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37 Cards in this Set
- Front
- Back
Definition of the nephrotic disease
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Spilling more than 3.5 g of protein in the urine per day.
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Primary Focal and Segmental Glomerulosclerosis: light microscopy
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See scarring of glomeruli
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Primary Focal and Segmental Glomerulosclerosis: Electron microscopy
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See effacement of podocytes in every glomerulus.
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What is the pathological consequence of FSGS and glomerular sclerosis in general?
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Hyperfiltration
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Minimal change disease: light microscopy
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Looks normal, nothing by immunofluorescence
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Minimal change disease: electron microscopy
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Effacement of podocytes
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If a nephron becomes sclerotic, what happens to the other nephons
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They become stressed and eventually become sclerotic themselves
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Minimal change disease: immune complexes?
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No
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FSGS: immune complexes?
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No
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What is the main difference between primary FSGS and secondary FSGS?
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In secondary FSGS you see some preservation of foot processes on EM
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Membranous Nephrophathy: cause?
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Immune complexes on the subEPITHELIAL side of the basement membrane.
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Membranous nephropathy: is there inflammation?
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No, immune cells can't get to immune complexes.
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What tries to reestablish the BM in membranous nephropathy?
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The podocyte
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In membranous nephrophathy, what are the structures that the podocyte creates as it tries to repair the BM?
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Puts down collagen --> forms spikes
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Membanous nephropathy is like what type of HSR?
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Type II
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What is the difference between membranous nephropathy and membranoproliferative glomerulonephritis?
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Location of immune complexes and immune reaction. No inflammation in membranous nephropathy.
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What is another thing that "spikes" in membranous nephropathy can look like on light microscope?
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"craters"
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What does membranous nephropathy look like on immunofluoresence microscopy?
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Granular deposits
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Hematuria and inflammation = what type of general renal disease?
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Nephritic disease
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Would a pt with minimal change disease have hematuria?
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No.
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One of the most important parts of the glomerular filtration apparatus?
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The slit pore.
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Normal protein filtration/excretion
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400 mg/day, < 200 mg/day in urine
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Amount of protein secretion in nephrotic disease.
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400,000 mg/day, 20,000 mg/day excreted
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Hypoalbuminemia reults when what happens?
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When albumin loss exceeds the capacity of the kidney to recycle filtered albumin and the liver to increase production.
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What is underfill
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Oncotic pressure down --> plasma volume down --> renin/ang up, symp nervous system --> renal sodium retention up --> edema
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EdemA
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Starling force + constant force to retain sodium
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Overfill edema
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Expanded volume.
Proteinuria --> renal sodium ret --> plasma volume up --> pressure in capillaris up --> edema |
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Pathogenesis of hyperlipidemia in the nephrotic syndrome
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Albumin is synthesized by the liver.
Protein lost in urine --> liver synthesizes more albumin --> at the same time the liver ALSO synthesizes more LIPIDS and CLOTTING FACTORS --> (leads to a hypercoagulable state because of ANTI-coagulants lost in the urine) |
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Morphology of lipid in urine
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Fatty casts. See a Maltese cross shape.
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In secondary nephrotic syndrome, what is the treatment?
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Treat the underlying disorder.
Supportive measures Diuretics Lipid lowering agents (ex FSGS pt that has cholesterol of 1440!) Anticoagulation prevention of progression to renal failure (antihypertension, etc) |
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As we lose nephrons we lose ____?
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GFR
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ACE inhibtors do what to the efferent arteriole
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Dilate the efferent arteriole. If do this, the pts GFR might go down, but DECREASES stress on nephrons.
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What are the major symptoms of the nephrotic syndrome?
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Bland urine sediment
Proteinuria (>3.5 g/day) Hypoalbuminemia Hyperlipidemia Hypercoagulability Edema |
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Pathogenesis of a procoagulant state in the nephrotic syndrome.
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Clotting factors are synthesized by the liver.
Protein lost in urine --> liver synthesizes more albumin --> at the same time the liver ALSO synthesizes more LIPIDS and CLOTTING FACTORS --> (leads to a hypercoagulable state because of ANTI-coagulants (antithrombin III) lost in the urine) Hypercoagulable especially when the albumin is below 2.0 mg/dL |
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The three most common causes of the nephrotic syndrome all share one morphologic feature on EM, what is it?
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See diffuse effacement of podocytes.
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What accounts for hyperfiltration in the nephrotic kidney?
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Effacement of podocytes --> podcytes smush down against the BM --> this creates thickened areas, but it also creates some large pores --> the slit pores are the "size filters" of the GBM, so now large molecules like albumin can escape (but RBCs cannot escape because the BM is still intact.)
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What is the etiology of minimal change disease?
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Hereditary form has been linked to mutations in nephrin and podocin, proteins that make up the slit pore.
Non-hereditary form: immune-mediated damage to the podocyte (explains why minimal change disease can happen after immunization or after transplantation or with B-cell lymphoma) |