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XIV - The Kidneys and Its Collecting System Flashcards

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USMLE® Step 1 flashcards
1
Q

A glomerular syndrome dominated by the acute onset of usually grossly visible hematuria, mildly moderate proteinuria, azotemia, edema and hypertension.

A

Acute nephritic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542

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2
Q

A glomerular syndrome characterized by heavy proteinuria, hypoalbunemia, severe edema, hyperlipidemia and lipiduria.

A

Nephrotic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542

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3
Q

Characterized by bacteriuria and pyuria, which may be asymptomatic.

A

Urinary tract infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542

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4
Q

Most common type of collagen found in glomerular basement membrane.

A

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 543

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5
Q

Most frequent cause nephrotic syndrome in children. Under light microscope, the glomerular basement membrane appears normal, but on electron microscopy, GBM shows uniform and diffuse effacement of foot processes of the podocytes. SEE SLIDE 14.1. Good response to corticosteroid therapy.

A

Minimal change disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550

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6
Q

A lesion characterized histologically by sclerosis affecting some but not all glomeruli and involving only segments of each affected glomerulus. SEE SLIDE 14.2.

A

Focal segmental glomerulosclerosis (FSGS)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550

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7
Q

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. SEE SLIDE 14.3. Often resistant to steroid therapy.

A

Membranous glomerulonephritis (Membranous Nephropathy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 551

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8
Q

Characterized by discrete SUBENDOTHELIAL electron-dense deposits in irregular granular pattern. SEE SLIDE 14.4.

A

Type I MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553

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9
Q

GBM is thickened, showing a “tram-track” appearance on PAS stains. There is proliferation of mesangial and endothelial cells as well as infiltrating leukocytes. SEE SLIDE 14.5.

A

MPGN(Membranoproliferative Glomerulonephritis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553

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10
Q

MPGN wherein the lamina densa and the SUBENDOTHELIAL space of the GBM are transformed into an irregular, ribbon-like extremely electron dense structure. SEE SLIDE 14.6.

A

Type II MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 554

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11
Q

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. SEE SLIDE 14.7.

A

Acute postinfectious (poststreptococcal) Glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555

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12
Q

Most common cause of recurrent microscopic or gross hematuria and is the most common glomerular disease revealed by renal biopsies.

A

IgA Nephropathy (Berger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555

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13
Q

Pathologic hallmark of this disease is the deposition of IgA in the mesangium. SEE SLIDE 14.8.

A

IgA nephropathy (Berger Disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556

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14
Q

Nephritis accompanied by nerve deafness, lens dislocation, posterior cataracts and corneal dystrophy. Pathogenesis is due to a mutation of one of the alpha chains of Type IV collagen, leading to these manifestations.

A

Alport syndrome(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 531

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15
Q

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. Interstitial cells also show foamy appearance.

A

Hereditay nephritis (Such as Alport Syndrome) (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 531

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16
Q

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. SEE SLIDE 14.9.

A

Rapidly Progressive Glomerulonephritis (Crescentic GN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557

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17
Q

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. SEE SLIDE 14.9.

A

Anti-Glomerular Basement Membrance Antibody (Type I) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557

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18
Q

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.

A

Immune Complex-Mediated (Type II) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558

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19
Q

CrGN defined by the lack of anti-GBM Ab and immune complex deposition. Glomeruli show segmental necrosis, negative immunofluorescence.

A

Pauci-immune (Type III) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558

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20
Q

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.

A

Chronic glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 559

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21
Q

A common suppurative inflammation of the kidney and renal pelvis caused by bacterial infection, either by hematogenous spread or through ascending infection.

A

Pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 560

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22
Q

Hallmark of this disease is scarring involving the pelvis or calyces, or both, leading to papillary blunting and marked calyceal deformities.

A

Chronic pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 562

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23
Q

Nephritis with prominent eosinophilic and mononuclear inflitrate, with pronounced edema in the INTERSTITIUM. SEE SLIDE 14.10

A

Acute Drug-Induced Interstitial Nephritis(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 536

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24
Q

A clinicopatholigic entity characterized by damaged tubular epithelial cells and clinically by acute suppression of renal function.Most common cause of acute renal failure. SEE SLIDE 14.11.

A

Acute tubular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564

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25
Q

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 (consisting of Tamm-Horsfall protein) in the distal tubules and collecting ducts.

A

Ischemic ATN(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 538

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26
Q

ATN characterized by necrosis and injury of the PCT with sparing of the tubular membranes.

