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NURS 2514 > Week 3 - Acute Kidney Injury > Flashcards

Week 3 - Acute Kidney Injury Flashcards

1
Q

what is prerenal kidney dsease

A
  • problem with blood flow into the kidney
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2
Q

what is intrarenal kidney disease

A
  • damage to the kidney
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3
Q

what is postrenal kidney disease

A
  • obstruction of the urinary tract
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4
Q

in pre and post renal disease is the kidney itself damaged? what does this mean?

A
  • no it is not

- means we have time to act to prevent damage to the kidney itself

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5
Q

what is acute kidney injury

A
  • represents a group of disorders that cause a rapid deterioration in renal function & resulting in azotemia
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6
Q

how does AKI present (2)

A
  1. rapid rising BUN and creatinine

2. diminished urine volume (oliguria)

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7
Q

what is one of the most common causes of AKI

A
  • sepsis
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8
Q

how does sepsis cause AKI (2)

A
  • sepsis causes hypotension thru systemic vasodilation = kidneys are not perfused
  • patients with sepsis are often exposed to nephrotoxic antibiotics to treat the infection
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9
Q

list 4 causes of prerenal disease

A
  • hypovolemia
  • septicemia & septic shock
  • heart failure
  • interruption of renal blood flow caused by surgery or other causes
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10
Q

how does hypovolemia cause prerenal disease

A
  • decreased blood vol = blood is diverted away from the kidneys to keep vital organs perfused
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11
Q

list 4 things that can cause hypovolemia

A
  • dehydration
  • loss of GI fluid
  • hemorrhage
  • fluid seqeuestration
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12
Q

what is fluid sequestration? how could this cause prerenal injury?

A
  • fluid shift from blood space to a 3rd space
    ex. ascites
  • although you still have the same volume of fluid in the body, there is less fluid available to circulate
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13
Q

how does heart failure cause prerenal disease

A
  • if the heart is not pumping enough blood it will cause decreased blood flow to the kidneys
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14
Q

list 2 examples of causes of postrenal disease

A
  • ureteral obstruction

- bladder outlet obstruction

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15
Q

list 2 examples of ureteral obstruction

A
  • calculi

- tumours

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16
Q

list 2 examples of bladder outlet obstruction

A
  • prostatic hyperplasia

- ureteral structures

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17
Q

list 7 causes of intrarenal disease

A
  • acute tubular necrosis
  • prolonged renal ischemia
  • exposure to nephrotoxic drugs
  • exposure to heavy metals
  • exposure to organic solvents
  • acute glomerulonephritis
  • acute pyelonephritis
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18
Q

list 3 examples of nephrotoxic drugs

A
  • aminoglycosides
  • radiocontrast agents
  • NSAIDs
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19
Q

what is an example of an aminoglycoside

A
  • gentamycin
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20
Q

what are 3 examples of conditions that cause preexisting renal hypoperfusion

A
  • HF
  • diabetes
  • renal stenosis
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21
Q

what is the effect of NSAIDs and ACE inhibtors on people with preexisting renal hypoperfusion? why does this occur?

A
  • may cause them to develop AKI
  • bc prostaglandins dilate the afferent arteriole
  • and angiotensin 2 acts to constrict the efferent artiole
    and both of these are blocked by the meds
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22
Q

describe the effect of heme-containing molecules on the renal tubules

A
  • heme is small enough to be filtered = toxic & cause damage to the tubules
23
Q

list 3 things that can cause AKI thru the release of heme

A
  • eclampsia
  • hemolysis
  • muscle damage due to trauma
24
Q

describe how hemolysis can cause AKI

A
  • breakdown of RBC = released hgb = heme-containing group is filtered & causes damage to the kidney
25
Q

describe how muscle damage can cause AKI

A
  • damage to muscle causes release of myoglobin which contains heme
26
Q

list 1 examples of muscle damage

A
  • hypermyoglobinemia / rhabdomyolysis
27
Q

what is eclampsia

A
  • seizures during or shortly after birth
  • follows preeclampsia: systemic vasoconstriction and HTN

not rlly sure how this contributes to heme being filtered

28
Q

what occurs in the early stages of prerenal disease? what does this result in?

