Ios3&4 Exam 1

Front 1

furosemide is excreted primarily by which organ?

Back 1

the kidneys (renally excreted)

Front 2

bumetanide and torsemide are excreted primarily by which organ?

Back 2

the liver (hepatically excreted)

Front 3

which two diuretic drug classes are secreted from the organic acid system in the PCT? what potential side effect might this lead to?

Back 3

loop and thiazide diuretics. this can lead to hyperuricemia and gout.

Front 4

which diuretic drug class can be used to treat hypercalciuria?

Back 4

thiazide diuretics (they increase the reabsorption of Ca++ from the tubule filtrate).

Front 5

eplerenone belongs to which drug class(es)?

Back 5

aldosterone antagonists (potassium sparing diuretic)

Front 6

why does an increase in delivery of Na+ to the collecting duct stimulate more K+ to be secreted to the tubule lumen?

Back 6

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)

Front 7

do glucocorticoids inhibit or stimulate the release of ADH?

Back 7

glucocorticoids inhibit the release of ADH

Front 8

does nicotine inhibit or stimulate the release of ADH?

Back 8

nicotine stimulates the release of ADH

Front 9

why is ADH/vasopression indicated for bleeding disorders?

Back 9

because it increases the secretion of von Willebrand factor and factor VIII, which ultimately decrease bleeding time.

Front 10

acetazolamide

Back 10

CA Inhibitor

Front 11

amiloride

Back 11

K+ Sparing

Front 12

8-arginine vasopression

Back 12

antidiuretic

Front 13

brinzolamide

Back 13

CA Inhibitor (glaucoma)

Front 14

bumetanide

Back 14

loop diuretic

Front 15

chlorthalidone

Back 15

thiazide

Front 16

desmopression

Back 16

antidiuretic

Front 17

dorzolamide

Back 17

CA inhibitor (glaucoma)

Front 18

eplerenone

Back 18

aldosterone antagonist

Front 19

ethacrynic acid

Back 19

loop diuretic

Front 20

furosemide

Back 20

loop diuretic

Front 21

glycerin

Back 21

osmotic

Front 22

hydrochlorothiazide

Back 22

thiazide

Front 23

indapamide

Back 23

thiazide

Front 24

8-lysine vasopressin

Back 24

antidiuretic

Front 25

mannitol

Back 25

osmotic

Front 26

metolazone

Back 26

thiazide

Front 27

tolvaptan

Back 27

v2 vasopressin receptor antagonist

Front 28

spironolactone

Back 28

aldosterone antagonist

Front 29

torsemide

Back 29

loop diuretic

Front 30

triamterene

Back 30

K+ sparing

Front 31

urea

Back 31

osmotic

Front 32

pharmacokinetic diuretic resistance due to decreased serum albumin is most often seen in patients with either or both of what two conditions?

Back 32

nephrotic syndrome and chronic liver disease

Front 33

decreased renal blood flow, increased organic acids, and proteinuria are all possible contributing factors to what?

Back 33

decreased concentration of diuretics at site of action (pharmcokinetic diuretic resistance)

Front 34

pharmacodynamic issues leading to diuretic resistance are only described with what class of diuretics?

Back 34

loop diuretics

Front 35

how is "braking" (decrease in response to a loop diuretic during acute dosing) managed?

Back 35

avoid over-aggressive diuresis and intravascular volume loss; remove fluid slowly

Front 36

how is rebound sodium retention managed?

Back 36

more frequent dosing of short-acting diuretics and maintaining a sodium restricted diet

Front 37

how is secondary sodium reabsorption (leading to decreased effectiveness of loop diuretic) managed?

Back 37

combine the loop diuretic with a thiazide diuretic (combination therapy)

Front 38

what is the first medication one should use to manage peripheral edema?

Back 38

loop diuretic. e.g. furosemide 20-40mg qd or bid.

Front 39

what is considered an adequate response to loop diuretics when treating acute severe edema?

Back 39

250-500ml urine over 2 hours (depending on kidney function)

Front 40

what is the diuretic of choice for management of ascites? what is this diuretic's MOA

Back 40

spironolactone - it blocks aldosterone

Front 41

when is combination therapy of spironolactone with a loop diuretic approrpiate? what is the ideal ratio between the two drugs?

Back 41

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)

Front 42

what is goal fluid loss in ascites without peripheral edema?

Back 42

500 mg/day (0.5 kg/day)

Front 43

what is goal fluid loss in ascites with peripheral edema?

Back 43

1000 ml/day (1.0kg/day)

Front 44

what are the 5 main adverse effects of diuresis?

Back 44

hypovolemia, azotemia, electrolye abrnomalities, acid-base disorders, ototoxicity

Front 45

is kideny secretion and reabsorption considered active or passive transport?

Back 45

active transport

Front 46

pre-renal kidney disease is related to a decrease in what physiological parameter?

Back 46

decrease in effective circulating volume

Front 47

glomerulonephritis, interstitial nephritis and acute tubular necrosis are all classified as what type of condition?

Back 47

acute intrinsic kidney injury

Front 48

if fractional excretion of sodium (FE-Na) is less than 1%, this might indicate what type of kidney dysfunction?

Back 48

pre-renal (low sodium means low circulating volume and more Na reabsorption by the kidneys.

Front 49

if fractional excretion of urea nitrogen (FE_un) is less than 35%, this might indicate what type of kidney dysfunction?

Back 49

pre-renal

Front 50

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?

Back 50

less than 500 ml/day urine. oliguria can indicate pre-renal or ATN.

Front 51

what is the range of normal urine osmolality?

Back 51

350-500 mosmol/kg

Front 52

persistant microalbuminuria with no other kidney function abnormalities (such as an increased SCr) is indicative of what condition?

Back 52

preclinical CKD

Front 53

constriction of the afferent artiole and dilation of the efferent arteriole in the kidney can lead to what condition?

Back 53

functional acute renal failure

Front 54

why are vasoactive agents commonly used to treat hepatorenal syndrome?

Back 54

to cause vasoconstriction in the body, which will improve pressure and flow of blood to the kidneys

Front 55

what are examples of some drugs used to treat hepatorenal syndrome?

Back 55

vasopressin, octreotide + midodrine (alpha agonists), norepinephrine.

Front 56

arginine vasopressin is often used to treat hepatorenal syndrome. what type of receptor does this drug act on?

Back 56

V1 receptors

Front 57

what is the mechanism of immunosuppressents (such as cyclosporine and tacrolimus) in drug-induced functional ARF?

Back 57

renal vasoconstriction

Front 58

the following conditions can lead to what kind of renal failure?
hypotension, hemmorrhage, dehydration, hypoalbuminemia, diuretic therapy, and renal artery occlusion

Back 58

pre-renal acute renal failure

Front 59

what are three compensatory mechanisms for prerenal acute renal failure?

Back 59

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.

Front 60

what volume of urine output per day would you expect in a patient with functional or pre-renal kidney failure?

Back 60

< 500 mL urine per day

Front 61

what percent fractional excretion of sodium (FENa) would you expect in a patient presenting with pre-renal or functional kidney failure?

Back 61

less than 1%

Front 62

which conditions accounts for 85% of all intrinsic acute renal failure? what are two general main causes of this condition?

Back 62

acute tubular necrosis. caused either by ischemia or toxins.

Front 63

what are the four main drug clases that can induce acute tubular necrosis?

Back 63

chemotherapy, aminoglycoside antibiotics, antifungals and radiocontrast media

Front 64

patients who take statins are at increased risk of what kind of kidney dysfunction?

Back 64

rhabdomyolysis induced acute tubular necrosis

Front 65

would you expect a high or low BUN/Scr ratio in instrinsic renal failure (especially compared to pre-renal failure)?

Back 65

low BUN/Scr ratio (less than 15:1)

Front 66

Would you expect a high or low FENa in instrinsic renal failure?

Back 66

high FENa. (greater than 2%)

Front 67

acyclovir, methotrexate, and cocaine are all example of drugs that can induce what kind of renal failure?

Back 67

postrenal ARF

Front 68

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?

Back 68

post-renal ARF

Front 69

a patient with a high FENa, dilute urine, and presence of eosinophils in urine is likely to have what condition?

Back 69

intersitial nephritis (intrinsic acute renal failure)

Front 70

what are general treatment approaches for interstitial damage of the kidneys?

Back 70

removal of inciting agent and/or immunosuppressive therapy (streoids)

Front 71

what is the reasoning behind treating a patient with hyperkalemia with sodium bicarbonate?

Back 71

inducing metabolic alkalosis will cause the potassium to shift from the ECF to the ICF.

Front 72

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?

Back 72

increase flow to the kidneys by giving volume prior to giving the diuretic drug.

Front 73

why do we avoid potassium sparing diuretics in patients with ARF?

Back 73

because hyperkalemia is already a concern with ARF.

Front 74

seizure, coma, death is the worst case scenario of build up of which substance during ARF?

Back 74

urea (uremia)

Front 75

AEIOU is an acronym used for the indications for renal replacement therapy (RRT). what does it stand for?

Back 75

acid-base abnormalities<br>
electrolye imbalance<br>
intoxications<br>
fluid overload<br>
uremia

Front 76

which type of ARF is dialysis most often indicated for?

Back 76

acute tubular necrosis

Front 77

in what three different ways does contrast media induce acute renal failure?

Back 77

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)

Front 78

why is bicarbonate used to prevent contrast media induced acute renal failure?

Back 78

bicarbonate infusions before and after contrast procedure provide antioxidant activity as well as they provide a source of fluid and hydration.

Front 79

which combination therapy for preventing constrast induced nephropathy is considered to be the most superior?

Back 79

sodium bicarbonate + NAC

Front 80

what is the most common cause of chronic kidney disease?

Back 80

diabetes

Front 81

what are the two defining pieces of chronic kidney disease?

Back 81

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

Front 82

at what stage of CKD does adaptation begin to occur?

Back 82

stage 2 (mild CKD)

Front 83

at what stage of CKD have patients reached the point of irreversible kidney damage?

Back 83

stage 3 (moderate CKD)

Front 84

if a patient has a persistant GFR of 45 ml/min/1.73 m^2, what stage of CKD are they classified as?

Back 84

stage 3 (gfr = 30-59 ml/min/1.73m^2)

Front 85

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?

Back 85

Stage 4 (severe CKD). progression to ESRD within 2-4 years.

Front 86

uremia is usually seen in which stage of CKD?

Back 86

stage 5.

Front 87

what changes in the kidney are related to diabetic kidney disease?

Back 87

mesangial expansion and glomerular basement membrane thickening --> damaging capillaries and ihibiting filtration

Front 88

proteinuria is an indicated of kidney damage, but can also inflict damage by itself. what is the mechanism of proteinuria induced damage?

Back 88

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.

Front 89

what gives the glomerular basement membrane (and podocytes) it's negative charge?

Back 89

glycosaminoglycans

Front 90

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?

Back 90

130/80 mmHg. ACE-i or ARB are first line choice. ACE/ARB + diuretic is preferred initial combo therapy.

Front 91

what agents are used to treat (persistant) microalbuminuria?

Back 91

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

Front 92

what is the post-prandial glucose goal in patients with CKD?

Back 92

<180 mg/dL

Front 93

what two main mechanisms are used in stages 3 and 4 CKD to maintain normal levels of K+?

Back 93

increased tubular secretion of K+ in remaining healthy nephrons and increased K+ secretion into the colon.