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GU2 - Urology > Pharm - AKI and CKD > Flashcards

Pharm - AKI and CKD Flashcards

1
Q

overview of the general management of a pt w/ AKI

A

management of life-threatening fluid and electrolyte abnormalities d/t AKI should be started immediately

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2
Q

indication for correction of fluid status

A
  • pt w/ clinical hx of fluid loss (v/d)
  • PE consistent w/ hypovolemia (hypotension and tachy)
  • and/or oliguria
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3
Q

what type of IV fluids are preferred?

A
  • crystalloid

- ex: isotonic saline

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4
Q

what is the overall goal of fluid therapy ?

A

increase CO and improve tissue oxygenation in pts who are preload dependent or volume responsive

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5
Q

what are fluids targeted at?

A
  • physiological endpoints such as:
  • mean arterial pressure
  • urine output
  • CO
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6
Q

what does the total amount of administered volume depend on?

A
  • degree of volume depletion

- ongoing losses

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7
Q

what indications during fluid treatment would lead you to think pre-renal vs. AKI?

A
  • pre-renal: restoration of adequate urine flow and improvement of renal fxn w/ fluid resuscitation
  • ADK: don’t respond to administered volume w/ increase urine output or have decrease Cr
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8
Q

what is the preferred method to treating volume overload?

A

diuretics

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9
Q

monitoring hypervolemia when using diuretics

A
  • pts should be regularly checked to see if urine output responds
  • if no increase, dyalsis should be considered
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10
Q

preferred diuretic

A
  • loop diuretic

- provides greater natriuretic effect than thiazides

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11
Q

starting dose and agent for fluid overload

A
  • IV furosemide
  • 40-80 mg
  • dose can be titrated up if needed
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12
Q

what is the approach to management of hyperkalemia?

A

in general, all pts w/ AKI and hyperkalemia that’s refractory to medical therapy should be dialyzed unless the cause is easily reversed

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13
Q

if it is hyperkalemic emergency, what is the treatment?

A
  • IV calcium
  • IV insulin
  • therapy to remove excess K from body:
  • diuretic
  • GI cation exchanger (Kayelexate)
  • and/or dialysis
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14
Q

when would immediate therapy to correct hyperkalemia while waiting on dialysis be warranted?

A
  • EKG changes

- peripheral neuromuscular abnormalities

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15
Q

specific tx of hyperkalemia is directed at what?

A

antagonizing the membrane effects of K, driving extracellular K into the cells, or removing excess K from the body

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16
Q

What is the general approach to management of metabolic acidosis?

A
  • dialysis
  • bicarb administration
  • the choice of therapy depends on absence/presence of vol. overload and the underlying cause and severity of acidosis
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17
Q

in a patient with metabolic acidosis that is also volume overloaded, what is the preferred tx?

A
  • dialysis

- bicarb could contribute to vol. overload

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18
Q

what is the goal for pts w/ metabolic acidosis d/t bicarb loss from diarrhea who are treated w/ bicarb?

A
  • 20-22 mEq/L serum bicarb

- pH > 7.2

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19
Q

what is the relationship b/w hypocalcemia and AKI?

A
  • hypocalcemia is common among AKI pts

- related to increases in serum phosphorus levels cause by reduced GFR

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20
Q

what to measure to monitor hypocalcemia in AKI pts

A
  • serum ionized Ca (metabolically active)

- total serum Ca

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21
Q

tx of hypocalcemia when the pt is asymptomatic and hyperphosphatemia is present

A
  • initial therapy is the correction of the hyperphosphatemia
  • tx w/ oral phosphate binders
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22
Q

tx of symptomatic pts w/ hypocalcemia

A
  • more aggressive
  • IV Calcium
  • caution: if pt is severely hyperphosphatemic, this may result in the deposition of Ca phosphate into vasculature and organs
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23
Q

tx of all AKI pts w/ moderately to severely elevated serum phosphate (>6mg/dL)

A
  • dietary phosphate binders

- selection of the binder depends on level of serum ionized Ca

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24
Q

if the serum ionized Ca concentration is low in a pt w/ hyperphosphatemia, what is the preferred tx?

A

calcium-containing phosphate binders

  • calcium acetate
  • calcium carbonate
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25
Q

if the serum ionized Ca concentration is high in a pt w/ hyperphosphatemia, what is the perferred tx?

A

non-calcium phosphate binders

  • lanthanum carbonate
  • sevelamer
  • Al(OH)3
26
Q

if a pt has nephrotoxic effects from an aminoglycoside, when would the ATN occur?

A

5-10 days after therapy is initiated

27
Q

lab findings in nephrotoxicity d/t aminoglycosides

A
  • gradual progressive rise in serum creatinine (.5-1.0 mg/dL) and BUN
  • decrease in CrCl
  • OR:
  • 50% increase in plasma creatinine concentration from baseline

other:
- mild proteinuria
- hyaline and granular casts
- FE(Na) > 1%

28
Q

what are the preventative action that can be taken to decrease the chance of nephrotoxicity when taking an aminoglycoside?

A
  • select other abx
  • avoid volume depletion
  • monitor aminoglycoside serum levels
  • monitor renal fxn
29
Q

if nephrotoxicity d/t aminoglycoside occurs, when does SCr return to nl?

A

after 3 weeks

30
Q

what are the risk factors for vancomycin nephrotoxicity?

