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76 Cards in this Set
- Front
- Back
What are the clinical features of acute kidney injury?
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acute kidney failure, with oliguria or anuria
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What is the pathogenesis of ischemic AKI?
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ischemia, proximal tubule is most seriously affected as it consumes the most energy
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What is the most common cause of acute renal failure?
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ischemic AKI
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What is the pathogenesis of toxic AKI?
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toxins cause direct tubular injury with resultant necrosis
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What does toxic AKI look like in histo?
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necrotic cells or sloughed epithelial cells within the lumen, hyaline and granular casts in distal nephron segments
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What causes toxic AKI?
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casts of hemoglobin/myoglobin, mercury, ethylene glycol, radio contrast, aminoglycosides
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What does ischemic AKI look like?
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regenerative changes, loss of proximal tubule brush border, tubule dilation, flattening of the epithelium
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What is the prognosis of AKI?
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recovery is common, mortality increased when part of multiorgan failure
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What is obstructive uropathy?
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structural or functional abnormality in urinary tract that blocks the normal outflow of urine
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What is the clinical presentation of unilateral renal obstruction?
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can be clinically silent unless there is a kidney stone
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How does bilateral urinary tract obstruction present?
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impaired urinary concentrating ability, polyuria, polydipsia
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How does obstruction of the bladder outlet present?
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micturition difficulties
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What casues urinary tract obstruction in kids?
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congenital anomalies, posterior urethral valves, ureteropelvic junction malformation
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What causes urinary tract obstruction in adults?
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kidney stones
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What causes urinary tract obstruction in older men?
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BPH
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What cause intrarenal urinary tract obstructions?
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deposits in tubule, stones, tumors, sloughed papillary tissue wihtin the renal pelvis
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What causes intrinsic extrarenal urinary tract obstruction?
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stones, tumors in ureter, ureteropelvic junction obstruction
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What causes extrinsic extrarenal urinary tract obstruction?
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neoplasms, inflammatory lesions of retroperitoneum
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What can cause urethral obstruction?
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strictures, posterior urethral valves
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What causes prostate obstruction?
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BPH, carcinoma
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What causes urinary bladder obstruction?
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carcinoma, neurogenic bladder
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What is hydronephrosis?
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dilation of the pelvis and calyces, thinning of overlying parenchyma
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What is the earliest morphologic change of obstructive nephropathy?
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dilation of the tubules, esp collecting ducts
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What is the course of obstructive nephropathy?
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dilation of the tubules, esp collecting ducts
Bowman's space may become enlarged, periglomerular fibrosis interstitial mononculear inflammation, atrophy of proximal tubules, worsening interstitial fibrosis, can have superimposed pyelonephrosis |
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What is a cystitis?
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bacterial infection of lower urinary tract
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What is pyelonephritis?
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infection of upper urinary tract
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What is the pathogenesis of acute pyelonephritis?
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ascending from cystitis or blood-borne seeding the kidney
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What is the pathogenesis of UTI in males and kids?
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anatomic or functional efect preventing normal emptying/urinary flow
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What pathogen causes mostt UTIs?
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E coli
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What other pathogens cause UTI?
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Staph faecalis, Staph albus, Klebsiella, Proteus
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What does Proteus mirabilis infection cause?
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urea splitting, staghorn calculi in pelvicaliceal system, can perpetuate infection
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How does acute cystitits present?
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urgency with pyuria
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How does acute pyelonephritis present?
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flank tenderness, pain, fever, pyuria, acute renal failure if bilateral
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What is the prognosis of acute UTI?
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excellent in uncomplicated acute
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What is the prognosis of chronic pyelonephritis?
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from repeated bouts, can be congenital or calculi, can develop chronic kidney disease and uremia
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What does acute pyelonephritis look like?
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plugs of neutrophils in tubular lamina and surrounding interstitium, tubular injury, abscess formation
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What does chronic pyelonephritis look like?
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broad-based scars, jig-saw pattern of interstitial fibrosis, tubular atrophy, interstitial mononuclear inflammatory cells with intervening spared areas
glomeruli are spared until late |
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What is acute interstitial nephritis?
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interstitial inflammation and edema
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Waht is chronic intersittial nephritis?
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insidious onset, fibrosis
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What are the clinical features of acute interstitial nephritis?
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oliguric kidney failure, features of hypersensitivity reaction: fever, rash, peripheral eosinophilia
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What do you see in urinalysis of acute intersitital nephritis?
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hematuria, pyuria, white cell casts, can have eosionphiluria
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What is NSAID-related AIN?
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Na retention/edema, hyperkalemia, decline in renal function/acute kidney failure, interstitial nephritis, with nephrotic syndrome
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What is the pathogenesis of NSAID-related AIN?
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inhibition of vasodilating renal PGs resulting in renal hypoperfusion
podocyte effacement, nephrotic range proteinuria AIN and minimal change-like lesion |
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What is the pathogenesis of AIN?
