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SAMS > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

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

A
  • ethylene glycol
  • grapes/raisins
  • aminoglycosides
  • lead
  • NSAIDs
  • amphotericin
  • melamine
  • easter lily
  • hemoglobin
  • myoglobin
  • cisplatin
  • hypercalcemia
25
Q

Infectious causes

A
  • leptospirosis
  • borreliosis (tubular and glomerular damage)
  • pyelonephritis (easy to treat, same antibiotic gets lepto)
26
Q

Tubular destruction

A
  • ischemia
  • toxin
  • infection
27
Q

Tubular obstruction

A
  • dead cell

- debris

28
Q

Tubular back-leak

A
  • filtrate resorbed between cells into renal interstitium

- inflammation, edema, azotemia

29
Q

Glomerular arteriole constriction

A

From increased solute delivery to macula densa

30
Q

Afferent arteriolar constriction

A

Sympathetically mediated vasoconstriction due to:
- hypotension
- pain
- anesthesia
Also due to vasomotor nephropathy –> loss of autoregulation

31
Q

Initiation

A

Immediately follows insult

  • renal tubular damage occurs
  • therapy may be helpful, not commonly instituted
  • usually <48 hrs
32
Q

Maintenance

A

Clinical signs of uremia occur following tubular damage

  • variable time
  • usually when they are presented
33
Q

Recovery

A

Tubular repair

  • days-months
  • does not occur if damage is too severe
  • remaining nephrons hypertrophy
34
Q

Clinical signs

A

Uremic syndrome, recent change in urine output

  • increased: polyuria (unable to concentrate urine)
  • decreased: oliguria, anuria (more severe injury)
35
Q

Uremia

A

Build up of uremic toxins

  • urea, creatinine
  • uremic syndrome (clinical signs that occur secondary to uremia)
36
Q

Uremic syndrome

A
  • depression
  • lethargy
  • anorexia
  • vomiting
  • diarrhea
  • stomatitis (ulcer)
  • weight loss
  • ataxia
  • seizures
37
Q

Polyuria

A

Increased urine production

  • > 50 ml/kg/day
  • different than pollakiuria –> increased frequency of urination, lower urinary tract sign
38
Q

Polydipsia

A

Increased drinking

- >100 ml/kg/day

39
Q

Oliguria

A

Urine productino <0.5 ml/kg/hr

40
Q

Anuria

A

Complete absence of urine production

41
Q

Physical exam findings

A
  • normal BCS
  • may see enlarged kidneys
  • dehydration
  • hypovolemia
  • uremic breath
  • oral ulceration
  • fever or hypothermia
42
Q

Clinicopathologic abnormalities

A

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
Q

Radiographs

A

Normal to increased kidneys

- rule out urolithiasis

44
Q

Ultrasound

A
  • normal to enlarged kidneys
  • loss of corticomedullary distinction
  • hyperechoic band with EtGly
  • pyelectasia with pyelonephritis
45
Q

Always perform a ______

A

Urine culture

46
Q

Arterial bp will often be ______

A

Increased

47
Q

_______ will differentiate AKI from CKD

A

Renal biopsy

48
Q

Goals of therapy

A
  • treat underlying disease
  • fluid therapy
  • manage metabolic acidosis and electrolyte abnormalities
  • symptomatic/supportive
49
Q

_____ is the primary treatment

A

Fluid therapy!!

  • treats pre renal azotemia and renal perfusion
  • replace deficit over 6 hrs
50
Q

Monitoring fluid therapy

A
  • BUN/creatinine: q12-48 hrs
  • electrolytes/blood gas: q6-12 hrs initially
  • urine output
  • weight: q6-12 hrs
51
Q

Monitoring electrolytes, acid/base

A

q6-12 hours

  • K, Na, P
  • acid/base
52
Q

Measuring Ins and Outs

A

Ins = (outs+insensible)

  • too much urine, increase fluid rate
  • too little urine (<1 ml/kg/hr), start furosemide BEFORE overload
53
Q

Fluid overload

A

Common with anuria/oliguria

  • difficult to correct
  • monitor urine output, weight, central venous pressure, pe findings
54
Q

Fluid overload physical exam

A

Appears after pulmonary edema has occurred

  • crackles, wheezes
  • tachycardia
  • restlessness
  • chemosis
  • serous nasal d/c
55
Q

Supportive therapy

A
  • anti-emetics
  • H2 blocker or proton pump inhibitor
  • oral ulceration
  • nutrition
  • manage BP
56
Q

Additional therapy for severe AKI

A
  • hemodialysis

- peritoneal dialysis

57
Q

AKI prognosis

A

Guarded to poor

  • mortality >50%
  • dependent on etiology and severity
  • may take 1-3 weeks to recover
  • may develop CKD
58
Q

Prevention

A
  • avoid nephrotoxins
  • avoid NSAIDs with dehydration
  • fluids/bp monitoring during anesthesia

SAMS (13 decks)

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