A
  • coadmin of vanc and aminoglycoside
  • total daily dose of vanc > 4g
  • duration of therapy
  • presence of underlying renal dysfunction
  • critical illness
31
Q

clinical manifestations d/y radiographic contrast dye

A
  • nonoliguria kidney injury w/i 24-48 hrs after admin
  • SCr peak at 3-4 days after exposure
  • muddy brown granular and epithelial casts
  • epithelial cells
  • low FE(Na)
  • low/absent proteinuria
32
Q

what preventative actions can be taken to prevent radiographic contrast dye toxicity?

A
  • minimize dose
  • use noniodinated contrast studies
  • avoid nephrotoxic drugs
  • IV fluids
  • n-acetylcysteine before and after
33
Q

what is the timeframe of ACE/ARB nephrotoxicity?

A
  • within 3-5 days of starting therapy

- stabilizes 1-2 weeks and is reversible when drug is stopped

34
Q

what is the mechanism by which ACE/ARB cause nephrotoxicity?

A
  • angiotensin II synthesis decreases –> dilation of the efferent arteriole –>
  • reduced outflow resistance from glomerulus –> decrease hydrostatic pressure in glomeruluar capillaries
  • decreased GFR
35
Q

given a pt w/ nephrotoxicity d/t ACE or ARB, when do you dc therapy?

A
  • when hyperkalemia can’t be controlled

- when serum Cr increases > 30% above baseline w/i 6-8 weeks when BP is reduced

36
Q

presentation of NSAID induced nephrotoxicity

A
  • c/o diminished urine output
  • weight gain
  • edema
  • urine Na concentration <20
  • elevated BUN, Scr, K, and BP
37
Q

what is the mechanism of NSAID and COX-2 inhibitors in causing nephrotoxicity

A
  • disruption of nl intraglomerular autoregulation

- PG inhibition results in renal ischemia and reduced GFR

38
Q

risk factors for NSAID and COX-2 inhibitor nephrotoxicity

A
  • > 60 yo
  • preexisting kidney dz
  • hepatic dz w/ acites
  • HF
  • dehydration
  • SLE
  • concurrent tx w/ ACE/ARB or diuretics
39
Q

prevention of NSAID and COX-2 inhibitor nephrotoxicity

A
  • avoid in high risk pts
  • lowest effective dose
  • use for shortest possible time
  • avoid dehydration
  • avoid hypotensive and nephrotoxic agents
  • optimal management of predisposing medical probs
40
Q

CrCl equation

A

(140-age)(weight in kg) / (72 x SCr)

x .85 if female

41
Q

what is the goal of iron therapy for pts w/ CKD?

A

to correct absolute iron deficiency and/or increase Hgb level

42
Q

What is needed before ESA (EPO-stimulating agents) therapy in CKD?

A
  • iron assessment
  • correction of anemia (if needed)
  • correction of BP
43
Q

what is the goal of ESA tx in dialysis pts?

A
  • avoid transfusions

- minimize or avoid anemia sx

44
Q

indication for ESA therapy in the tx of anemia in dialysis pts

A

hemoglobin level <10 g/dL

45
Q

what is the hgb goal to attain in ESA therapy?

A

11-12 g/dL

46
Q

ESA agents

A
  • epoetin alfa (Epogen, Procrit)

- darbepoetin alfa (Aranesp)

47
Q

MoA of ESAs

A
  • induces erythropoesis by stimulating the division and differentialtion of committed erythroid progenitor cells
  • induces the release of reticulocytes from the bone marrow into the blood stream where they mature
  • reticulocytes increase followed by a rise in hct and hgb
48
Q

what is nl serum phosphate?

A

2.5 - 4.5 mg/dL

49
Q

what is the therapy goal for serum phosphorus in non-dialysis pts?

A

<4.5 in nl range

50
Q

what is the therapy goal for serum phosphorus in dialysis pts?

A

between 3.5 - 5.5 mg/dL

51
Q

Ca-containing phosphate binders

A
  • calcium carbonate (tums)

- calcium acetate (phoslo)

52
Q

ADRs of ca-containing phosphate binders

A
  • hypercalcemia
  • extraskeletal Ca phosphate deposition
  • increase risk of vascular and tissue calcification
53
Q

non-calcium containing phosphate binders

A
  • sevelamer HCl (renagel)

- sevelamer carbonate (renvela)

54
Q

iron based binder products

A
  • sucroferric oxyhydroxide (velphoro)

- ferric citrate (auryxia)

55
Q

pt status: hypocalcemic

-what product to use?

A

ca-containing binder

56
Q

pt status: normocalcemic

-what product to use?

A
  • pts w/o vascular calcification or adynamic bone dz: Ca-containing binder
  • pts taking vit. D: non-Ca containing binder
57
Q

pt status: hypercalcemic

-what product to use?

A

non-Ca containing binder

58
Q

pt status: adynamic bone dz

-what product to use?

A

non-Ca containing binder

59
Q

pt status: vascular calcification

-what product to use?

A

non-Ca containing binder

60
Q

the amount of elemental Ca contained in the phosphate binder should not exceed ____ ?

A

1500 mg per day

61
Q

tx parameters for the use of ergocalciferol in CKD

A
  • check 25,hydroxy vit. D level
  • deficiency = calcidiol < 30 ng/mL
  • replace w/ vit. D2 if low
62
Q

be able to . . .

A
  • use CrCl equation

- use the calculated CrCl to select appropriate drug dose

GU2 - Urology (10 decks)

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