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26 Cards in this Set
- Front
- Back
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within the glomerular structure, what are the four cell types
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parietal epithelial (bowman's capsule)
visceral epithelial (podocyte) endothelial cell (afferent and efferent arterioles) mesangial cell |
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through the glomerular filtration, LARGER/SMALLER proteins will be more permeable. the MORE/LESS cationic, the more permeable.
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smaller; more (positive charged molecules will get through more, negative-negative charge opposition will keep neg molecules from getting through filtration)
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what is the critical component of the glomerular filtration model that is responsible for proteinuria?
a. basement membrane b. slit diaphragm c. endothelial cell fenestri d. podocyte foot processes |
slit diaphragm (the mutation of these molecules are responsible for heavy proteinuria seen in nephrotic syndrome)
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what is the pathogenesis of glomerular dz (in general)? mainly, i'm asking about nephritis syndrome.
what are the clinical manifestations? |
streptococaal antigen gets into the glomerular area --> Ig-antigen complex will activate complement system --> cytotoxic molecules/chemokines are recruited to cause glomerular cell proliferation and inflammatory cell infiltrates
clincial manifestations: Hematuria, proteinuria, renal failure (Nephritic syndrome) |
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what are the two types of barrier in glomeruli?
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"charge" barrier due to negatively charged BM (heparin sulfate)
"size" barrier due to porous nature of blomerular BM and size of pores in the slit diaphragm |
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Major glomerular capillary abnormalities resulting in an excessive leak of protein through the glomerulary capillary wall into the urinary space.
what dz is this? what would clinical findings be? |
nephrotic syndrome
-heavy proteinuria (>3.5 gm/day) - hypoalbuminemia (low albumin in serum bc of the problem) -edema (due decreased oncotic pressure) - hyperlipidemia (increased lipoprotein synthesis in liver bc of dec plasma oncotic pressure) - lipiduria (increased glomerular capillary wall permeability) |
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there is increased synthesis of albumin to compensate for loss of albumin due to nephrotic syndrome. is this compensation usually enough?
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NO.
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what are the most common causes of nephrotic syndrome? remember to differntiate b/w primary and secondary glomerular dz's
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Primary glomerular dz's:
- Minimal change disease -Focal segmental glomerulosclerosis- -Membranous glomerulonephritis -Membranoproliferative glomerulonephritis, secondary glomerular dz's: -diabetic nephropathy -amyloidosis |
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define nephritic syndrome
what's the main difference in terms of capillary wall disruption with nephrotic syndrome? |
Active inflammation within the glomerulus --> inflammatory rupture of glomerular capillaries w/ bleeding into urinary space --> Loss of filtration and a reduction in the blood flow to the glomeruli
nephritic = focal disruptions in the capillary well (meaning only some of the glomeruli are affected) and thus, lower amts of proteinuria nephrotic = the entire glomerular capillary wall is affected and has increased permeability; and thus, high amts of proteinuria |
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what would the PEx/lab findings be for nephritic syndrome
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-Non-nephrotic proteinuria (Urine protein > 500 mg and < 3.5 g/day - less than nephrotic syndrome)
-Reduced glomerular filtration rate (due to acute inflammation of glomeruli --> glomerular vasoconstriction, occlusion, thrombosis --> reduced filtrating surface area) -Active urine sediment (RBCs, WBCs, casts in urine, due to glomerular inflammation and disruption of GBM) -Edema (from reduced, glomerular perfusion but still intact salt/water reabsorption mechanisms) -Hypertension (increased salt/water retention) |
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causes of nephritic syndrome
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Primary:
-Postinfectious glomerulonephritis -Membranoproliferative glomerulonephritis -IgA nephropathy -Crescentic glomerulonephritis -Lupus nephritis (secondary dz) |
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what is acute renal failure
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Rapid deterioration of renal function that occurs over days to weeks. It is often associated with low or no urine output, red cell casts, hypertension and edema.
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what is the most common cause of acute renal failure (glomerular dz wise)...
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crescentic glomerulonephritis
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Prolonged (spanning months to years), progressive and irreversible decrease in glomerular filtration rate, increased blood urea nitrogen, increased serum creatine level (azotemia), resulting in a constellation of systemic signs and symptoms (uremia)
what is this? |
chronic renal failure (this is common final pathway for any chronic progressive renal dz incuding glomerular dz's)
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what is focal segmental glomerulosclerosis characterized by histologically?
what about crescentic glomerulonephritis? |
visceral epithelial cell proliferation
parietal epithelial cell proliferation (Proliferating cells in the urinary space, and thus outside of the glomerular capillary lumen ) |
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what's the main differnece b/w mesangial cell proliferation and endocapillary cell proliferation?
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with mesangial cell proliferation, you still can see capillary lumen, whereas with endocapillary cell proliferation the lumen is obliteratedvi
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visceral epithelial cell proliferation is associated with ______ _______ ______________, whereas parietal epithelial cell proliferation is associated with _______ ________.
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focal segmental glomerulosclerosis
crescentic glomerulonephritis |
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give location of immune complex deposition:
IgA nephropathy = membranous GN = lupus GN = |
mesangial (within mesangium)
subepithelial (b/w podocyte cytoplasm and glomerular BM) subendothelial (bw endothelial cell cytoplasm and glomerular BM) |
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give type of immunoglobulin:
IgA nephropathy = membranous GN = lupus GN = |
IgA
IgG IgG |
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what would you call glomerular dz where some glomeruli are affected, but only portions of the glomerulus itself is affected?
what if the whole glomerulus were affected? what if all the glomeruli were affected and the whole glomerulus itself is affected? |
focal segmental glomerulosclerosis
focal global diffuse global |
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explain the mechanism of postinfectious GN (start from bigger to smaller category on your flow chart...can you remember it?')
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it is an immune-mediated mechanism, driven by Antibodies that form immune complexes with antigens WITHIN THE CIRCULATION.
they then are deposited within the kidneys (example of a CIRCULATING immune complex deposition) |
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what is the mechanism for lupus nephritis?
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immune-mediated, Ab-mediated, IN-SITU immune complex deposition where the antigen of lupus is not a normal component of the kidney but the autoAb's are directed against the antigen located IN THE KIDNEY
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what are the 3 different immune-mediated mechanisms of glomerular dz's?
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Ab-mediated (can be IN SITU or CIRCULATING)
cell-mediated (T cells attacking kidneys) cytotoxic Ab's (Ab's against diff glomerular cells can cause glomerulonephritis) |
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What glomerular properties account for the very low urinary protein content of normal urine?
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the size barrier of the slit diaphragm keeps large molecules like albumin from escaping the capillary lumen
the negative charge barrier of the heparin sulfate-rich glomerular BM provides electronegative repulsion against the negatively charged proteins |
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list the morphologic changes of the glomeruli in response to injury
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- glomerular cell proliferation
-inflammatory cell infiltration (lymphocytes, neutrophils, macrophages) - deposition of immune complexes - glomerular scarring |
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Match pathologic finding with the type of glomerular injury:
1. electron dense deposits 2. mesangial IgA deposition 3. glomerular BM damage 4. visceral epithelial cell (podocyte) injury a. passing of protein molecules through glomerular capillary barrier b. autoAb's to type IV collagen c. mesangial injury d. immune complexes and complement activation |
1. D
2. C 3. B 4. A |