A
  • GFR is decreased due to renal hypoperfussion

= prerenal azotemia

29
Q

manifestations of AKI are a result of what??

A
  • tubule obstruction by necrotic tissue
30
Q

what does tubule obstruction by necrotic tissue in AKI cause?

A
  • increases the intratubular pressure

= offsets the glomerular filtration pressure = dramatic reduction in GFR

31
Q

what 2 things does acute tubular necrosis result in?

A
  • loss of tubular function (reabsorb & secrete)

- failure to conc. urine

32
Q

describe the effects of nephortoxins on the kidney (6)

A
  1. meds enter the filtrate & become v conc
  2. concentrated nephrotoxin causes the tubule wall to become swollen & necrotic
  3. lumen becomes shrunken = increased resistance
  4. filtrate has high back pressire
  5. = decreased GFR
  6. oliguria
33
Q

what are casts?

A
  • cell debris & protein that combine together within the tubule & are excreted in the urine
34
Q

what are the early signs of AKI (4)

A
  1. elevated BUN and creatinine
  2. oliguria
  3. hyperkalemia
  4. fatigue & malaise
35
Q

what causes elevated BUN and creatine in the early signs of AKI

A
  • decreased GFR (due to the high back pressure in the filtrate)
36
Q

describe the ratio of BUN:creatinine during prerenal azotemia; what causes this?

A
  • high ratio
  • during prerenal azotemia, the tubules still function properly
  • urea is filtered & reabsorbed while creatinine is only filtered
  • since urea is still being reabsorbed, the BUN is higher
37
Q

what might cause BUN to increase rapidly? include 2 examples

A
  • increased protein catabolism

ex. during fever & sepsis

38
Q

what might cause creatinine to be unusually high

A
  • if rhabdomyolysis is the cause
39
Q

what causes oliguria during early AKI

A
  • decreased GFR and/or tubule obstruction
40
Q

what % of patients do not have oliguria? this will occur especially when it is caused by???

A
  • 25% of patients will not have oliguria

- especially if AKI is caused by nephrotoxins

41
Q

what causes hyperkalemia during early AKI (2)

A
  • if GFR is significantly reduced

- & there is significant acidosis

42
Q

what can hyperkalemia cause during early AKI (2)

A
  • ECG changes

- arrhythmias

43
Q

list 4 things that can treat hyperkalemia during early AKI

A
  • insulin/glucose
  • salbuterol
  • Kayexalate
  • furosemide
44
Q

what causes fatigue & malaise during early AKI (4)

A
  • water intoxication & hyponatremia
  • hyperkalemia
  • acidosis
  • elevated metabolic wastes
45
Q

list late symptoms of AKI (5)

A
  • low ratio of BUN:creatinine
  • pulmonary/CVS effects
  • edema
  • altered mental status
  • urinalysis abnormalities
46
Q

why is there now a low ratio of BUN; creatinine during late AKI

A
  • during acute tubular necrosis, the tubules are now damaged so it is no longer reabsorbing urea
47
Q

what pulmonary manifestations occur with late AKI? what causes them?

A
  • dyspnea
  • orthopnea
  • rales & crackles
  • 3rd heart sound

due to fluid overload

48
Q

what causes edema in late AKI

A
  • fluid overload
49
Q

what causes altered mental status in late AKI (3)

A
  • when metabolic wastes become increasing elevated in the blood
  • altered electrolytes
  • acidosis
50
Q

what is a good indicator of toxicity

A
  • BUN
51
Q

what might the urinalysis show during late AKI

A
  • hematuria
  • proteinuria
  • pyuris
  • with acute tubular necrosis: casts & very dilute urine
52
Q

what is pyuris? what is it a sign of?

A
  • pus in the urine

- sign of infection

53
Q

regardless of eitology, AKI will likely result in what? why?

A
  • this will result in necrotic death of the tubule epithelial cells bc they are furthest away (=acute tubular necrosis) without successful treatment

NURS 2514 (75 decks)

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