Flashcards in XIV - The Kidneys and Its Collecting System Deck (132):
1
A glomerular syndrome dominated by the acute onset of usually grossly visible hematuria, mildly moderate proteinuria, azotemia, edema and hypertension.
Acute nephritic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
2
A glomerular syndrome characterized by heavy proteinuria, hypoalbunemia, severe edema, hyperlipidemia and lipiduria.
Nephrotic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
3
Characterized by bacteriuria and pyuria, which may be asymptomatic.
Urinary tract infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
4
Most common type of collagen found in glomerular basement membrane.
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 543
5
Most frequent cause nephrotic syndrome in children. Under light microscope, the glomerular basement membrane appears normal, but on electrin microscopy, GBM shows uniform and diffuse effacement of foot processes of the podocytes. Good response to corticosteroid therapy.
Minimal change disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
6
A lesion characterized histologically by sclerosis affecting some but not all glomeruli and involving only segments of each affected glomerulus.
Focal segmental glomerulosclerosis (FSGS)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
7
Slowly progressive disease characterized by the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane. Histologically, there is diffuse thickening of the BM. (+) spike and dome pattern on electron microscopy. Often resistant to steroid therapy.
Membranous glomerulonephritis (Membranous Nephropathy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 551
8
Characterized by discrete SUBENDOTHELIAL electron-dense deposits in irregular granular pattern.
Type I MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
9
GBM is thickened, showing a "tram-track" appearance on PAS stains. There is proliferation of mesangial and endothelial cells as well as infiltrating leukocytes.
MPGN(Membranoproliferative Glomerulonephritis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
10
MPGN wherein the lamina densa and the SUBENDOTHELIAL space of the GBM are transformed into an irregular, ribbon-like extremely electron dense structure.
Type II MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 554
11
Caused by glomerular deposition of immune complexes resulting in diffuse proliferation and swelling of resident glomerular cells. There is uniformly increased cellularity of glomerular tufts. Electron microscopy show subepithelial "humps" against the GBM, with granular deposits of IgG and complement.
Acute postinfectious (poststreptococcal) Glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
12
Most common cause of recurrent microscopic or gross hematuria and is the most common glomerular disease revealed by renal biopsies.
IgA Nephropathy (Berger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
13
Pathologic hallmark of this disease is the deposition of IgA in the mesangium.
IgA nephropathy (Berger Disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556
14
Nephritis accompanied by nerve deafness, lens dislocation, posterior cataracts and corneal dystrophy.
Alport syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556
15
Caused by mutations in genes encoding GBM collagen, manifest as hematuria and slowly progressing proteinuria and declining renal function. GBM has "basket-weave" appearance due to splitting and lamination of the lamina densa.
Hereditay nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
16
A clinical syndrome characterized by rapid and progressive lossof renal function with features of nephritic syndrome,often with severe oliguria. Histologic feature is the presence of crescents.
Rapidly Progressive Glomerulonephritis (Crescentic GN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
17
CrGN characterized by linear deposits of IgG and C3 on the GBM. anti-GBM Ab also bind to pulmonary alveolar capillary basement membranes to produce pulmonary hemorrhages associated with renal failure.
Anti-Glomerular Basement Membrance Antibody (Type I) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
18
CrGN which are immune complex-mediated disorders, as a complication of any of the IC nephritides including PSGN, IgA Nephropathy and HSP. There is segmental necrosis and characteristic granular pattern of the underlying immune complex disease.
Immune Complex-Mediated (Type II) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
19
CrGN defined by the lack of anti-GBM Ab and immune complex deposition. Glomeruli show segmental necrosis, negative immunofluorescence.
Pauci-immune (Type III) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
20
An important cause of end-stage renal disease presenting as chronic renal failure. Kidneys are symmetrically contracted, surfaces are red-brown and diffusely granular. Glomeruli are obliterated with marked interstitial fibrosis.
Chronic glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 559
21
A common suppurative inflammation of the kidney and renal pelvis caused by bacterial infection, either by hematogenous spread or through ascending infection.
Pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 560
22
Hallmark of this disease is scarring involving the pelvis or calyces, or both, leading to papillary blunting and marked calyceal deformities.
Chronic pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 562
23
Nephritis with prominent eosinophilic and mononuclear inflitrate, with pronounced edema.
Acute Drug-Induced Interstitial Nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 563
24
A clinicopatholigic entity characterized by damaged tubular epithelial cells and clinically by acute suppression of renal function.Most common cause of acute renal failure.
Acute tubular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
25
Characterized by necrosis of short segments of the tubules, seen in the straight portions of the PCT and TALOH. There is a variety of tubular injuries, associated with proteinaceous casts in the distal tubules and collecting ducts.
Ischemic ATN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
26
ATN characterized by necrosis and injury of the PCT with sparing of the tubular membranes.
