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140 Cards in this Set
- Front
- Back
What type of AKI has a high survival rate of 70-95%
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community acquired AKI
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What AKI has a high mortality rate and has a most common etiology of prerenal?
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Hospital acquired AKI
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What kind of AKI accounts for 18-33% of hospital occurrences?
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Drug-induced
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20-60% of all AKI patients will require what kind of initial therapy?
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dialysis (25% of those will progress to chronic renal insufficiency, requiring long-term dialysis)
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What is the main participant in regulating a constant extracellular balance?
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kidney
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When the kidney has achieved a steady state of extracellular balance, what is the rate of excretion equal to?
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intake + endogenous production OR gfr
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What are the normal GFRs (m&f)?
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130-145L/d women and 165-180L/d men
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What are the three main functions of the kidney?
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main participant in regulating a constant extracellular balance, hormone secretion, gluconeogenesis/peptide catabolism
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What is prerenal AKI?
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results from decreased renal perfusion
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What is intrinsic AKI?
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results from structural damage to the kidney
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What is postrenal AKI?
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results from obstruction of urine flow from the renal tubule to the urethra
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What is the kidney responsible for secreting?
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renin, prostaglandins, kinins, erythropoietin
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What is the kidney responsible for metabolizing?
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Vit D (final metabolism to active form, first metabolism occurs in liver)
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What are the 3 basic physiologic events for the production and elimination of urine?
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1. Delivery of blood flow to glomeruli
2. Formation and processing of ultra filtrate by the glomerulus and tubular cells 3. Urine excretion through the ureters, bladder, and urethra |
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What is GFR?
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excretion rate of toxins and drugs (slides); is the volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman's capsule per unit time (wiki)
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What is the time frame fro GFR decline and associated uring output drop and AKI?
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generally occurs over hours to days but can occur over weeks
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What are the clinical definitions for AKI?
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imcrease in Scr of 0.5mg/dL over 24h when baseline Scr < 3, increase in Scr of 1 mg/dL over 24h when baseline Scr >=3mg/dL, decrease of >50% of baseline CrCl
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What is True GFR?
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total filtration rate x number of functioning nephrons
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What three factors maintain glomerular pressure?
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1. Arterial pressure
2. Afferent arteriolar resistance 3. Efferent arteriolar resistance. |
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What happens during afferent arterilolar constriction at the glomerulus?
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increased vascular resistance, decreased intraglomerular pressure, decreased gfr
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What happens during efferent arterilolar constriction at the glomerulus?
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increased vascular resistance, increased intraglomerular pressure, increased GFR
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Where does the ultrafiltrate go after leaving the glomerulus?
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proximal tubule
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What is the best method for assessing renal function in acutely ill, renally unstable patients?
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urine formation
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In renal function decline, what phase occurs over <1-2 days after initial insult?
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oliguric phase
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In renal function decline, what phase is a period of increased urine production that occurs only after cause of injury is removed or reduced?
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diuretic phase
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In renal function decline what phase is characterized by several weeks to months in length, return of normal kidney function, and normalization of urine production?
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recovery phase
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Does the recovery phase occur in all renal function decline cases?
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No
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What are patient risk factors for AKI?
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co-morbid disease that increase kidney injury, volume depletion, urinary tract obstruction, age > 60, male gender, infection, cancer, previous history of AKI, pre-existing renal dysfunction
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What are possible medication related risk factors for AKI?
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IV radiographic contrast, nephrotoxic abx drugs, nsaids, angiotensin-converting enzyme (ACE), angiotensin II receptor blockers (ARBs)
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Why is a decline in renal excretion bad?
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reduces toxin elimination, promotes retenetion of BUN&creatinine&urea, presons will then begin to show symptoms of this accumulation and increases chances for severe morbidity and death
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In rifle risk category, what is the GFR/Scr criteria?
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increased Scr by 50% or decreased GFR by 25%
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In rifle risk category, what is urine output criteria?
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UOP < 0.5 ml/kg/h x 6 h
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In rifle injury category, what is urine output criteria?
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Scr increased 100% or GFR decreased 50%
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In rifle injury category, what is urine output criteria?
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UOP < 0.5 ml/kg/h x 12h
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In rifle failure category, what is urine output criteria?
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UOP < 0.3 ml/kg/h x 24 h or anuria x 12 h
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in rifle loss category, what is the general criteria?
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persistant ARF > 4 wks
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In rifle ESRD category, what is the general criteria?
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ESRD > 3 months
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What is the clinical presentation in AKI?
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changes in urine ouput, signs of hypovolemia, unique color and composition of urine (cola-colored suggests bleeding, foaming suggest proteinuria), symptoms of uremia, flank pain, increased weight, increased blood pressure, signs/symptoms of electrolyte abnormalities, bladder distention or prostate enlargement
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In clinical presentation of AKI, what is the progression of musculoskeletal and neurologic s/sx?
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weakness --> peripheral neuropathy --> renal osteodystrophy or seizures
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In clinical presentation of AKI, what is the progression of hematologic s/sx?
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platelet dysfunction --> anemia
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In clinical presentation of AKI, what is the progression of electrolytes s/sx?
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hyponatremia or metabolic acidosis --> edema or hyperphosphatemia --> hypocalcemia
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In clinical presentation of AKI, what is the progression of cardiovascular s/sx?
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fluid overload --> hypertension or hyperlipidemia
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In clinical presentation of AKI, what is the progression of dermatologic s/sx?
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itching --> worsening itching --> rash/inflammatory skin reactions
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In clinical presentation of AKI, what is the progression of endocrine s/sx?
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erythropoetin secretion reduction --> infertility in women
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What are the monitoring parameters for AKI?
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urine output, GFR, labs (bun, scr, Na, K, Cl, total C02, calcium, uric acid, phosphate, hematocrit), urinalysis, renal biopsy
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What in nonoliguric in ml/d?
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urine output > 500ml/d
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What in oliguric in ml/d?
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urine output < 500ml/d
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What in anuric in ml/d?
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urine ouput < 50ml/d
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What is the result of a reduction in urine output on scr?
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increased accumulation
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What is the single most important calculation that you will as a pharmacist (will use) on a daily basis in the evaluation of patient clinical presentation? :P
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Estimated Gfr
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What is estimated gfr equal?
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calculated CrCl
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What is normal BUN?
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7.0-20mg/dL
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What is normal Scr?
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0.6-1.2 mg/dL
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What is normal Na?
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135-145 mEq/L
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What is normal K?
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3.6-5.0 mEq/L
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What is normal Cl?
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98-108 mEq/L
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What is normal total C02 (HC03)?
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22-38 mEq/L
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What is normal calcium?
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8.5-10.5 mg/dL
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What is normal uric acid?
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2-7 mg/dL
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What is normal phosphate?
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2.6-4.6 mg/dL
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What is normal hematocrit (male)?
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40-50%
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What is normal hematocrit (female)
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35-45%
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What is the Cockcroft-gault equation?
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CrCl ml/min = ((140-age)(IBW)) / (72*Scr); multiply product by 0.85 if female
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What does Cockcroft-Gault equation assume?
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stable renal function
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In calculating CrCl, when should you uses actual body weight?
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if actualy body weight is less than IBW
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What is the calculation for IBW (males)?
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Males (kg) = 50kg + 2.3(for each inch >5ft)
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What is the calculation for IBW (females)?
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Females (kg) = 45kg +2.3 (for each inch > 5ft)
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What is a non-pathological occurrence that can yield a increased BUN?
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high protein diet
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In prerenal ARF, what are some causes of intravascular volume depletion?
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excessive diuresis, hemorrhage, dever diarrhea, loss of intravascular fluid into the extravascular space "third spacing"
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In prerenal ARF, what are some causes of decreased systemic circulation?
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congestive heart failure, cirrhosis, nephrotic syndrome, hepatorenal syndrome
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In prerenal ARF, what are some causes of systemic vasodilation?
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sepsis, liver failure, anaphylaxis
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In prerenal ARF, what are some causes of large vessel renal vascular disease?
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renal artery thrombosis, renal artery stenosis
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What are possible drug-induced causes of prerenal ARF?
