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26 Cards in this Set
- Front
- Back
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Renal cystic disease |
cystic renal dysplasia and simple cysts IMPT adult type AD-PKHD1 gene, childhood type AR, medullary sponge kidney, acquired diaylsis related |
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Renal dysplasia pathology |
immature tubules, rudimentary glomeruli, surrounding mesenchyme with cartilage and smooth muscle proliferation |
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Renal dysplasia general |
development disorder, abrnomal metanephric differentiation often present shortly after birth as flank mass stimulatiing tumor, uni or bilateral, bi is not compatible with life |
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Simple renal cysts |
very common in greater than 50% patients over age 50 usually incidental finding = rarely produce symptoms large cysts may be mistake for tumors may be solitary or multiple usually in renal cortex, filled with flluid and can spontan hemorrhage |
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Urinary tract obstruction |
may occur at any level gross pathology indicated level, entire system hydroureter, hydronephrosis many causes = congenital atresia of urethra, proliferative/neoplastic, calculi |
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UTO |
sudden or insidiou onset, pain when sudden partial or complete unilateral or bilaterla may be silent especially if unilateral, impaired urine concentration when bilateral due to tubular damage reversible early on |
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Hydronephrosis |
dilation of renal pelvis and calyces, blunting of pyraminds early = dilated bowmans and tubules later = tubular dilatation and atrophy, glomerular collapse and intersitial fibrosis |
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terrible abdominal pain |
36 yo male with sudden onset of severe LLQ ab pain several previous episodes but much less severe than this one, otherwise good health micro shows hematuria |
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Urinary calculi |
in the kidney they are called nephrolithiasis very common disease incidence is greater in men peak age of symptoms is younger adults most stones are unilateral 80% arise in pelvis more than bladder many pts have no underlying disease |
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Clinical signs of calculi |
severe pain hematuria obstruction superimposed infection dx using imagine treat using lithotripsy |
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Causes of urolithiaisis |
increased urinvary conc. of stones constituents low urine volume pH of urine may play a role infection many pts have no underlying reason or disease |
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stone composition |
calcium in 75% oxalate or oxalate and phosphate; caused by hypercalcemia, hypercalciuria, inceased uric acid with nucleation of calcium oxalate, hyperoxaluria urates 1-% gout and hyperuricemia magnesium ammonium phos 15% large staghorn calculi in pelvis, urea splitting bacteria, alkaline urine cystine 1% cystinuria low urine pH |
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Randalls plaque |
stone formation forms in loop of Henle starts in tubular basement membrane proagation of crystal |
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Staghorn |
Mg-NH4 and PO4 |
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Tubulointersitial nephrtiis |
realtive sparing of glomerulus infection-pyelonephritis toxins drugs metabolic urates myeloma transplant |
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Acute pyelonephritis |
acute suppurative infection UTI second in frequency to URI predisposing factors; urinary tract obstruction, catheterization esp long term indwelling, instrumentaiton, shroter urethra in femlales |
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Acute pyelo |
most infections are ascending usually there is bladder infection, 85% infections due to gram - bacteria 50% are due to e. coli from fecal flora endogenous infection involve bacterial adhesions some infectionas are hematogenous; sepsis endocarditis |
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Acute in clinic |
sudden onset flank CVA pain fever dysuria and frequency and urgency pyuria and WBC casts in urine may resovle or become chronic |
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Gross acute |
many small yellow abscess pelvis involved extension thru capsul causes perinephritis abscess severe pain fever chills and spread to adjacent organs and spesis |
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micro acute |
polys in tubule and intersitial tissues abscess formation glomeruli spread |
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Acute tubular necrossi |
potentially reversible form of ARF oliguria increasing serum creatinine fluid renteiton hyperkalemia |
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ATN caues |
ischemic shock nephrotoxins in gross kidneys swollen and cortex pale with red medulla nucleted WBCs in vasa recta, early phase eosionphilic tubules, loss of nuclei, edema, early phase sloughing of tubular cells, high tubular obstructionmeans lower GFR due to increased luminal oncotic late phase = tubular regenation with flat epithelium and basophilia |
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Kidney and hypertension |
benign = nephrosclerosis caused by chronic hypertension gradual ischmia of okdney occurs and siease is bilateral accrts for one third cases of end stage renal disease |
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gross of nephroscelrosis |
moroccan leather surface alternating scars and normal tissue forming tiny nodules |
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5/6 renal ablation hyperfiltration model |
reduction in nephrons increases flow to remaining causing glomerular injury resulting in mesangial proliferation and scarring |
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small arterrolar lesions |
transuction of plasma proteins into wall, excessive matrix produce by smooth muscles cells, hylaine arteriolar sclerosis afferent arterioles esspecialyl affected arterial lession comon glomerular obsolescence = thickening of capps, shrinking gloms, scarring, intersitial inflammation |