A

Toxic ATN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566

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27
Q

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.

A

Initiation phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566

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28
Q

Phase of ATN where urine output falls markedly, between 50-400mL/day. Dominated by signs and symptoms of uremia and fluid overload.

A

Maintenance phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566

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29
Q

Phase of ATN characterized by a steady increase in urine volume, electrolyte imbalance and increased vulnerability to infection.

A

Recovery(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566

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30
Q

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. SEE SLIDE 14.12.

A

Analgesic nephropathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564

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31
Q

T-cell mediated immune reaction of the kidneys to an offending agent, characterized by interstitial inflammation, with abundant eosinophils and edema.

A

Drug-induced interstitial nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564

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32
Q

Renal changes in benign hypertension, associated with hyaline arteriolosclerosis, appearing as homogenous, pink hyaline thickening of arterial walls. Larger blood vessels show fibroelastc hyperplasia.

A

Benign nephrosclerosis. SEE SLIDE 14.13. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566

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33
Q

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 (hyperplastic arteriolosclerosis).

A

Malignant hypertension. SEE SLIDE 14.14. (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 540

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34
Q

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.

A

Thrombotic microangiopathies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568

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35
Q

One of the main causes of acute renal failure in children.

A

Hemolytic Uremic Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568

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36
Q

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.

A

Simple renal cyst(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569

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37
Q

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.

A

Adult polycystic kidney disease (APKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569

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38
Q

What is the pathology behind APKD?

A

Defective gene PKD1,which codes for polycystin-1.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569

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39
Q

Function of policystin-1?

A

Protein that is involved in cell-cell or cell-matrix adhesion.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569

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40
Q

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.

A

Childhood Polycystic Kidney Disease (CPKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 570

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41
Q

An under-recognized cause 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.

A

Medullary cystic disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571

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42
Q

Calculus formation at any level of the urinary collecting system.

A

Urolithiasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571

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43
Q

Most common composition of kidney stones.

A

Calcium oxalate and/or calcium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571

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44
Q

Most important cause of kidney stone formation.

A

Supersaturation(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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45
Q

Kidney stones occuring in patients with alkaline urine due to UTI, particularly Proteus vulgaris and Staphylococci.

A

Struvite stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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46
Q

Component of struvite stones.

A

Magnesium ammonium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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47
Q

Kidney stones seen in patients with gout and leukemias. Urine pH is decreased.

A

Uric acid stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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48
Q

Kidney stones associated with a defect in the renal transportation of certain amino acids. Forms in acidic urine.

A

Cystine stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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49
Q

Branching structures which create a cast of the renal pelvis and calyceal system.

A

Stagnorn calculi(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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50
Q

Most common composition of staghorn calculi.

A

Magnesium ammonium phosphate (Struvite)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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51
Q

Dilation of the renal pelvis and calyces, accompanied by atrophy of the renal parenchyma, caused by obstruction to urine outflow. Histologically, there is tubular dilation followed by atrophy and fibrous replacement of the tubular epithelium.

A

Hydronephrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572

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52
Q

Dilation of the ureters secondary to obstruction.

A

Hydroureter(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573

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53
Q

Most common malignant tumor of the kidney.

A

Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573

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54
Q

Tumors derived from renal tubular epithelium, located primarily at the cortex. With three common forms, clear cell, papillary renal cell and chromophobe renal carcinomas.

A

Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573

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55
Q

Most common form of renal cell carcinoma and associated with homozygous loss of the VHL tumor suppressor gene.

A

Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 549

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56
Q

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. Often invades the renal vein. SEE SLIDE 14.14.

A

Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 549

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57
Q

Renal carcinoma exhibiting varying degrees of papilla formation with fibrovascular cores. Cells have clear to pink cytoplasm. Associated with increased activity of MET oncogene. Tend to be bilateral.

A

Papillary renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 549

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58
Q

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.

A

Chromophobe-type renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574

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59
Q

Tumor of the urinary bladder, characterized as small, frond-like structures having delicate fibrovascular core covered by multilayered, well-differentiated transitional epithelium.

A

Benign papilloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575

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60
Q

Dominant clinical presentation of bladder carcinoma.

A

Painless hematuria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575

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61
Q

Protozoa associated with increased risk of bladder carcinoma.

A

Schistosoma haematobium(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576

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62
Q

Chemotherapeutic agent associated with development of hemorrhagic cystitis and increased risk of bladder carcinoma.