Toxic ATN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
27
Phase of ATN lasting about 36 hrs, dominated by the inciting medical, surgical or obstetric event. Slight decline in renal output and a rise in serum creatinine.
Initiation phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
28
Phase of ATN where urine output falls markedly, between 50-400mL/day. Dominated by signs and symptoms of uremia and fluid overload.
Maintenance phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
29
Phase of ATN characterized by a steady increase in urine volume, electrolyte imbalance and increased vulnerability to infection.
Recovery(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
30
Chronic interstitial nephritis associated with renal papillary necrosis. The necrotic papillae appear yellowish-brown, showing coagulative necrosis associated with loss of cellular detail with preservation of tubular outlines.
Analgesic nephropathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
31
T-cell mediated immune reaction of the kidneys to an offending agent, characterized by interstitial inflammation, with abundant eosinophils and edema.
Drug-induced interstitial nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
32
Renal changes in benign hypertension, associated with hyaline arteriolosclerosis, appearing as homogenous, pink hyaline thickening of arterial walls. Larger blood vessels show fibroelastc hyperplasia.
Benign nephrosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
33
Acute renal injury assiciated with malignant hypertension. The kidneys show small, pinpoint petechial hemorrhages, "flea-bitten" appearance. Concentric arrangement of cells, described as "onion-skin" lesions cause marked narrowing of arterioles and small arteries.
Malignant nephrosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 567
34
Characterized by widespread thrombosis and presence of fibrin thrombi in glomeruli and small vessels resulting in acute renal failure. Consequence of childhood HUS and TTP.
Thrombotic microangiopathies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568
35
One of the main causes of acute renal failure in children.
Hemolytic Uremic Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568
36
Innocuous lesions of the kidney, 1-5cm in diameter, translucent, lined by a gray, glistening, smooth membrane, filled with clear fluid. Composed of a single layer of cuboidal or flattened cuboidal epithelium, usually confined to the cortex.
Simple renal cyst(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
37
Autosomal dominant. Kidneys are enlarged, composed solely of cysts without intervening parenchyma. Cysts are filled with clear or turbid fluid. Cysts may arise at any level of the nephron, with variable, often atrophic lining.
Adult polycystic kidney disease (APKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
38
What is the pathology behind APKD?
Defective gene PKD1,which codes for polycystin-1.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
39
Function of policystin-1?
Protein that is involved in cell-cell or cell-matrix adhesion.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
40
Autosomal recessive. There are numerous small cysts in the cortex and medulla, giving the kidney a "sponge-like" appearance. Cysts have uniform cuboidal epithelium. Associated with multiple cysts in the liver.
Childhood Polycystic Kidney Disease (CPKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 570
41
An under-recognized vause of chronic kidney disease in children and young adults, associated with mutations in several genes that encode neohrocystins that may be involved in ciliary function. Kidneys are contracted and contain multiple cysts.
Medullary cystic disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
42
Calculus formation at any level of the urinary collecting system.
Urolithiasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
43
Most common composition of kidney stones. Precipitates in the presence of alkaline urine.
Calcium oxalate and/or calcium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
44
Most important cause of kidney stone formation.
Supersaturation(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
45
Kidney stones occuring in patients with alkaline urine due to UTI, particularly Proteus vulgaris and Staphylococci.
Struvite stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
46
Component of struvite stones.
Magnesium ammonium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
47
Kidney stones seen in patients with gout and leukemias. Urine pH is decreased.
Uric acid stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
48
Kidney stones associated with a defect in the renal transportation of certain amino acids. Forms in acidic urine.
Cystine stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
49
Branching structures which create a cast of the renal pelvis and calyceal system.
Stagnorn calculi(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
50
Most common composition of staghorn calculi.
Magnesium ammonium phosphate (Struvite)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
51
Dilation of the renal pelvis and calyces, accompanied by atrophy of the renal parenchyma, caused by obstruction to urine outflow.
Hydronephrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
52
Dilation of the ureters secondary to obstruction.
Hydroureter(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
53
Most common malignant tumor of the kidney.
Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
54
Tumors derived from renal tubular epithelium, located primarily at the cortex. With three common forms, clear cell, papillary renal cell and chromophobe renal carcinomas.
Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
55
Most common form of renal cell carcinoma.
Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
56
Renal carcinoma, usually solitary and large, spherical masses reaching up to 15cms in diameter. Cut surface show yellow orange to gray-white, with prominent areas of cystic softening and hemorrhage. Cells appear vacuolated or may be solid.
Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
57
Renal carcinoma exhibiting varying degrees of papilla formation with fibrovascular cores. Cells have clear to pink cytoplasm.
Papillary renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
58
Renal cell carcinoma which tends to be tan-brown, cells have clear, flocculent cytoplasm with very prominent, distinct cell membranes. Nuclei surrounded by halos of cleared cytoplasm.
