Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

GU2 - Urology > Pharm - AKI and CKD > Flashcards

Pharm - AKI and CKD Flashcards

(62 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what type of IV fluids are preferred?

A
  • crystalloid

- ex: isotonic saline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are fluids targeted at?

A
  • physiological endpoints such as:
  • mean arterial pressure
  • urine output
  • CO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does the total amount of administered volume depend on?

A
  • degree of volume depletion

- ongoing losses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the preferred method to treating volume overload?

A

diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

preferred diuretic

A
  • loop diuretic

- provides greater natriuretic effect than thiazides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

starting dose and agent for fluid overload

A
  • IV furosemide
  • 40-80 mg
  • dose can be titrated up if needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A
  • EKG changes

- peripheral neuromuscular abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what to measure to monitor hypocalcemia in AKI pts

A
  • serum ionized Ca (metabolically active)

- total serum Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
if the serum ionized Ca concentration is high in a pt w/ hyperphosphatemia, what is the perferred tx?
non-calcium phosphate binders - lanthanum carbonate - sevelamer - Al(OH)3
26
if a pt has nephrotoxic effects from an aminoglycoside, when would the ATN occur?
5-10 days after therapy is initiated
27
lab findings in nephrotoxicity d/t aminoglycosides
- 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
what are the preventative action that can be taken to decrease the chance of nephrotoxicity when taking an aminoglycoside?
- select other abx - avoid volume depletion - monitor aminoglycoside serum levels - monitor renal fxn
29
if nephrotoxicity d/t aminoglycoside occurs, when does SCr return to nl?
after 3 weeks
30
what are the risk factors for vancomycin nephrotoxicity?
- coadmin of vanc and aminoglycoside - total daily dose of vanc > 4g - duration of therapy - presence of underlying renal dysfunction - critical illness
31
clinical manifestations d/y radiographic contrast dye
- 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
what preventative actions can be taken to prevent radiographic contrast dye toxicity?
- minimize dose - use noniodinated contrast studies - avoid nephrotoxic drugs - IV fluids - n-acetylcysteine before and after
33
what is the timeframe of ACE/ARB nephrotoxicity?
- within 3-5 days of starting therapy | - stabilizes 1-2 weeks and is reversible when drug is stopped
34
what is the mechanism by which ACE/ARB cause nephrotoxicity?
- angiotensin II synthesis decreases --> dilation of the efferent arteriole --> - reduced outflow resistance from glomerulus --> decrease hydrostatic pressure in glomeruluar capillaries - decreased GFR
35
given a pt w/ nephrotoxicity d/t ACE or ARB, when do you dc therapy?
- when hyperkalemia can't be controlled | - when serum Cr increases > 30% above baseline w/i 6-8 weeks when BP is reduced
36
presentation of NSAID induced nephrotoxicity
- c/o diminished urine output - weight gain - edema - urine Na concentration <20 - elevated BUN, Scr, K, and BP
37
what is the mechanism of NSAID and COX-2 inhibitors in causing nephrotoxicity
- disruption of nl intraglomerular autoregulation | - PG inhibition results in renal ischemia and reduced GFR
38
risk factors for NSAID and COX-2 inhibitor nephrotoxicity
- >60 yo - preexisting kidney dz - hepatic dz w/ acites - HF - dehydration - SLE - concurrent tx w/ ACE/ARB or diuretics
39
prevention of NSAID and COX-2 inhibitor nephrotoxicity
- 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
CrCl equation
(140-age)(weight in kg) / (72 x SCr) x .85 if female
41
what is the goal of iron therapy for pts w/ CKD?
to correct absolute iron deficiency and/or increase Hgb level
42
What is needed before ESA (EPO-stimulating agents) therapy in CKD?
- iron assessment - correction of anemia (if needed) - correction of BP
43
what is the goal of ESA tx in dialysis pts?
- avoid transfusions | - minimize or avoid anemia sx
44
indication for ESA therapy in the tx of anemia in dialysis pts
hemoglobin level <10 g/dL
45
what is the hgb goal to attain in ESA therapy?
11-12 g/dL
46
ESA agents
- epoetin alfa (Epogen, Procrit) | - darbepoetin alfa (Aranesp)
47
MoA of ESAs
- 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
what is nl serum phosphate?
2.5 - 4.5 mg/dL
49
what is the therapy goal for serum phosphorus in non-dialysis pts?
<4.5 in nl range
50
what is the therapy goal for serum phosphorus in dialysis pts?
between 3.5 - 5.5 mg/dL
51
Ca-containing phosphate binders
- calcium carbonate (tums) | - calcium acetate (phoslo)
52
ADRs of ca-containing phosphate binders
- hypercalcemia - extraskeletal Ca phosphate deposition - increase risk of vascular and tissue calcification
53
non-calcium containing phosphate binders
- sevelamer HCl (renagel) | - sevelamer carbonate (renvela)
54
iron based binder products
- sucroferric oxyhydroxide (velphoro) | - ferric citrate (auryxia)
55
pt status: hypocalcemic | -what product to use?
ca-containing binder
56
pt status: normocalcemic | -what product to use?
- pts w/o vascular calcification or adynamic bone dz: Ca-containing binder - pts taking vit. D: non-Ca containing binder
57
pt status: hypercalcemic | -what product to use?
non-Ca containing binder
58
pt status: adynamic bone dz | -what product to use?
non-Ca containing binder
59
pt status: vascular calcification | -what product to use?
non-Ca containing binder
60
the amount of elemental Ca contained in the phosphate binder should not exceed ____ ?
1500 mg per day
61
tx parameters for the use of ergocalciferol in CKD
- check 25,hydroxy vit. D level - deficiency = calcidiol < 30 ng/mL - replace w/ vit. D2 if low
62
be able to . . .
- use CrCl equation | - use the calculated CrCl to select appropriate drug dose

GU2 - Urology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions