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93 Cards in this Set
- Front
- Back
furosemide is excreted primarily by which organ?
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the kidneys (renally excreted)
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bumetanide and torsemide are excreted primarily by which organ?
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the liver (hepatically excreted)
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which two diuretic drug classes are secreted from the organic acid system in the PCT? what potential side effect might this lead to?
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loop and thiazide diuretics. this can lead to hyperuricemia and gout.
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which diuretic drug class can be used to treat hypercalciuria?
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thiazide diuretics (they increase the reabsorption of Ca++ from the tubule filtrate).
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eplerenone belongs to which drug class(es)?
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aldosterone antagonists (potassium sparing diuretic)
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why does an increase in delivery of Na+ to the collecting duct stimulate more K+ to be secreted to the tubule lumen?
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As more Na+ reaches the collecting duct, more of it is reabsorbed, increasing the negative potential of the lumen. this pulls the positively charged K+ out of the tubular cell into the lumen to be secreted. (since normally, Na+ exit from the lumen >>> K+ exit from the cell - this imbalance causes the negative potential to begin with)
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do glucocorticoids inhibit or stimulate the release of ADH?
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glucocorticoids inhibit the release of ADH
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does nicotine inhibit or stimulate the release of ADH?
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nicotine stimulates the release of ADH
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why is ADH/vasopression indicated for bleeding disorders?
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because it increases the secretion of von Willebrand factor and factor VIII, which ultimately decrease bleeding time.
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acetazolamide
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CA Inhibitor
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amiloride
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K+ Sparing
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8-arginine vasopression
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antidiuretic
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brinzolamide
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CA Inhibitor (glaucoma)
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bumetanide
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loop diuretic
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chlorthalidone
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thiazide
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desmopression
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antidiuretic
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dorzolamide
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CA inhibitor (glaucoma)
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eplerenone
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aldosterone antagonist
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ethacrynic acid
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loop diuretic
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furosemide
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loop diuretic
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glycerin
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osmotic
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hydrochlorothiazide
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thiazide
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indapamide
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thiazide
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8-lysine vasopressin
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antidiuretic
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mannitol
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osmotic
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metolazone
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thiazide
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tolvaptan
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v2 vasopressin receptor antagonist
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spironolactone
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aldosterone antagonist
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torsemide
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loop diuretic
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triamterene
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K+ sparing
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urea
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osmotic
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pharmacokinetic diuretic resistance due to decreased serum albumin is most often seen in patients with either or both of what two conditions?
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nephrotic syndrome and chronic liver disease
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decreased renal blood flow, increased organic acids, and proteinuria are all possible contributing factors to what?
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decreased concentration of diuretics at site of action (pharmcokinetic diuretic resistance)
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pharmacodynamic issues leading to diuretic resistance are only described with what class of diuretics?
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loop diuretics
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how is "braking" (decrease in response to a loop diuretic during acute dosing) managed?
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avoid over-aggressive diuresis and intravascular volume loss; remove fluid slowly
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how is rebound sodium retention managed?
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more frequent dosing of short-acting diuretics and maintaining a sodium restricted diet
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how is secondary sodium reabsorption (leading to decreased effectiveness of loop diuretic) managed?
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combine the loop diuretic with a thiazide diuretic (combination therapy)
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what is the first medication one should use to manage peripheral edema?
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loop diuretic. e.g. furosemide 20-40mg qd or bid.
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what is considered an adequate response to loop diuretics when treating acute severe edema?
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250-500ml urine over 2 hours (depending on kidney function)
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what is the diuretic of choice for management of ascites? what is this diuretic's MOA
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spironolactone - it blocks aldosterone
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when is combination therapy of spironolactone with a loop diuretic approrpiate? what is the ideal ratio between the two drugs?
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when managing ascites, if spironolactone is inadequate, if there is concern for hyperkalemia, or if the patient also has peripheral edema - combination therapy is appropriate. <br>
ideal ratio is 100 mg/day spironolactone to 40mg/day furosemide (oral for both) |
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what is goal fluid loss in ascites without peripheral edema?