Chromophobe-type renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
59
Tumor of the urinary bladder, characterized as small, frond-like structures having delicate fibrovascular core covered by multilayered, well-differentiated transitional epithelium.
Benign papilloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575
60
Dominant clinical presentation of bladder carcinoma.
Painless hematuria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575
61
Protozoa associated with increased risk of bladder carcinoma.
Schistosoma haematobium(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576
62
Chemotherapeutic agent associated with development of hemorrhagic cystitis and increased risk of bladder carcinoma.
Cyclophosphamide(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576
63
Electron Microscopy: Subepithelial humps
PSGN (TOPNOTCH)
64
Light Microscopy: Hyalinized glomeruli
Chronic Glomerulonephritis (TOPNOTCH)
65
Electron Microscopy: Subepithelial deposits
Membranous glomerulopathy (TOPNOTCH)
66
Electron Microscopy: Loss of foot processes
Minimal Change Disease (TOPNOTCH)
67
Electron Microscopy: Subendothelial deposits
MPGN Type 1 (TOPNOTCH)
68
Flourescence Microscopy: Linear IgG and C3
Goodpasture's disease (TOPNOTCH)
69
Light Microscopy: Normal, with lipid in tubules
Minimal Change Disease (TOPNOTCH)
70
What is the most common type of Renal Cell Carcinoma (RCC)?
Clear cell RCC (TOPNOTCH)
71
What are the 3 classic diagnostic features of RCC?
1. Costovertebral Pain (TOPNOTCH)2. Palpable Mass3. Hematuria
72
Among the 3 classic diagnostic features of RCC, which feature is the most reliable?
Hematuria (TOPNOTCH)
73
RCC morphology: pale eosinophilic cells, often with a perinuclear halo, arranged in solid sheets with a concentration of the largest cells around the blood vessels
Chromophobe RCC (TOPNOTCH)
74
RCC morphology: rounder or polygonal shape and have abundant clear or granular cytoplasm with stains with glycogen and lipid
Clear Cell RCC (TOPNOTCH)
75
RCC morphology: arise from DCT and are typically hemorrhagic and cystic
Papillary RCC (TOPNOTCH)
76
RCC morphology: irregular channels lined by highly atypical epithelium with a hobnail pattern.
Collecting Duct Carcinoma (TOPNOTCH)
77
RCC morphology: Interstitial foam cells and psamomma bodies
Papillary Carcinoma (TOPNOTCH)
78
Urolithiasis: most common type
Calcium Oxalate stones (TOPNOTCH)
79
Urolithiasis: staghorn calculi
Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)
80
Urolithiasis: caused by genetic defects in the renal absorption of amino acids
Cystine stones (TOPNOTCH)
81
Urolithiasis: associated with urea-splitting bacteria
Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)
82
Urolithiasis: radiolucent
Uric Acid Stones (TOPNOTCH)
83
Urolithiasis: common in patients with leukemia
Uric Acid Stones (TOPNOTCH)
84
What is the most common cause of renal artery stenosis?
Occlussion by an atheromatous plaque at the origin of the renal artery (TOPNOTCH)
85
What is the most common type of Fibromuscular Dysplasia; intimal, medial, or adventitial?
Medial (TOPNOTCH)
86
Gross morphology: flea bitten appearance of the kidneys
Malignant Hypertension (TOPNOTCH)
87
What are the two histological alterations in the blood vessels of patients with malignant hypertension?
1. Fibrinoid Necrosis of arterioles2. Onion-skinning (TOPNOTCH)
88
What are the 3 complications of acute pyelonephritis?
1. Papillary Necrosis2. Pyonephrosis3. Perinephric Abscess (TOPNOTCH)
89
Among the 3 complications of acute pyelonephritis, which one is mainly seen in diabetics and in those with urinary tract obstruction?
Papillary necrosis (TOPNOTCH)
90
Morphology: acute neutrophilic exudate within tubules and the renal substance
Acute pyelonephritis (TOPNOTCH)
91
ATN morphology: focal tubular epithelial necrosis at multiple points along the nephron, with large skip areas in between
Ischemic ATN (TOPNOTCH)
92
ATN morphology: manifested by acute tubular injury with non specific tubular necrosis
Toxic ATN (TOPNOTCH)
93
ATN morphology: Eosinophilic hyaline casts containing Tamm Horsfall protein
Ischemic ATN (TOPNOTCH)
94
ATN morphology: severely injured cells that are not yet dead might contain large acidophilic inclusions
Mercuric Chloride ATN (TOPNOTCH)
95
ATN morphology: accumulation of neutral lipids in injured cells
Carbon Tetrachloride poisoning (TOPNOTCH)
96
ATN morphology: marked ballooning and hydrophic or vacuolar degeneration of proximal convulated tubules and often times calcium oxalate crystals are seen in the lumen
Ethylene Glycol ATN (TOPNOTCH)
97
Morphology: patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, and tubular necrosis
Acute pyelonephritis (TOPNOTCH)
98
Gross morphology: irregularly scarred; if bilateral, the involvement is asymmetric
Chronic pyelonephritis (TOPNOTCH)
99
Gross morphology: kidneys are diffusely and symmetrically scarred
Chronic glomerulonephritis (TOPNOTCH)
100
Morphology: hallmark is the coarse, discrete, corticomedullary scar overlying a dilated, blunted, or deformed calyx
Chronic pyelonephritis (TOPNOTCH)
101
What is the main cause of renal dysfunction in Multiple Myeloma?
Bence Jones protein (TOPNOTCH)
102
Morphology: bence jones tubular casts appear as pink to blue amorphous masses, sometimes concentrically laminated, often with fractured and angulated appearance, filling and idstending the lumens
Multiple Myeloma (TOPNOTCH)
103
Morphology: narrowing of the lumens of arterioles and small arteries, caused by thickening and hyalinization of the walls (hyaline arteriolosclerosis)
Benign nephrosclerosis (TOPNOTCH)
104
Morphology: classic diagnostic finding is enlarged hypercellular glomeruli
PSGN (TOPNOTCH)
105
Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla
Renal infarcts (TOPNOTCH)
106
What is the most common cause of clinical pyelonephritis?
Ascending infection (TOPNOTCH)
107
What is the first step in the pathogenesis of ascending infection that leads to pyelonephritis?
Colonization of the distal urethra and introits by coliform bacteria (TOPNOTCH)
108
Morphology: "fibrin caps" and "capsular drops"
Diabetic kidney (TOPNOTCH)
109
Morphology: diffuse increase in mesangial matrix and characteristic PAS positive nodules
Diabetic glomerulosclerosis (TOPNOTCH)
110
Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region
Henoch Schonlein Purpura (TOPNOTCH)
111
Morphology: "tram track" "double contour" glomerular capillary walls
Membranoproliferative Glomerulonephritis (TOPNOTCH)
112
Morphology: collapsed glomerular tufts and the crescent shaped mass of proliferating cells and leukocytes internal to Bowman capsule
Rapidly Progressive Glomerulonephritis (TOPNOTCH)
113
Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla
Renal infarcts (TOPNOTCH)
114
What is the most common cause of clinical pyelonephritis?
Ascending infection (TOPNOTCH)
115
What is the first step in the pathogenesis of ascending infection that leads to pyelonephritis?
Colonization of the distal urethra and introits by coliform bacteria (TOPNOTCH)
116
Morphology: "fibrin caps" and "capsular drops"
Diabetic kidney (TOPNOTCH)
117
Morphology: diffuse increase in mesangial matrix and characteristic PAS positive nodules
Diabetic glomerulosclerosis (TOPNOTCH)
118
Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region
Henoch Schonlein Purpura (TOPNOTCH)
119
Morphology: "tram track" "double contour" glomerular capillary walls
Membranoproliferative Glomerulonephritis (TOPNOTCH)
120
Morphology: collapsed glomerular tufts and the crescent shaped mass of proliferating cells and leukocytes internal to Bowman capsule
Rapidly Progressive Glomerulonephritis (TOPNOTCH)
121
Morphology: glomeruli show thickening and sometimes splitting of capillary walls, due largely to endothelial and subendothelial swelling, and deposits of fibrin-related materials in the capillary lumens, subendothelially, and in the mesangium.
Childhood Hemolytic Uremic Syndrome(TOPNOTCH)
122
Gross morphology: flea bitten appearance of the kidney
Malignant hypertension(TOPNOTCH)
123
Gross morphology: fine, leathery granularity of the surface of the kidney
nephrosclerosis(TOPNOTCH)
124
What is the emerging viral pathogen that causes pyelonephritis in kidney allografts?
Polyoma virus(TOPNOTCH)
125
Morphology: enlarged tubular epithelial cells with nuclear inclusions
Polyoma kidney (TOPNOTCH)
126
Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region
Henoch Schonlein Purpura (TOPNOTCH)
127
Electron microscopy: irregular thickening of the BM of the glomerulus, lamination of the lamina densa, and foci of rarefaction
Alport Syndrome (TOPNOTCH)
128
Morphology: lamina densa of the GBM is transformed into an irregular, ribbon like, extremely electron dense structure
Dense Deposti Disease or Type II MPGN (TOPNOTCH)
129
ESRD is defined as GFR less than how many percent of normal?
5%(TOPNOTCH)
130
Renal failure is defined as GFR less than how many percent of normal?
20%-25%(TOPNOTCH)
131
In renal insufficiency is defined as GFR less than how many percent of normal?
20%-50%(TOPNOTCH)
132