muscle arterioles and artery
Petechial hemorrhage on cortical surface

A

Malignant hypertension

107
Q

Fibrin thrombi in glomeruli and small vessel -> AKI

A

Thrombotic microangiopathy

108
Q

Childhood HUS is caused by endothelial injury from

A

E coli toxin

109
Q

TTP is caused by

A

defect in vWF ADAMST 13 leading to thrombosis

110
Q 
Symmetrically contracted kidney
Diffusely granular scarring of glomeruli
Obliteration of glomeruli 
Marked interstitial fibrosis 
Unable to ascertain origin of injury
A

End stage kidney disease

111
Q

Pathophysiology of hereditary cystic disease

A

defect in ciliacentrosome complex of tubular epithelial cell

112
Q

1-5cm
transluscent gray glistening smooth membrane filled with clear fluid
single layer of cuboidal cell confined to cortex
Smooth contours on xray, avascular

A

Simple cyst

113
Q

Occur in kidneys of dialysis pxs
Both in cortex and medulla
Hematuria

A

Dialysis acquired cyst

114
Q

Defective gene in 85-90% of families in AD PKD

A

PKD1 on ch 16

115
Q

PKD1 encodes

A

complex cell membrane assoc proten Polycystin-1

116
Q

Renal cystic disease is a type of

A

Ciliopathy

bec polycystin is closely linked to primary cilium of tubular cells

117
Q

hairlike organelles projecting into lumina from apical surface serving as mechanosensor of fluid flow

A

Cilia

Polycystin mutation dysregulates mechanosensing

downregulates cell polarity, proliferation and cell to cell adhesion

118
Q

Mutations in 10-20% of cases caused by this gene

Residing on chromosome

Encoding protein

A

PKD2

4

Polycystin2

119
Q

Ca permeable membrane channel expressed in cilia

Similar phenotype but slower rate of progression

A

Polycystin2

120
Q

Large kidneys palpable with mass of cysts arising from nephrons on all levels
Some may develop asymptomatic liver cyst 1/3
Produces symptoms only on 4th decade of life
Intermittent gross hematuria

A

PCK

75% HTN
10-30% Saccular aneurysm of Circle of Willis and SAH

121
Q

Autosomal recessive childhood PKD is from a mutation in

A

PKHD1 gene encoding receptor protein fibrocystin at ch6

122
Q

Numerous small cyst in cortex and medulla
Spongy kidney
Bilateral
Multiple cysts in liver and bile duct prolif

A

AR Childhood PKD

123
Q

Most common form of nephronopthisis

A

Juvenile

Others: infantile, adolescent, medullary cystic

124
Q

Autosomal recessive form of nephronopthisis affects gene

A

NHP1-9

Encode components of cilia

125
Q 
Small contracted kidneys
Small cysts at corticomedullary junction
Chronic tubulointerstitial nephritis 
Polyuria polydypsia
Unexplained chronic renal failure (diff to dx)
A

Nephronopthisis

126
Q

AD inheritance by mutation in genes encoding polycystin1 and 2
10% of renal chronic failure
Very large kidneys with cyst

A

Adult Polycystic Kidney Disease

127
Q

Mutations in gene encoding fibrocystin
Assoc with liver abnormality
Numerous small cyst

A

Autosomal recessive PKD

128
Q

Cause of chronic kidney disease in children
AR
Mutations encoding epithelial cell protein nephrocysti
Contracted kidney with multiple
SMALL cyst

A

Nephronopthisis

129
Q

3 major stones

A

80% calcium oxalate or calcium phosphate
10% magnesium ammonium phosphate
6-9% uric acid or cysteine

130
Q

Factors contributing to stone formation (4)

A

Concentration of solute
Changes in pH
Bacterial infection
Inc urinary concentration of constituents exceeding solubility in urine (most important) supersaturation

131
Q

50% of patients with calcium stone have

A

hypercalciuria but not hypercalcemia

132
Q

50% of said patients with ca stone absorb ca in gut and excrete promptly in urine

A

absorptive hypercalciuria

133
Q

primary renal defect of calcium reabsorption

A

renal hypercalciuria

134
Q

Occurs in persistently alkaline urine from UTI

Proteus vulgaris, staph

A

Magnesium ammonium phosphate

135
Q

Tendency to excrete persistently acidic urine less than 5.5

Leukemia Gout

A

Uric acid stone

136
Q

Genetically determined defect in renal transport protein of AA
Acidic urine

A

Cysteine stone

137
Q

80% unilateral, stones form in

A

Pelves and calyx

bladder

138
Q

Branching structure creating cast on pelvis made up of magnesium phosphate

A

Staghorn calculi

139
Q

Atresia of ureter, valve formation, aberrant renal artery compression, renal ptosis, kinking of ureter

A

Congenital hydronephrosis

140
Q

Calculi, sloughed necrotic papillae

A

Acquired hydronephrosis foreign

141
Q

BPH, Prostate carcinoma, papilloma and carcinoma tumor, malignant disease

A

Proliferative lesion

142
Q

Prostatitis, uretritis, urethritis, retroperitoneal fibrosis

A

Inflammation

143
Q

SC damage with paralysis of bladder

A

Neurogenic

144
Q

Mild and reversible

A

Hydronephrosis from pregnancy

145
Q

Blockage below level of ureters

A

Bilateral hydronephrosis

146
Q

Dilation of pelvic calyx bec of continued filtration

Initial functional disturbance largely tubular manifested by impaired concentrating ability

A

Hydronephrosis

Serious damage occurs after 3 weeks of complete obstruction

3 months in incomplete

147
Q

Tumors of urinary tract are

A

twice as common as RCC

148
Q

benign tumor from intercalated cells

central stellate scar, plethora of mitochondria

A

Oncocytoma

149
Q

80-85% of primary malignant kidney tumors
2-3% of all cancers in adult
6-7th decade M>F

A

Renal Cell Carcinoma

150
Q

RCC risk factors

A

Smoker
HTN
Cadmium exposure
30x in px with dialysis acquired cyst

151
Q

65% most common
Assoc with homozygous loss of VHL TSP
Invades renal vein

A

Clear cell carcinoma

152
Q

CCC of Kidney strongly assoc to

A

von Hippel Lindau

153
Q

AD
Predisposition to hemangioblastoma of cerebellum and retina
Bilateral renal cyst

154
Q

Palpable abdominal mass
Painless hematuria
Dull flank pain

A

Renal cell carcinoma

155
Q

Assoc with increased expression and mutations of MET oncogene
Bilateral, multiple

A

Papillary renal cell

156
Q

Less common, not as clear as other renal cell carcinoma

A

Chromophobe renal cell carcinoma

157
Q

3rd most common organ CA in children

A

Wilms tumor

158
Q

Cells and tissue components of the tumor in Wilms are derived from

A

mesoderm

epithelial
serosa
blastema

Pathology (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions