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renal path

renal pathology

QuestionAnswer
clinical manifestations of nephrotic syndrom massive proteinuria, hypoalbuminemia, edema, hyperlipidemia
minimal change disease normal appearing glomeruli in light miscroscopy, but with the disappearance or fusing of epithelial foot process
minimal change disease lipid laden renal cortices, most often seen in young children and responds well to corticosteriods
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
nephrotic syndrom a group of conditions characterized by increased basement membrane permeability
membranous glomerulonephritis should be suspected in teens and young adults when nephrotic syndrom is accompanied by azotemia
membranous glomerulonephritis characterized by greatly thickened capillary walls, immune complexes in intramembranous and epimembranous location and granular immunoflourescence, sometimes causing renal vein thrombosis
diabetic nephropathy increase thickness of basement membrane and mesangial matrix wither diffuse or nodular glomerulosclerosis
nephritic syndrom characterized by inflammatory rupture of glomerular capillaries
clinical manifestations of nephritic syndrome oliguria, azotemia, HTN, and hematuria
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
rapidly progressive glomerulonephritis nephritic syndrome, progressing rapidly to renal failure, crescentic
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
alport syndrome hereditary nephritis associated with nerve deafness and ocular disoreders caused by a muation in the alpha5 chain of type IV colagen
IgA nephropathy characterized by benign recurrent hamaturia in children usually following an infection
membranoproliferative glomerulonephritis slow progression to chronic renal disease, basement membrane thickening and cellular proliferation, tram track appearance
PKD manifests between the ages of 15 and 30, autosomal dominant
PKD parital replacement of renal parenchyma by cysts, often associated with berry aneurisms of the circle of Willis, can cause polycythemia
infantile PKD multiple cysts evident at birth, autosomal recessive, reults in death shortly after birth
renal papillary necrosis ischemic necrosis of the tips of the renal papillae
renal papillary necrosis often associated with diabetes mellitus or phenacetin, ocassionally a consequence of acute pyelonephritis
ATN most common cause of acute renal failure
ATN is reversible; patient may need dialysis as repair of tubules takes 2 weeks
ATN can lead to cardiac arrest due to hyperkalemia, usually during th oliguric phase
ATN most frequently precipitated by renal ischemia, also assocaited with crush injury with myoglobinuria, or direct injury from toxins
Fanconi Syndrome manifestation of generilzed dysfunction of proximal tubule, may be hereditary, ccharacterized by impaired reabsorption of glucose, amino acids, phosphate, and bicarb
cystinuria genetically determined impairment of tubular reabsorption of cystine, mainifests clinically as cystine stones
hartnup disease genetically determined impairment of tubular reabsorption of tryptophan, leads to pellagra-like manifestations
chronic pyelonephritis coarse asymmetric corticomedullary scarring and deformit of renal pelvis and calyces; stars as interstitial inflammatory infiltrate followed by fibrosis and tubular atrophy
chronic pyelonephtritis results of chronic urinary tract obstruction, leads to renal hypertension and end-stage renal disease
uremia azotemia, acidosis, hyperkalemia, abnormal control of fluid volume, hypocalcemia, anemia, HTN
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
adenoma bengn tumor, small and asymptomatic derived from renal tubules, may be a precursor to carcinoma
angiomyolipma benign renal tumor that consists of fat, smooth muscle, and blood vessles
renal cell carcinoma most common renal malignancy, originates in tubules most commonly in upper poles, frequently invades renal veins and vena cava
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
wilms tumor most common renal malignancy of early childhood, highest incidence from 2-4 years, most often presents with palpable mass
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)
squamous cell carcinoma can result from chronic inflammatory process, can be associated with renal calculi
Created by: swohlers
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