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renal pathology

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Answer
clinical manifestations of nephrotic syndrom   massive proteinuria, hypoalbuminemia, edema, hyperlipidemia  
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minimal change disease   normal appearing glomeruli in light miscroscopy, but with the disappearance or fusing of epithelial foot process  
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minimal change disease   lipid laden renal cortices, most often seen in young children and responds well to corticosteriods  
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focal segmental glomerulosclerosis   similar to minimal change but occurs in older patients, characterized by sclerosis within capillary tufts of deep juxtamedullary glomeruli with focal or segmental distribution  
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nephrotic syndrom   a group of conditions characterized by increased basement membrane permeability  
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membranous glomerulonephritis   should be suspected in teens and young adults when nephrotic syndrom is accompanied by azotemia  
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membranous glomerulonephritis   characterized by greatly thickened capillary walls, immune complexes in intramembranous and epimembranous location and granular immunoflourescence, sometimes causing renal vein thrombosis  
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diabetic nephropathy   increase thickness of basement membrane and mesangial matrix wither diffuse or nodular glomerulosclerosis  
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nephritic syndrom   characterized by inflammatory rupture of glomerular capillaries  
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clinical manifestations of nephritic syndrome   oliguria, azotemia, HTN, and hematuria  
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post strep glomerulonephritis   group A beta hemolytic strep, complete recovery, characterized by innumerable punctate hemorrhages on the surface, enlarged hpercellular, bloodless glomeruli and lumpy bumpy immunoflourescence of IgG or C3  
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rapidly progressive glomerulonephritis   nephritic syndrome, progressing rapidly to renal failure, crescentic  
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good pasture syndrome   caused by anti-GBM antibodies, demonstrates linear immunoflourescence and is manifested by nephritic syndrom, pneumonitis with hemoptysis, affects men in their 20's  
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alport syndrome   hereditary nephritis associated with nerve deafness and ocular disoreders caused by a muation in the alpha5 chain of type IV colagen  
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IgA nephropathy   characterized by benign recurrent hamaturia in children usually following an infection  
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membranoproliferative glomerulonephritis   slow progression to chronic renal disease, basement membrane thickening and cellular proliferation, tram track appearance  
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PKD   manifests between the ages of 15 and 30, autosomal dominant  
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PKD   parital replacement of renal parenchyma by cysts, often associated with berry aneurisms of the circle of Willis, can cause polycythemia  
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infantile PKD   multiple cysts evident at birth, autosomal recessive, reults in death shortly after birth  
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renal papillary necrosis   ischemic necrosis of the tips of the renal papillae  
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renal papillary necrosis   often associated with diabetes mellitus or phenacetin, ocassionally a consequence of acute pyelonephritis  
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ATN   most common cause of acute renal failure  
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ATN   is reversible; patient may need dialysis as repair of tubules takes 2 weeks  
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ATN   can lead to cardiac arrest due to hyperkalemia, usually during th oliguric phase  
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ATN   most frequently precipitated by renal ischemia, also assocaited with crush injury with myoglobinuria, or direct injury from toxins  
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Fanconi Syndrome   manifestation of generilzed dysfunction of proximal tubule, may be hereditary, ccharacterized by impaired reabsorption of glucose, amino acids, phosphate, and bicarb  
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cystinuria   genetically determined impairment of tubular reabsorption of cystine, mainifests clinically as cystine stones  
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hartnup disease   genetically determined impairment of tubular reabsorption of tryptophan, leads to pellagra-like manifestations  
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chronic pyelonephritis   coarse asymmetric corticomedullary scarring and deformit of renal pelvis and calyces; stars as interstitial inflammatory infiltrate followed by fibrosis and tubular atrophy  
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chronic pyelonephtritis   results of chronic urinary tract obstruction, leads to renal hypertension and end-stage renal disease  
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uremia   azotemia, acidosis, hyperkalemia, abnormal control of fluid volume, hypocalcemia, anemia, HTN  
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prerenal azotemia   results from decreased blood flow and characterized by increased tubular reabsorption of sodium and water resulting in oliguria, concentrated urin, decreased urinary sodium excretion BUN/Creatinine ratio greater than 15  
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adenoma   bengn tumor, small and asymptomatic derived from renal tubules, may be a precursor to carcinoma  
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angiomyolipma   benign renal tumor that consists of fat, smooth muscle, and blood vessles  
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renal cell carcinoma   most common renal malignancy, originates in tubules most commonly in upper poles, frequently invades renal veins and vena cava  
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renal cell carcinoma   polygonal clear cells, can present with triad of flank pain, palpable mass, and hematuria, may have fever, secondary polycythemia, ectopic production of hormones  
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wilms tumor   most common renal malignancy of early childhood, highest incidence from 2-4 years, most often presents with palpable mass  
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transitional cell carcinoma   has been associated with phenacetin abuse, presents with hematuria, tends to spread by local extension to surrounding tissues (can be caused/ associated with benxidine or beta naphthylamine, cigarette smoking, and long term treatment with cyclophophamide)  
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squamous cell carcinoma   can result from chronic inflammatory process, can be associated with renal calculi  
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