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hypersensitivity reaction/immunologic injury from drugs, infections, systemic immunologic disorders
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What drugs cause AIN?
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sulfa drugs, methicillin, beta-lactam antibiotics, rifampin, thiazides, furosemide, NSAIDs
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What is the prognosis of AIN?
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glmerular and tubulointersitital abnormalities reversible on discontinuation of drugs,
NSAID related injury reversible within days with discontinuation of offending agent |
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What is the pathology of AIN?
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edematous interstitium, increased space between tubules, interstitial inflammation, lymphocytes, eosinophils, can invade tubular epithelium, tubules show injury or degenerative changes/necrosis
non-necrotizing granulomatous inflammation |
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What is the prognosis of AIN?
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typically reversible, may require dialysis
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What causes papillary necrosis?
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diabetes, sickle cell, analgesic abuse nephropathy, obstruction
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What are the clinical features of chronic intersitital nephritis?
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insidious decline in renal function, aminoaciduria, glycosuria, renal tubular acidosis, decreased urinary concentrating ability, mild proteinuria
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What can cause chronic interstitial nephritis?
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crystal deposition, analgesics, Sjogren syndrome, sarcoidosis, multiple myeloma causing light chain nephropathy
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What is the pathogenesis of CIN?
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deposits that precipitate in tubules, ongoing immunological injury
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What is the pathology of CIN?
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inflammation with tubule injury in absence of proportional glomerular/vascular disease, interstitial fibrosis, tubular atrophy, also specific deposits
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What is the prognosis of CIN?
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fibrosis is irreversible, can improve renal function and prevent ESRD if contributing factors are removed and aggravating factors are controlled
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What is the clinical presentation of hyperacute rejection?
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0 - 3 days after transplant, typically while still in OR, patient is swollen, acute rise in serum creatinine
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What is the pathogenesis of hyperacute rejection?
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preformed antibodies, esp ABO or HLA, seldom seen because of matching
antibodies bind to antigens on vascular endothelial cells, complexes fix complement, activates neutrophils, active coagulation cascade |
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What is the pathology of hyperacute rejection?
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widespread thrombosis wiht extensive ischemic injury, necrotizing vasculitis, influx of neutrophils in arteries and peritubular capillaries, thrombosis of blood vessels and ischemic necrosis, C4d in peritubular capillaries
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When does accelerated acute rejection present?
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3-7 days
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What is the clinical presentation of accelearated acute rejection?
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fever and tenderness over graft site
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What si the pathogenesis of accelerated acute rejection?
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humoral mechanisms, de novo antibodies or induction of amnestic response
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What is the pathology of accelearated acute rejection?
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similar to hyperacute with arterial and capillary thrombosis, infiltration of neutrophils in arteries and peritubular capillaries, ischemic injury, C4d positive in peritubular capillaries
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When does acute rejection occur?
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more than 7 days after transplant, usually within first several months
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How does acute rejection present?
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abruptly increased creatinine, graft tenderness
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What is the pathogenesis of acute rejection?
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humoral and cellular (CD4 and CD8)
acute cellular or acute vascular vascular is due to humoral mechanisms (ABs to HLA-Class I antigens), C4d is present in most cases with humora mechanisms |
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What is the pathogenesis of acute cellular rejection?
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lymphocytic interstitial infiltrate and lymphocytes invading tubular epithelium
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What is the pathogenesis of acute vascular rejection?
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lymphocytes under endothelium of arteries
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What is pathogenesis of severe acute vascular rejection?
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full thickness infiltration of inflammatory cells in arterial walls, transmural necrosis
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Waht ist he prognosis for acute cellular rejection?
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responds well to increased anti-rejection therapy
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What is the prognosis for vascular rejection?
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needs more aggressive therapy, less responsive to treatment
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What is chronic allograft nephropathy?
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scarring of renal graft
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What causes chronic allograft nephropathy?
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preexisting disease in donor, recurrent/de novo disease, preceding acute rejection, scarring due to drug toxicity
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What does chronic allograft nephropathy look like?
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interstitial, vascular and glomerular scarring, arteries show concentric fibrointimal thickening of arteries
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What is the prognosis of chronic allograft nephropathy?
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inexorable decline, can lose the graft
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What is calcineurin inhibitor nephrotoxicity?
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acute or chornic nephrotoxicity, in kdineys from patients on CNI after receiving other transplants
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What is the pathogenesis of calcineurin inhibitor nephrotoxicity?
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CNI is toxic to renal cells, induces vasoconstriction, casues concentric arteriole hyalinosis, due to vascular smooth muscle cell necrosis
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What does chronic CNI toxicity look like?
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pattern of scarring in which fibrotic tubulointerstitial areas are interspersed with more normal regions,s triped fibrosis, prolonged vasoconstrction along medullary rays
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