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NSAIDS, ace inhibitors, arbs, cox-2 inhibitors, cyclosporin, tacrolimus, diuretics, radiocontrast dye
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How do nsaids cause auto-regulatory failure in AKI?
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decrease formation of prostaglandin precursors which usually prevent the over vasconstriction in the kidney
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How can ACEi cause AKI?
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Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor.
Results in decreased levels of angiotensin II. Causes an increase in plasma renin activity and a reduction in aldosterone secretion. Ultimately blocks ability of kidney to self regulate |
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What were the four listed in class types of intrinsic ARF?
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Vascular damage, glomerular damage, tubular injury, acute interstitial nephritis
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What can cause vascular damage during intrinsic ARF?
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inflammation, emboli, medications (amphetamines, cisplatin, cyclosporin, mitomycin C)
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What can cause glomerular damage during intrinsic ARF?
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systemic lupus erythematosus, medications (heroin, lithium, Nsaids, phenytoin)
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What can cause tubular damage during intrinsic ARF?
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Ischemia, acute tubular necrosis, toxins
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For tubular injury of intrinsic ARF, what are the causes of acute tubular necrosis?
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90% of intrinsic cases - caused by intrarenal vasoconstriction, direct tubular toxicity, intratubular obstruction, or prolonged ischemia from pre-renal causes
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what are the sources of toxin induced tubular injury during intrinsic ARF?
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Endogenouos (myoglobin, hemoglobin, uric acid) or exogenous (medications - aminoglycosides, amphotericin B, chemo, cidofocvir, cocaine, foscarnet, radiocontrast dye, tacrolimus; ethylene glycol, pesticides
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During instrinsic AKI, what are the causes of acute interstitial nephritis?
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ischemia, infections, medications (PCN, sulfas, NSAIDS, lithium, cyclosporin, tacrolimus)
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During postrenal AKI, what are the possible causes of obstruction?
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crystal deposition in renal tubules, ureteral tumor or stricture or stones, bladder carcinoma, bladder neck obstruction secondary to prostatic hypertrophy
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During postrenal AKI, what are the possible medicinal causes?
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obstructive: acyclovir, methotrexate, uric acid; nephrolithiasis: allopurinal, indinavir, sulfadiazine, triamterene
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What is the rph role AKI?
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medication hx, patient assessment of risk factors and pmh and hpi, estimate GFR, dose meds based off of renal function (Scr can NOT be the only determinate for the dose), recognize AKI early
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What is normal GFR?
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100-125ml/min/1.73m^2
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What population is Scr an unreliable marker in?
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elderly, malnourished, children, critically ill
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During urinalysis, what does a high specific gravity, osmolality suggest?
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high values indicate prerenal causes and stimulation of sodium and water retention
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During urinalysis, what does urine sediment mean?
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hyaline casts normal; granular casts and cellular debris suggest structural damage
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During urinalysis, what does WBC mean?
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suggests inflammation
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During urinalysis, what does eosinophils mean?
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associated with acute allergic intersitial nephritis
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What is the measure for microalbuminuria?
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>30mg/24h
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What is the measure for overt proteinuria?
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>300mg/24h
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What is the equation for the calculation of fractional excretion of sodium?
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FEna = ((Una X Scr) / (Ucr X Sna)) x 100
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What is the advantage of fractional excretion of sodium calculation?
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differentiating prerenal from acute intrinsic renal failure
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If the fractional excretion of sodium yields a value <1% in AKI, what does it mean?
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suggests retention of sodium and water -> prerenal etiology versus intrinsic cause
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In prerenal and function, what are the possible physical examination findings?
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hypotension, dehydration, petechia if thrombotic, ascites
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In intrinsic, what are the possible physical examination findings?
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rash, fever
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In postrenal, what are the possible physical examination findings?
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distended bladder, enlarged prostate
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In prerenal and function, what is the BUN/Scr ratio?
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>20:1
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In intrinsic, what is the BUN/Scr ratio?
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15:1
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In postrenal, what is the BUN/Scr ratio?
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15:1
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In prerenal and function, what is the Urine sodium?
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<20 mEq/L
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In intrinsic, what is the Urine sodium?
