Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
33 Cards in this Set
- Front
- Back
|
acute tubular necrosis etiology
|
any cause of hypoperfusion or hypodrainage (pre or postrenal azotemia) can lead to tubular necrosis if prolonged;
|
|
|
acute tubular necrosis phases
|
prodromal (between injury and acute renal failure)
oliguric or anuric post oliguric (polyuria due to tubular death and lack of urine concentration function) |
|
|
acute tubular necrosis diagnosis
|
BUN/creatinine ration close to 10:1
low urine osmolarity (<350) high urine sodium (>40) high fractional Na (>1%) brown pigmented granular casts and epithelial casts |
|
|
acute tubular necrosis management
|
no effective medical therapy, just hydration and if life-threatening, dyalisis
dopamine or diuretics cannot reverse it |
|
|
What are the intrinsic causes of acute renal failure?
|
ATN (MC)
contrast induced nephropathy direct tubular necrosis:NSAIDS, aminoglycosides obstructive urupathy renal ischemia, Acute inerstital nephritis: penicillins acute renal vasculitis |
|
|
allergic interstitial nephritis etiology
|
accounts for 10-15% of intrinsic renal failure
Inflammation of the interstitial region of the kidney often associated with acute onset of renal insufficiency. penicillins, methicillin induced is the prototype happens 7-14 days and has a manfisted sequelae |
|
|
allergic interstitial nephritis presentation
|
begins 7-14days after drug exposure
fever (90%) PRURITIC MORBILLIFORM RASH (25-50%) hemolysis (95%, nonspecific) eosinophilia, eosinophiluria, proteinuria, increased IgE |
|
|
allergic interstitial nephritis management
|
remove offending agent; if persistent failure then short course of steroids
|
|
|
A patient has acute renal failure and hearing loss. What do you suspect?
|
history of NSAIDS
|
|
|
renal failure from pigments etiology
|
hemoglobin and myoglobin are toxic to tubules and also precipitate
rhabdomyolisis can be caused by crush injury, seizures, severe exertion, statins, hypokalemia, hypophosphatemia, ABO incompatibility |
|
|
acute renal failure from urate
|
(obstructive uropathy)
seen in tumor lysis syndrome of leukemia/lymphoma patients treat with hydration to induce diuresis, allopurinol and alkalinization of urine before chemo confirm with uric acid crystals in urinalysis also with crystallization of methotrexate and its 7-oh metabolite |
|
|
A patient has acute renal failure and muddy casts in his urine. What do you suspect?
|
ATN
|
|
|
aminoglycoside renal toxicity
|
10-20% of drug-induced nephrotoxocity and usually reversible; due to high trough levels, not peak levels therefore give once a day to allow same bactericidal effect (peak level) and low trough levels (less toxicity)
|
|
|
amphotericin B renal toxicity
|
leads to renal insufficiency and proximal tubular acidosis after several days from cumulative dosing; find high creatinine; stop medication
|
|
|
atheroembolic renal failure
|
usually angioplasty patient after several days
presents with eosinophilia, low complement, bluish discoloration of fingers and toes, livedo reticularis |
|
|
contrast agent renal failure
|
osmostic pressure produces a transient inc in RBF followed by prolonged decrease
ROS -> dec. RBF rise in creatinine >= 25% BUN/creatinine ratio may be as high as 20:1 clinical manifestation of osmotic diuresis |
|
|
What do you need to be aware of befor initiating fluid in acute renal failure?
|
ATN
|
|
|
nephrotoxic drugs
|
aminoglycosides
contrast agents pentamidine vancomycin cyclosporine ampB NSAIDs cysplatine |
|
|
What are the indications to do dialysis in treating acute renal failure?
|
volume overload
hyperkalemia acid/base disorders symptomatic uremia uremia (BUN>100) dialyzable intoxications (aspirin, lithium) |
|
|
NSAID nephropathy
|
mechanisms: inhibition of vasodilatory prostaglandins. kidney can't compensate for drop in RBF in patients with renin mediated renal vasoconstriction
risk factors are elderly, hypertension, diabetes or other renal impairment diagnose with history of NSAIDs + rise in BUN/creatinine and sterile pyuria |
|
|
What is the most common cause of intrinsic ARF?
|
ATN
|
|
|
papillary necrosis
|
precipitated by NSAIDs, lead causing renal failure, gout, hypertension
|
|
|
How do you differentiate ATN from ARF?
|
urine
ATN: - urine brown with muddy casts - SG <1.012 - osmolality <500 - sodium >40 - Plasma BUN/Cr ratio <10-15 |
|
|
prevention of contrast-induced renal failure
|
most importantly is hydration; then bicarbonate and N-acetyl cysteine have been shown to decrease it
|
|
|
What can cause ATN?
|
insult or injury to the kidney
- ischemia, prolonged hypotension, sepsis, dehydration |
|
|
glomerulonephritis general presentation
|
hematuria with dysmorphic red cells, edema, hypertension, proteinuria <2gm/24h
biopsy is extremely important for specific Rx |
|
|
How do you treat ATN?
|
Avoid fluid overload and hyperkalemia
Loop diuretics |
|
|
drug induced lupus caused by?
|
hydralazine, procainamide, isoniazid
|
|
|
nephrotic syndrome etiology
|
primary: membranous GN, Nil, membranoproliferative, focal-segmental GN
1/3 associated with diabetes, hypertension or myeloma any glomerulonephritis can convert to nephrotic syndrome if severe enough |
|
|
nephrotic syndrome presentation
|
proteinuria >3.5g/24h, edema, hyperlipidemia, hypoalbuminemia
can have hyperlipiduria (maltese cross) and hypercoagulable states (arterial or venous thrombosis from loss of antithrombin, proteins C and S) |
|
|
nephrotic syndrome diagnosis
|
initial test is proteinuria >3.5g/24h or albumin/creatinine ratio >3.5 on urinalysis
renal biopsy is most accurate |
|
|
cyclosporine, tacrolimus cause
|
renal ischemia through reversible vasoconstriction, injury to glomerular afferent arterioles
|
|
|
renal tubular acidosis type I etiology
|
ampB, acetazolamide, outdated tetracycline
|