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500 mg/day (0.5 kg/day)
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what is goal fluid loss in ascites with peripheral edema?
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1000 ml/day (1.0kg/day)
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what are the 5 main adverse effects of diuresis?
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hypovolemia, azotemia, electrolye abrnomalities, acid-base disorders, ototoxicity
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is kideny secretion and reabsorption considered active or passive transport?
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active transport
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pre-renal kidney disease is related to a decrease in what physiological parameter?
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decrease in effective circulating volume
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glomerulonephritis, interstitial nephritis and acute tubular necrosis are all classified as what type of condition?
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acute intrinsic kidney injury
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if fractional excretion of sodium (FE-Na) is less than 1%, this might indicate what type of kidney dysfunction?
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pre-renal (low sodium means low circulating volume and more Na reabsorption by the kidneys.
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if fractional excretion of urea nitrogen (FE_un) is less than 35%, this might indicate what type of kidney dysfunction?
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pre-renal
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what is the definition of oliguria in the context of urine volume output per day? what types of renal dysfunction does oliguria play a role in?
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less than 500 ml/day urine. oliguria can indicate pre-renal or ATN.
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what is the range of normal urine osmolality?
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350-500 mosmol/kg
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persistant microalbuminuria with no other kidney function abnormalities (such as an increased SCr) is indicative of what condition?
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preclinical CKD
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constriction of the afferent artiole and dilation of the efferent arteriole in the kidney can lead to what condition?
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functional acute renal failure
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why are vasoactive agents commonly used to treat hepatorenal syndrome?
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to cause vasoconstriction in the body, which will improve pressure and flow of blood to the kidneys
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what are examples of some drugs used to treat hepatorenal syndrome?
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vasopressin, octreotide + midodrine (alpha agonists), norepinephrine.
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arginine vasopressin is often used to treat hepatorenal syndrome. what type of receptor does this drug act on?
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V1 receptors
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what is the mechanism of immunosuppressents (such as cyclosporine and tacrolimus) in drug-induced functional ARF?
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renal vasoconstriction
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the following conditions can lead to what kind of renal failure?
hypotension, hemmorrhage, dehydration, hypoalbuminemia, diuretic therapy, and renal artery occlusion |
pre-renal acute renal failure
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what are three compensatory mechanisms for prerenal acute renal failure?
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sympathetic nervous system activation. <br>
renin-angiotensin-aldosterone activation<br> antidiuretic hormone activation<br> this will result in thirst, increased fluid intake, and sodium and water retention. |
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what volume of urine output per day would you expect in a patient with functional or pre-renal kidney failure?
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< 500 mL urine per day
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what percent fractional excretion of sodium (FENa) would you expect in a patient presenting with pre-renal or functional kidney failure?
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less than 1%
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which conditions accounts for 85% of all intrinsic acute renal failure? what are two general main causes of this condition?
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acute tubular necrosis. caused either by ischemia or toxins.
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what are the four main drug clases that can induce acute tubular necrosis?
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chemotherapy, aminoglycoside antibiotics, antifungals and radiocontrast media
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patients who take statins are at increased risk of what kind of kidney dysfunction?
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rhabdomyolysis induced acute tubular necrosis
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would you expect a high or low BUN/Scr ratio in instrinsic renal failure (especially compared to pre-renal failure)?
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low BUN/Scr ratio (less than 15:1)
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Would you expect a high or low FENa in instrinsic renal failure?
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high FENa. (greater than 2%)
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acyclovir, methotrexate, and cocaine are all example of drugs that can induce what kind of renal failure?
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postrenal ARF
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a patient with increased SCr, low urine output, urine crystals and cellular debris, with variable FENa and BUN/Scr ratios is likely presenting with what condition?
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post-renal ARF
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a patient with a high FENa, dilute urine, and presence of eosinophils in urine is likely to have what condition?
