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SAMS > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

(58 cards)

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1
Q

Functions of the kidney

A
  • excretion of metabolic waste and toxins (urea, creatinine)
  • regulation of water and electrolyte balance
  • regulation of acid base balance
  • regulation of arterial bp
  • secretion of erythropoietin
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2
Q

Acute kidney injury is an abrupt decline in renal function leading to _______

A
  • azotemia
  • fluid abnormalities
  • electrolyte abnormalities
  • acid/base disturbances
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3
Q

AKI is caused by loss of _____ of functioning nephrons

A

75%

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4
Q

Azotemia

A

Increased blood urea and creatinine concentrations

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5
Q

Urea

A

Product of protein catabolism

  • hepatic production
  • freely filtered thru glomeruli
  • passively resorbed by renal tubules (increased w/ decreased tubular flow)
  • increased by high dietary protein intake
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6
Q

Creatinine

A

Product of muscle metabolism

  • constant and proportional to muscle mass (unaffected by diet)
  • freely filtered by glomerulus
  • NOT resorbed by tubules!
  • blood concentration increased by decreased renal excretion
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7
Q

Pre-renal causes of azotemia

A

Decreased renal blood flow

- dehydration, decreased cardiac output

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8
Q

Renal causes of azotemia

A

Renal failure

- kidneys cannot excrete urea/creatinine

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9
Q

Post-renal causes of azotemia

A

Decreased excretion of urine

- urethral obstruction, ruptured bladder

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10
Q

Pre-renal azotemia

A

Decreased renal blood flow

  • kidneys should function properly initially by conserving water and sodium (aldosterone)
  • decreased perfusion may lead to primary renal dz
  • physiologic oliguria
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11
Q

Renal azotemia

A

Result of nephron loss or damage

  • associated w/ renal failure
  • inability to excrete BUN/creatinine due to nephron loss
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12
Q

Post-renal azotemia

A

Inability to excrete urea/creatinine from body

  • urinary tract obstruction, rupture of bladder/urethra/ureter
  • kidneys normal initially, may be damaged due to ischemia
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13
Q

Urine specific gravity

A
  • hyposthenuria: USG<1.008, dilution of filtrate, ADH deficiency
  • isosthenuria: USG 1.008-1.012, no dilution or concentration of filtrate
  • hypersthenuria: USG > 1.012
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14
Q

Pre-renal azotemia differentiation

A
  • USG > 1.030 (dog)
  • USG > 1.035 (cat)
  • exceptions: diuretics, hypoadrenocorticisim
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15
Q

Renal azotemia differentiation

A
  • isosthenuria (1.008-1.012)
  • less than 1.030 (dog) or 1.035 (cat)
  • inadequately concentrated
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16
Q

Post renal azotemia differentiation

A
  • history (trauma)
  • PE (large bladder, ascities)
  • radiographs (urethral obstruction)
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17
Q

Etiologies of AKI

A
  • ischemia
  • toxicity
  • infection
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18
Q

Ischemia and AKI

A

Large renal oxygen demand (20% of CO)

  • hypovolemia
  • anesthesia (hypotension)
  • NSAIDs
  • heat stroke
  • ACE inhibitors
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19
Q

Decreased renal perfusion leads to

A

Decreased O2 –> decreased Na/K pump activity –> cell swelling –> cell injury and death

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20
Q

Renal cortex

A

90% of RBF

- proximal tubule and thick ascending loop most often hit with nephrotoxins due to high metabolic rate

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21
Q

Toxicants hinder ________

A

ATP production

- same mechanism of death as with ischemia

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22
Q

Nephrotoxins

A

Exert deleterious effects directly on the kidney after binding to tubular cell membranes

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23
Q

Nephrotoxicant

A

Chemical or drug that can result in renal injury regardless of whether it is by direct nephrotoxic injury (aminoglycosides) or by renal ischemia (NSAIDs)