A

Cyclophosphamide(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576

63
Q

Electron Microscopy: Subepithelial humps

A

PSGN. SEE SLIDE 14.7. (TOPNOTCH)

64
Q

Light Microscopy: Hyalinized glomeruli

A

Chronic Glomerulonephritis. SEE SLIDE 14.15. (TOPNOTCH)

65
Q

Electron Microscopy: Subepithelial deposits

A

Membranous glomerulopathy. SEE SLIDE 14.3.(TOPNOTCH)

66
Q

Electron Microscopy: Loss of foot processes

A

Minimal Change Disease. SEE SLIDE 14.1 (TOPNOTCH)

67
Q

Electron Microscopy: Subendothelial deposits

A

MPGN Type 1. SEE SLIDE 14.4. (TOPNOTCH)

68
Q

Flourescence Microscopy: Linear IgG and C3

A

Goodpasture’s disease. SEE SLIDE 14.9. (TOPNOTCH)

69
Q

Light Microscopy: Normal, with lipid in tubules

A

Minimal Change Disease. SEE SLIDE 14.1 (TOPNOTCH)

70
Q

What are the 3 classic diagnostic features of RCC?

A
  1. Costovertebral Pain (TOPNOTCH)2. Palpable Mass3. Hematuria
71
Q

Among the 3 classic diagnostic features of RCC, which feature is the most reliable?

A

Hematuria (TOPNOTCH)

72
Q

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

A

Chromophobe RCC (TOPNOTCH)

73
Q

RCC morphology: rounder or polygonal shape and have abundant clear or granular cytoplasm with stains with glycogen and lipid

A

Clear Cell RCC (TOPNOTCH)

74
Q

RCC morphology: arise from DCT and are typically hemorrhagic and cystic

A

Papillary RCC (TOPNOTCH)

75
Q

RCC morphology: irregular channels lined by highly atypical epithelium with a hobnail pattern.

A

Collecting Duct Carcinoma (TOPNOTCH)

76
Q

RCC morphology: Interstitial foam cells and psamomma bodies

A

Papillary Carcinoma (TOPNOTCH)

77
Q

Urolithiasis: most common type

A

Calcium Oxalate stones (TOPNOTCH)

78
Q

Urolithiasis: staghorn calculi

A

Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)

79
Q

Urolithiasis: caused by genetic defects in the renal absorption of amino acids

A

Cystine stones (TOPNOTCH)

80
Q

Urolithiasis: associated with urea-splitting bacteria

A

Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)

81
Q

Urolithiasis: radiolucent

A

Uric Acid Stones (TOPNOTCH)

82
Q

Urolithiasis: common in patients with leukemia

A

Uric Acid Stones (TOPNOTCH)

83
Q

What is the most common cause of renal artery stenosis?

A

Occlusion by an atheromatous plaque at the origin of the renal artery (TOPNOTCH)

84
Q

What is the most common type of Fibromuscular Dysplasia; intimal, medial, or adventitial?

A

Medial (TOPNOTCH)

85
Q

Gross morphology: flea bitten appearance of the kidneys

A

Malignant Hypertension (TOPNOTCH)

86
Q

What are the two histological alterations in the blood vessels of patients with malignant hypertension?

A
  1. Fibrinoid Necrosis of arterioles2. Onion-skinning (TOPNOTCH)
87
Q

What are the 3 complications of acute pyelonephritis?

A
  1. Papillary Necrosis2. Pyonephrosis3. Perinephric Abscess (TOPNOTCH)
88
Q

Among the 3 complications of acute pyelonephritis, which one is mainly seen in diabetics and in those with urinary tract obstruction?

A

Papillary necrosis (TOPNOTCH)

89
Q

Morphology: acute neutrophilic exudate within tubules and the renal substance

A

Acute pyelonephritis (TOPNOTCH)

90
Q

ATN morphology: focal tubular epithelial necrosis at multiple points along the nephron, with large skip areas in between

A

Ischemic ATN (TOPNOTCH)

91
Q

ATN morphology: manifested by acute tubular injury with non specific tubular necrosis

A

Toxic ATN (TOPNOTCH)

92
Q

ATN morphology: Eosinophilic hyaline casts containing Tamm Horsfall protein

A

Ischemic ATN (TOPNOTCH)

93
Q

ATN morphology: severely injured cells that are not yet dead might contain large acidophilic inclusions

A

Mercuric Chloride ATN (TOPNOTCH)

94
Q

ATN morphology: accumulation of neutral lipids in injured cells

A

Carbon Tetrachloride poisoning (TOPNOTCH)

95
Q

ATN morphology: marked ballooning and hydrophic or vacuolar degeneration of proximal convulated tubules and often times calcium oxalate crystals are seen in the lumen

A

Ethylene Glycol ATN (TOPNOTCH)

96
Q

Morphology: patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, and tubular necrosis

A

Acute pyelonephritis (TOPNOTCH)

97
Q

Gross morphology: irregularly scarred; if bilateral, the involvement is asymmetric

A

Chronic pyelonephritis (TOPNOTCH)

98
Q

Gross morphology: kidneys are diffusely and symmetrically scarred

A

Chronic glomerulonephritis (TOPNOTCH)

99
Q

Morphology: hallmark is the coarse, discrete, corticomedullary scar overlying a dilated, blunted, or deformed calyx

A

Chronic pyelonephritis (TOPNOTCH)

100
Q

What is the main cause of renal dysfunction in Multiple Myeloma?

A

Bence Jones protein (TOPNOTCH)

101
Q

Morphology: bence jones tubular casts appear as pink to blue amorphous masses, sometimes concentrically laminated, often with fractured and angulated appearance, filling and distending the lumens

A

Multiple Myeloma (TOPNOTCH)

102
Q

Morphology: classic diagnostic finding is enlarged hypercellular glomeruli

A

PSGN (TOPNOTCH)

103
Q

Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla

A

Renal infarcts (TOPNOTCH)

104
Q

What is the first step in the pathogenesis of ascending infection that leads to pyelonephritis?

A

Colonization of the distal urethra and introits by coliform bacteria (TOPNOTCH)

105
Q

Morphology: “fibrin caps” and “capsular drops”

A

Diabetic kidney (TOPNOTCH)

106
Q

Morphology: diffuse increase in mesangial matrix and characteristic PAS positive nodules

A

Diabetic glomerulosclerosis (TOPNOTCH)

107
Q

Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region

A

Henoch Schonlein Purpura (TOPNOTCH)

108
Q

Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla

A

Renal infarcts (TOPNOTCH)

109
Q

What is the most common cause of clinical pyelonephritis?

A

Ascending infection (TOPNOTCH)

110
Q

Morphology: collapsed glomerular tufts and the crescent shaped mass of proliferating cells and leukocytes internal to Bowman capsule

A

Rapidly Progressive Glomerulonephritis (TOPNOTCH)

111
Q

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.

A

Childhood Hemolytic Uremic Syndrome(TOPNOTCH)

112
Q

Gross morphology: fine, leathery granularity of the surface of the kidney

A

Nephrosclerosis(TOPNOTCH)

113
Q

What is the emerging viral pathogen that causes pyelonephritis in kidney allografts?

A

Polyoma virus(TOPNOTCH)

114
Q

Morphology: enlarged tubular epithelial cells with nuclear inclusions

A

Polyoma kidney (TOPNOTCH)

115
Q

Electron microscopy: irregular thickening of the BM of the glomerulus, lamination of the lamina densa, and foci of rarefaction

A

Alport Syndrome (TOPNOTCH)

116
Q

Morphology: lamina densa of the GBM is transformed into an irregular, ribbon like, extremely electron dense structure

A

Dense Deposit Disease or Type II MPGN. SEE SLIDE 14.6. (TOPNOTCH)

117
Q

ESRD is defined as GFR less than how many percent of normal?

A

5%(TOPNOTCH)

118
Q

Renal failure is defined as GFR less than how many percent of normal?

A

20%-25%(TOPNOTCH)

119
Q

In renal insufficiency is defined as GFR less than how many percent of normal?

A

20%-50%(TOPNOTCH)

120
Q

Diminished renal reserve is define as GFR less than how many percent of normal?

A

50%(TOPNOTCH)

121
Q

An 18 y/o female presented with decreased in urine volume and edema. BP = 150/100. RBC cast was present in the urine. What is the most likely light microscopy pattern of this condition?

A

Acute glomerulonephritis (TOPNOTCH)

122
Q

An 18 y/o female presented with decreased in urine volume and edema. BP = 150/100. RBC cast was present in the urine. Two weeks prior, patient had sore throat and tonsillar swelling. What is the clinical impression?

A

PSGN (TOPNOTCH)

123
Q

Patient presented with fever, nausea, and flank pain. Urinalysis showed gross hematuria, increased pus cells, and presence of WBC cast. The most likely diagnosis is:

A

Acute pyelonephritis (TOPNOTCH)

124
Q

A 10 y/o male presents with generalized edema. BP is 90/60. Urinalysis showed Protein 3+, and presence of fatty cast. The most likely diagnosis is:

A

Nephrotic syndrome (TOPNOTCH)

125
Q

A 50 y/o patient with long standing hypertension and diabetes presented with complaints of pruritus, lower extremity edema, nausea and vomiting. Urinalysis showed presence of protein and waxy casts. Presence of waxy casts may indicate:

A

Chronic kidney disease (TOPNOTCH)

126
Q

A 5 y/o child presents with short history of facial edema that has now progressed to swelling of the feet and abdomen. Other symptoms include nausea, vomiting and abdominal pain. High levels of protein was noted in the urine. The parents reported that the child had fever few days before the development of the swelling. Biopsy was done. On light microscopy, no significant structural changes were noted except for the few lipids in the tubules. What can be expected on electron microscopy?

A

Loss of foot processes (TOPNOTCH)

127
Q

Characterized by rapid decline in GFR, with concurrent dysreglation of fluid and electrolyte balance, and retention of metabolic waste products.

A

Acute kidney injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 898

128
Q

Most frequent clinical presentation of this disease is rapidly progressive glomerulonephritis (with crescent formation). The anti-GBM antibodies cross react with pulmonary alveolar basement membranes to produce pulmonary hemorrhage, associated also with renal failure.

A

Goodpasture syndrome. SEE SLIDE 14.9. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 912

129
Q

The most common cause/mechanism of acut nephritic syndrome

A

immune-mediated glomerular injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 914

130
Q

Its presence in the urine represents lipoprotein resorbed by tubular epithelial cells and then shed along with injured tubular cells.Present in Nephrotic syndrome

A

Oval fat bodies(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 914

131
Q

Most frequent systemic causes of nephrotic syndrome

A

Diabetes, amyloidosis, SLE(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 914

132
Q

Most common cause of nephrotic syndrome in older adults

A

FSGS 35%, Membranous glomerulopathy 30% (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 524

133
Q

A 6 y/o male presented with massive proteinuria and edema. There is no hypertension or hematuria noted. Patient responded well to corticosteroid. The principal lesion in this condition:

A

Uniform and diffuse effacement of foot processes(Minimal change disease) (TOPNOTCH)

134
Q

Most common type of glomerulonephritis worldwide

A

IgA Nephropathy/Berger Disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 923

135
Q

Presents with gross hematuria after an infection of the respiratory, GIT or urinary tract, microscopic hematuria, with or without proteinuria. Hematuria last for several days, only to return every few months. These are the clinical features of what renal pathology?

A

IgA Nephropathy/Berger Disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 923

136
Q

This childhood syndrome consists of purpuric skin lesions, abdominal pain, intestinal bleeding, and arthralgia along with renal abnormalities.

A

Henoch Schonlein Purpura (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 926

137
Q

Most common renal manifestation of multiple myeloma

A

Chronic kidney disease (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 938

138
Q

True or False. Patients with malignant hypertension have markedly elevated levels of plasma renin.

A

True (TOPNOTCH)

139
Q

Most common cause of renal artery stenosis

A

Narrowing by an atheromatous plaque (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 940

140
Q

Following a prodrome of influenza-like or diarrheal symptoms, this syndrome presents with sudden onset of bleeding manifestation, severe oliguria, hematuria, associated with microangiopathic hemolytic anemia, thrombocytopenia and prominent neurologic changes.

A

Hemolytic Uremic Syndrome(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 942

141
Q

Earliest manifestation in bilateral partial obstruction of the ureter

A

Polyuria and nocturia(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 951

142
Q

Patient presents with flank pain, hematuria, and flank mass. Abdominal CT revealed a mass on the upper pole of the left kidney. CT guided biopsy showed a tumor that are made up of cell with basophilic cytoplasm and are non-papillary. The most likely histologic type of renal carcinoma described is:

A

Clear cell carcinoma(TOPNOTCH)

143
Q

Most common site of metastasis of renal cell carcinoma

A

Lungs(TOPNOTCH) Robbins Basic Pathology, 9th ed. P. 955

144
Q

A 32 year old woman develops tea-colored urine, periorbital edema, and decreasing urine output. A renal biopsy shows glomeruli with collapsed glomerular tufts and crescent-shaped masses of proliferating cells and leukocytes internal to the Bowman’s capsule. Which immunofluorescence pattern indicates that she is amenable to plasmapheresis? (A) linear staining of IgG and C3 along the GBM (B) granular “lumpy bumpy” deposits of Ig and/or complement in the GBM and/or mesangium (C) no distinct Ig or complement deposition (D) none of the above

A

linear staining of IgG and C3 (Anti-GBM antibody CrGN/Type I) (B - Type II - immune complex mediated; C - Type III - pauci immune; neither are helped by plasmapharesis). SEE SLIDE 14.9. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557-558.

145
Q

An 18 year old female has sore throat and fever. The next day, she develops tea-colored urine for a week, which spontaneously resolves. Six months later, her hematuria recurs. She is also found to have increased serum IgA. Which of the following renal biopsy findings is consistent with her disease? (A) presence of C1q and C4 deposits in the glomeruli (B) IgA deposits in the mesangium (C) granular deposits of IgG and complement (D) subepthelial “humps” on electron microscopy

A

IgA deposits in the mesangium (Berger disease) (all other choices are seen in PSGN, which develops 1 to 4 weeks after infection). SEE SLIDE 14.8.

146
Q

A 10 year old male presents with periorbital edema. Urinalysis shows persistent albuminuria. Which renal biopsy finding will indicate that he will respond to short coursse corticosteroid therapy? (A) normal-looking glomerulus by light miscroscopy, with podocyte foot process effacement on electron microscopy (B) some glomeruli with segmental increased mesangial matrix and hyaline deposits (C) diffusely thickened GBM on light microscopy, with subepithelial deposits in a “spike and dome” pattern on electron microscopy (D) a “tram track” appearance of the thickened GBM on PAS stain

A

normal-looking glomerulus on light microscopy, with podocyte foot process effacement on electron microscopy (minimal change disease) (B - FSGS; C - membranous GN; D - membranoproliferative GN) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550-554

147
Q

A 38 year old male presents with gross hematuria. Imaging workup shows three renal masses. He undergoes radical nephrectomy, where gross examination of the kidney specimen showed yellowish masses with foci of hemorrhage. The mass nearest the hilum appears to infiltrate into the renal vein. On histopathology, the masses are composed of sheets of clear, vacuolated cells with round to oval nuclei, and occasional mitoses. The patient also had a history of brain surgery at 14 years old for a cerebellar hemangioblastoma. This association raises the possibility which syndrome? (A) Li Fraumeni (B) Von Hippel-Lindau (C) Tuberous sclerosis (D) Gardner

A

von Hippel-Lindau (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573-74

148
Q

Which of the following is the most important prognostic factor in bladder tumors? (A) histologic grade (B) painless hematuria (C) histologic type (D) depth of invasion

A

depth of invasion (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576

149
Q

One of the most common causes of nephrotic syndrome in adults. Initially presents as increased mesangial matrix, obliterated capillary lumina, with deposition of hyaline masses and lipid droplets. In time, causes global sclerosis.

A

FSGS (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.526

150
Q

Pathogenesis: Auto-antibodies react to endogenous or planted glomerular antigens, most recognized of which is the phospholipase A2 receptor. Immune complex formation activates membrane attack complex (COMPLEMENT C5 to C9) which damages mesangial cells and podocytes.

A

Membranous nephropathy (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.526

151
Q

Pathogenesis: Excessive complement activation, with autoantibodies against C3 CONVERTASE, which lead to uncontrolled cleavage of C3 and activation of the pathway.

A

Dense deposit disease (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.527

152
Q

How do you differentiate the three main causes of crescenteric glomerulonephritis from one another (Anti-GBM-mediated, Immune complex-mediated, and pauci-immune)?

A

Anti-GBM on IF shows LINEAR IgG and C3 deposits; Immune-complex mediated on IF shows granular pattern; pauci-immune on IF shows NO deposits (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.532-533

153
Q

Pathognomonic gross feature of papillary necrosis.

A

Gray-white to yellow necrosis of the apical two thirds of the pyramids. Remember also the three predisposing conditions: Diabetes, urinary tract obstruction, and analgesic abuse. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.535

154
Q

Grossly, kidneys are symmetrically atrophic due to ischemia. Histology will reveal hyaline arteriolosclerosis (extensive hyaline thickening) in the small arteries and arterioles and fibroelastic hyperplasia in the larger blood vessels. It’s an important renal cause of seconday hypertension.

A

Arterionephrosclerosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.539

medical board (24 decks)

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