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intersitial nephritis (intrinsic acute renal failure)
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what are general treatment approaches for interstitial damage of the kidneys?
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removal of inciting agent and/or immunosuppressive therapy (streoids)
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what is the reasoning behind treating a patient with hyperkalemia with sodium bicarbonate?
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inducing metabolic alkalosis will cause the potassium to shift from the ECF to the ICF.
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you can overcome diuretic resistance with loop diuretics by combining the loop diuretic with a thiazide diuretic, by giving higher doses and/or more frequent dosings of the diuretic, by decreasing sodium intake, and what other method?
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increase flow to the kidneys by giving volume prior to giving the diuretic drug.
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why do we avoid potassium sparing diuretics in patients with ARF?
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because hyperkalemia is already a concern with ARF.
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seizure, coma, death is the worst case scenario of build up of which substance during ARF?
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urea (uremia)
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AEIOU is an acronym used for the indications for renal replacement therapy (RRT). what does it stand for?
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acid-base abnormalities<br>
electrolye imbalance<br> intoxications<br> fluid overload<br> uremia |
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which type of ARF is dialysis most often indicated for?
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acute tubular necrosis
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in what three different ways does contrast media induce acute renal failure?
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vasoconstriction (leading to renal medullary ischemia)<br>
increased osmotic load which increases blood viscosity and cell oxygen consumption (leading to renal medullary ischemia)<br> direct toxicity (from free radical formation) |
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why is bicarbonate used to prevent contrast media induced acute renal failure?
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bicarbonate infusions before and after contrast procedure provide antioxidant activity as well as they provide a source of fluid and hydration.
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which combination therapy for preventing constrast induced nephropathy is considered to be the most superior?
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sodium bicarbonate + NAC
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what is the most common cause of chronic kidney disease?
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diabetes
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what are the two defining pieces of chronic kidney disease?
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kidney damage for greater or equal to 3 months with or without a decrease in gfr _OR_ gfr less than 60ml/min/1.73m^2 for greater or equal to 3 months with or without kidney damage
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at what stage of CKD does adaptation begin to occur?
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stage 2 (mild CKD)
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at what stage of CKD have patients reached the point of irreversible kidney damage?
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stage 3 (moderate CKD)
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if a patient has a persistant GFR of 45 ml/min/1.73 m^2, what stage of CKD are they classified as?
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stage 3 (gfr = 30-59 ml/min/1.73m^2)
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at which point in CKD staging is a patient guaranteed to reach ESRD? how long does progression to ESRD usually take once the patient reaches this stage?
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Stage 4 (severe CKD). progression to ESRD within 2-4 years.
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uremia is usually seen in which stage of CKD?
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stage 5.
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what changes in the kidney are related to diabetic kidney disease?
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mesangial expansion and glomerular basement membrane thickening --> damaging capillaries and ihibiting filtration
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proteinuria is an indicated of kidney damage, but can also inflict damage by itself. what is the mechanism of proteinuria induced damage?
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release of cytokines which leads to an increase in inflammatory cell infiltration into the glomerulus and tubules, eventually leading to glomerular and tubulointerstitial fibrotic scarring.
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what gives the glomerular basement membrane (and podocytes) it's negative charge?
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glycosaminoglycans
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what is the blood pressure goal for reversing/slowing progression of CKD in patients without severe proteinuria? what medications are most commonly used to reach BP goals?
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130/80 mmHg. ACE-i or ARB are first line choice. ACE/ARB + diuretic is preferred initial combo therapy.
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what agents are used to treat (persistant) microalbuminuria?
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ACE-i, regardless if patient has HTN or not. If patient has uncontrolled HTN, combo therapy of ACE-i and ND-calcium channel blocker is recommended
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what is the post-prandial glucose goal in patients with CKD?
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<180 mg/dL
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what two main mechanisms are used in stages 3 and 4 CKD to maintain normal levels of K+?
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increased tubular secretion of K+ in remaining healthy nephrons and increased K+ secretion into the colon.
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