Fang 2 Flashcards

1
Q

NephrITIC vs nephrOTIC syndrome

A
  • Nephrtic syndorme
    • HTN
    • HEMATURIA
    • RBC cast
  • NephrOTIC syndrome
    • PROTEINURIA > 3.5g/24hr
    • generalized PITTING EDEMA (due to HYPOALBUMINEMIA
    • hypercholesterolemia (due to hypoalbuminemia)
    • FATTY CASTS
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2
Q

NephrITIC syndrome

A
  • Due to breaks in the glomerular capillary loop
    • erythrocytes spill out into urinary space
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3
Q

nephrotic syndrome

A
  • due to glomerular capillary filtration defects
    • epithelial cell foot process EFFACEMENT AND DETACHEMENT
      • shortening and or thinning of podocytes
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4
Q

Chronic renal failure pathology

A
  • Caused by untreated pathology leads to scarring/fibrosed kidney
    • slow rise in creatinine over months to years
  • GrOSS
    • kidneys are small
    • cortex is thinned
    • increase pelvic fact
  • MICRO
    • glomerular sclerosis
    • interstitial fibrosis
    • tubular atrophy
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5
Q

Causes of NEPHROTIC SYNDROME

A
  • Priamry
    • minimal change disease
    • focal segmental glomerulosclerosis
    • membranous nephropathy
  • Secondary
    • Diabetic nephropathy
    • Amyloidosis, SLE, DRUGS, infections, malginancies etc
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6
Q

Minimal chagne glomerulopathy

A
  • most COMMON CAUSE of nephrotic syndrome in CHILDREN (2-6)
  • normal glomeruli on LM and Iimmunofluorescence
  • EFFACEMENT OF FOOT PROCESSES ON ELECTRON MICROSCOPE
    • DIFFUSE EPITHELIAL FOOT PROCESS EFFACEMENT
  • lipid in tubular cells
  • usually respond to steroids (cortisol)
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7
Q

Focal segmental GlomeruloSclerosis (FSGS)

A
  • Proteinuria is defining feature
  • PROGRESSIVE GLOMERULAR SCARRING
  • early in disease course: focal and segmental –> progress to diffuse and global
  • Symtpoms
    • HYPERTENSION
    • common in African americans
    • microscopic HEMATURIA
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8
Q

Causes of FSGS

A
  • 80% are IDIOPATHIC
  • VIRUS associated
    • HIV, CMV, EBV, etc
  • DRUG-INDUCED associated
    • HEROIN, anabolic steroids
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9
Q

Pathology of FSGS

A
  • LM = SEGMENTAL SCLEROSIS (hyalinosis)
  • IF = mild IgM and CS or negative
  • EM = diffuse epithelial cell injury (foot process effacement)
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10
Q

Membranous glomerulopathy

A
  • DEPOSITION OF Ag-Ab COMPLEXES
  • LM = thickened capillary walls; SPIKES on silver stain
  • IF = GRANULAR IgG and C3 along the GBM
  • EM = subEPITHELIAL DEPOSITS

SEE POWERPOINT FOR PICS

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11
Q

Membranoproliferative GLOMERULONEPHRITIS (MPGN)****

A
  • nephrotic syndrome with a nephritic component (hematuria)
  • steroids and immunosuppressive drugs are NOT effect
  • MESENGIAL HYPERCELLULARITY + CAPILLARY wall remodeling (with the formation of double contours)
  • TYPES
    • Type I = subendothelial depositis
    • Type 2 = intramembranous deposits
      • predominant MESANGIAL INVOLVEMENT
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12
Q

MPGN TYPE I

A
  • LM = TRAM TRACKS (on silver stain)
  • IF = granular CS (and often with IgG)
  • EM = subendothelial and mesangial depositis (SubENDO vs SubEPI in membranous GN)
    • mesangial interpositioning between endothelial cels and GBM
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13
Q

MPGN TYPE 2

A
  • LM = tram track (on silver stain
  • IF = C3 ONLY (NO IgG)
  • EM = INTRAMEMBRANE DEPOSIT
    • lamina densa - electron dense material

LOW SERUM C3!!!

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14
Q

Acute nephrITIC syndrome

A
  • caused by 2 conditions
    • DIFFUSE PROLIFERATIVE glomerulonephritis
      • ACUTE POST-STREP GN
    • CRESCENTIC GLOMERULONEPHRITIS
      • Goodpasture’s disease
      • lupus nephritis
      • ANCA-assocaited diseases
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15
Q

Acute glomerulonephritis

A
  • Hematuria, azotemia, oliguria, HTN
  • IN CHILDREN after a latent period of 1-3 WEEKS following STREP INFECTION
    • POST-INFECTIOUS
  • LOW COMPLEMENT 3 LEVELS (vs MPGN)
  • 95% of recovery
  • LM = diffuse proliferative GN with NEUTROPHILS
  • IF = scattered granular (starry sky) IgG, IgM, and CS along GBM and in mesenagium
  • EM = SUBEPITHELIAL HUMPS
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16
Q

Crescentic glomerulonephritis

A
  • GLOMERULAR CRESCENTS ARE FORMED
    • SEVERE glomerular injury
  • CRESCENTIC
    • anti-GMB Ab
    • IC’s
    • ANti-PMN Ab
  • Components of crescentic
    • Anti-fibrinogen IF causes Fibrin to form and there is then proliferation of epithelial cells from the parietal wall of bowman’s capsul as well as influx of monocytes/macrophages resulting in Crescent formation
17
Q

Types of Crescent glomerulonephritis

A
  • Type I = Linear capilalry loop (cigarette smoke like structures in IF)
    • good pasture disease (serum anti-GBM antibody will be elevated
    • Tx with steroids, cytotoxic agens and plasmapheresis
  • Type 2 = Lumpy Bumpy world (Granular deposits in mesangium or capillary loops
    • SLE
  • Type 3 = Negative (or few) depositis
    • elevated serum anti-neutrophil cytoplasmic antibodies (ANCA)
      • ANCA-associated diseases
18
Q

Rapidly Progressive GlomeruloNephritis (RPGN)

A
  • Clinical definition, NOT a specific pathologic one, but most associated with CRESCENTIC GN