XIV - The Kidneys and Its Collecting System (with pics) Flashcards Preview

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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 electron microscopy, GBM shows uniform and diffuse effacement of foot processes of the podocytes. SEE SLIDE 14.1. 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. SEE SLIDE 14.2.

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. SEE SLIDE 14.3. 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. SEE SLIDE 14.4.

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. SEE SLIDE 14.5.

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. SEE SLIDE 14.6.

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. SEE SLIDE 14.7.

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. SEE SLIDE 14.8.

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. Pathogenesis is due to a mutation of one of the alpha chains of Type IV collagen, leading to these manifestations.

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

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. Interstitial cells also show foamy appearance.

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

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. SEE SLIDE 14.9.

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. SEE SLIDE 14.9.

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 in the INTERSTITIUM. SEE SLIDE 14.10

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

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. SEE SLIDE 14.11.

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

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

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. SEE SLIDE 14.12.

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