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24
Q

Nephrotoxins

Study These Flashcards
A
  • ethylene glycol
  • grapes/raisins
  • aminoglycosides
  • lead
  • NSAIDs
  • amphotericin
  • melamine
  • easter lily
  • hemoglobin
  • myoglobin
  • cisplatin
  • hypercalcemia
25
Infectious causes
- leptospirosis - borreliosis (tubular and glomerular damage) - pyelonephritis (easy to treat, same antibiotic gets lepto)
26
Tubular destruction
- ischemia - toxin - infection
27
Tubular obstruction
- dead cell | - debris
28
Tubular back-leak
- filtrate resorbed between cells into renal interstitium | - inflammation, edema, azotemia
29
Glomerular arteriole constriction
From increased solute delivery to macula densa
30
Afferent arteriolar constriction
Sympathetically mediated vasoconstriction due to: - hypotension - pain - anesthesia Also due to vasomotor nephropathy --> loss of autoregulation
31
Initiation
Immediately follows insult - renal tubular damage occurs - therapy may be helpful, not commonly instituted - usually <48 hrs
32
Maintenance
Clinical signs of uremia occur following tubular damage - variable time - usually when they are presented
33
Recovery
Tubular repair - days-months - does not occur if damage is too severe - remaining nephrons hypertrophy
34
Clinical signs
Uremic syndrome, recent change in urine output - increased: polyuria (unable to concentrate urine) - decreased: oliguria, anuria (more severe injury)
35
Uremia
Build up of uremic toxins - urea, creatinine - uremic syndrome (clinical signs that occur secondary to uremia)
36
Uremic syndrome
- depression - lethargy - anorexia - vomiting - diarrhea - stomatitis (ulcer) - weight loss - ataxia - seizures
37
Polyuria
Increased urine production - >50 ml/kg/day - different than pollakiuria --> increased frequency of urination, lower urinary tract sign
38
Polydipsia
Increased drinking | - >100 ml/kg/day
39
Oliguria
Urine productino <0.5 ml/kg/hr
40
Anuria
Complete absence of urine production
41
Physical exam findings
- normal BCS - may see enlarged kidneys - dehydration - hypovolemia - uremic breath - oral ulceration - fever or hypothermia
42
Clinicopathologic abnormalities
Get blood/urine before fluids!! - normal CBC - increased BUN/creatinine (concurrent isosthenuria or lack of hypersthenuria) - normal to increased K+ - hyperphoosphatemia - metabolic acidosis - hypocalcemia - cylinduria - USH
43
Radiographs
Normal to increased kidneys | - rule out urolithiasis
44
Ultrasound
- normal to enlarged kidneys - loss of corticomedullary distinction - hyperechoic band with EtGly - pyelectasia with pyelonephritis
45
Always perform a ______
Urine culture
46
Arterial bp will often be ______
Increased
47
_______ will differentiate AKI from CKD
Renal biopsy
48
Goals of therapy
- treat underlying disease - fluid therapy - manage metabolic acidosis and electrolyte abnormalities - symptomatic/supportive
49
_____ is the primary treatment
Fluid therapy!! - treats pre renal azotemia and renal perfusion - replace deficit over 6 hrs
50
Monitoring fluid therapy
- BUN/creatinine: q12-48 hrs - electrolytes/blood gas: q6-12 hrs initially - urine output - weight: q6-12 hrs
51
Monitoring electrolytes, acid/base
q6-12 hours - K, Na, P - acid/base
52
Measuring Ins and Outs
Ins = (outs+insensible) - too much urine, increase fluid rate - too little urine (<1 ml/kg/hr), start furosemide BEFORE overload
53
Fluid overload
Common with anuria/oliguria - difficult to correct - monitor urine output, weight, central venous pressure, pe findings
54
Fluid overload physical exam
Appears after pulmonary edema has occurred - crackles, wheezes - tachycardia - restlessness - chemosis - serous nasal d/c
55
Supportive therapy
- anti-emetics - H2 blocker or proton pump inhibitor - oral ulceration - nutrition - manage BP
56
Additional therapy for severe AKI
- hemodialysis | - peritoneal dialysis
57
AKI prognosis
Guarded to poor - mortality >50% - dependent on etiology and severity - may take 1-3 weeks to recover - may develop CKD
58
Prevention
- avoid nephrotoxins - avoid NSAIDs with dehydration - fluids/bp monitoring during anesthesia

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