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>40 mEq/L
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In post renal, what is the Urine sodium?
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>40 mEq/L
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What is the fractional sodium excretion in prerenal and functional?
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<1%
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What is the fractional sodium excretion in intrinsic?
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>2%
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What is the fractional sodium excretion in postrenal?
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variable
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What is the urine sediment in prerenal and functional?
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hyaline casts, may be normal
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What is the urine sediment in intrinsic?
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muddy brown granular casts, tubular epithelial casts
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What is the urine sediment in postrenal?
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variable, may be normal
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What is the urine WBC in prerenal and functional?
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negative
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What is the urine WBC in intrinsic?
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2-4+
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What is the urine WBC in postrenal?
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variable
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What is the urine RBC in prerenal and functional?
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negative
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What is the urine RBC in intrinsic?
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2-4+
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What is the urine RBC in postrenal?
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1+
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What is the proteinuria in prerenal and functional?
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negative
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What is the proteinuria in intrinsic?
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positive
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What is the proteinuria in postrenal?
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negative
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What are the desired goals of therapy in AKI?
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recognize aki early, anticipate and prevent potential problems, remove primary cause of acute renal failure, limit further nephrotoxic exposures/events, correcnt and maintain euvolemia (restore electrolyte and acid-base balance), regain life-sustaining renal function
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What are the non-pharmacologic prevention points in AKI?
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hydration (prevent vascular depletion), hydration and sodium loading prior to amphotericin or contrast dye admin, slow infusion rate of amphotericin B, use liposomal formulation of amphotericin B as is less nephrotoxic
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What are the EBM nephrotoxic preventive drugs mentioned?
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acetylcystein (most common; 600mg po bid on day before contrast dye), theophylline (not common; 200mg IV 30 mins prior to radiocontrast dye), insulin (maintains tight glycemic control which is associated with 41% reduction in ARF)
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What are the non-EBM nephrotoxic preventive drugs mentioned?
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dopamine, loop diuretics, fenoldopam
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In established ARF, what is the treatment goal?
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eliminate further harm to kidneys, prevent extension of injury
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What are the indications for renal replacement therapies?
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AEIOU - Acidosis, Electrolyte abnormalities, intoxication, volume overload, uremia (BUN > 100mg/dl) or uremic symptoms
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What is the goal urine output in diuretic use for ARF?
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0.5-1ml/kg/h
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What is used to produce diuresis in patients with ARF?
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mannitol and loop diuretics (reserved for fluid-overloaded patients who make adequate urine in response to diuretics)
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What are the proposed mechanisms of benefit in mannitol for diuresis in AKI?
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increased filtration pressure, improved urine flow rates, reduced tubular cell inflammation, improved renal blood flow caused by a decrease in renal vascular resistance; BENEFIT NOT established
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Who should not get mannitol?
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anuric or oliguric patients ---> hyperosmolar state
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What is the moa of loop diuretics?
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decrease tubule obstruction and cause renal vasodilation resulting in increased renal blood flow by affecting the ascending limb of loop of Henle to increase solute diuresis
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What were the loop diuretics mentioned in class?
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bumetanide, furosemide, torsemide, ethacrynic acid (typicall reserved for patients with sulfa compound allergies)
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What is the equipotent dosing for furosemide, torsemide, and bumetanide?
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furosemide 40mg = torsemide 20mg = bumetanide 1mg
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What are the ADEs of loop diuretics?
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worsen ARF, electrolyte abnormalities, ototoxicity
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What is the most commonly used loop diuretic?
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furosemide
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What are used synergistically with loop diuretics for resistant edema and fluid overload?
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metolazone and chlorothiazide
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What is an advantage of metazolone over other thiazide diuretics?
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effective at GFR <20 ml/min; other diuretics generally not effective at GFR this low
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What is the dosing for metolazone?
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5-10mg po
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What is the dosing for chlorothiazide?
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500-1000mg IV
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What meds are used in acute tx of hyperkalemia?
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calcium gluconate (protects heart), insulin (shifts K out of vascular space and into cells), albuterol (shifts K into the cells), lasix (increases renal excretion of K), kayexalate (removes K from gut in exchange for sodium)
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