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SAM 2 > Acute Renal Failure > Flashcards

Acute Renal Failure Flashcards

1
Q

What is acute renal injury?

A

Encompasses mild damage that does not cause azotemia to severe damage associated with anuria

May be pre-, post-, or renal

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2
Q

Is acute renal injury reversible or irreversible?

A

Reversible

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3
Q

What is acute renal failure?

A

Decreased GFR leading to retention of nitrogenous wastes

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4
Q

What is the RIFLE criteria?

A

Allows the clinician to objectively and uniformly define AKI

R: Risk
I: Injury
F: Failure
L: Loss
E: End stage kidney disease
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5
Q

What is the RIFLE criteria based on?

A

Proportion of serum creatinine increases and urine output decreases

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6
Q

What is the issue with using the RIFLE criteria in vet med?

A

Good baseline references for creatinine may not have been established at presentation

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7
Q

What is the IRIS AKI subgrading based on?

A

Same thing as RIFLE, creatinine to urine output

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8
Q

What is pre renal AKI due to?

A

Anything that causes insufficient blood flow to the kidney

Hypoxia, ischemia, dehydration, hypovolemia, hypotension, decreased circulatory volume, anesthesia, hypoadrenocorticism, trauma, sx, shock, heatstrocke, hypoalbuminemia, hypoperfusion (NSAID tox)

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9
Q

What is pre-renal AKI characterised by?

A

Reduced fractional excretion of sodium

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10
Q

What are some renal etiologies for AKI?

A
  • Prolonged hypoperfusion
  • Prolonged obstruction
  • Excessive vasoconstriction
  • Thrombosis/DIC
  • Transfusion reaction
  • Infection
  • Immune diseases
  • Neoplasia
  • Secondary to systemic disease
  • Nephrotoxins
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11
Q

What are some post-renal etiologies for AKI?

A

Urine leakage or obstruction causing damage to collecting tubules

May result in urine leakage and uroabdomen

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12
Q

What are the four phases of acute renal failure?

A

Initial, extension, maintenance, and recovery

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13
Q

What are the characteristics of the initial phase of AKF?

A
  • Usually little to no clinical signs

- Decrease in urine output or increase in creatinine

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14
Q

Is intervention necessary in the initial phase of ARF?

A

Yes

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15
Q

What are the characteristics of the extension phase of ARF?

A

Continued hypoxia and inflammation

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16
Q

What part of the nephron is particularly susceptible to toxins and ischemia?

A

Proximal tubule and loop of henle

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17
Q

What is the maintenance phase of ARF?

A

Lasts 1-3 weeks typically, urine is usually ultrafiltrate and may be decreased or increased volume

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18
Q

What is the recovery phase of ARF?

A

Characterized by polyuria and extreme los of sodium

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19
Q

How long may the recovery phase of ARF last?

A

Weeks to months depending on damage

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20
Q

What causes intra-renal vasoconstriction?

A

Imbalance between the vasoconstrictors (endothelin) and vasodilators (NO)

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21
Q

What is the consequence of intra-renal vasoconstriction?

A

Endothelial injury, decreased oxygen, ATP deficiency, mitochondrial damage, oxidant injury, intracellular acidosis and hypercalcemia

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22
Q

What are the causes of tubular dysfunction?

A
  • Tubular obstruction from crystals or detached RTE cells
  • Cytoskeletal injury with loss of polarity
  • Loss of tight junctions between cells
  • Cell necrosis
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23
Q

What are some risk factors for ARF?

A

Dehydration, hypovolemia, anesthesia, hypoxia, SIRS

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24
Q

How do you prevent ARF?

A

Aggressive treatment of shock and dehydration, avoid nephrotoxic drugs especially in compromised patients

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25
Q

What needs to be monitored closely in acute renal patients?

A

Dehydration status, blood volume and pressure, cardiac and urine output, GFR (direct if necessary)

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26
Q

What are some renoprotective drugs?

A
  • Calcium channel blockers (prevent Ca influx)
  • Selective DA-2 receptor agonists (vasodilation)
  • Selective DA-1 receptor agonists (prevents vasoconstriction)
  • Erythropoeitin analogues (protect against hypoxia)
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27
Q

Should fluids be given to accute renal patients?

A

Yes, always, helps correct electrolyte abnormalities as well as pressure and volume issues

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28
Q

Why should ECG be monitored in acute kidney patients?

A

To asses patient for electrolyte associated arrhythmias

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29
Q

Can pressors be given to acute renal patients?

A

Yes, if hypotension cannot be resolved with fluid therapy

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30
Q

How do you diagnose acute renal issues?

A
  • Correction of underlying cause
  • Detection of reduced urine output
  • Urinalysis
  • Azotemia
  • Reduced fractional excretion of sodium
  • Renal tubular biomarkers
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31
Q

What are the initial bolus doeses to correct shock in the dog and the cat?

A

Dog: 60-90 mL/kg
Feline: 45 mL/kg

Over 60 min in 15 min interval boluses

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32
Q

What is the formula to correct dehydration?

A

%dehydration x 10 x BK kg = mL to be given over 6-12 hours

33
Q

What volume accounts for insensible fluid loss?

A

22 mL/kg/day

34
Q

What volume accounts for sensible fluid loss?

A

44 mL/kg/day

35
Q

What is the maintenance fluid rate?

A

60 mL/kg/Day but adjust for abnormal urinary losses

36
Q

What should be used for rehydration of the ARF patient?

A

Crystalloids or hypertonic saline

37
Q

What are the four fluid requirements?

A
  1. Dehydration
  2. Insensible losses
  3. Ongoing losses
  4. Sensible losses
38
Q

What is oliguria defined as?

A
39
Q

Is oliguria always a bad thing?

A

No, normal in a dehydrated patient

40
Q

How do you treat pathological oliguria?

A

Mannitol, furosemide, dopamine, Ca channel blockers

41
Q

Is treatment of oliguria usually successful?

A

No, no evidence that treatment improves outcome

42
Q

What is mannitol?

A

An osmostic diuretic used to decrease cell swelling

Has some free radical scavenging ability

43
Q

What are some contraindications for mannitol use?

A

Dehydration or anuria

44
Q

What is furosemide?

A

Loop diuretic that inhibits Na-K-2Cl symporter in thick ascending loop of henle

45
Q

What is the advantage of fruosemide?

A

Decreases O2 requirement of the kidney and increases urine production without increase in GFR, renoprotective and fast acting

46
Q

What are some contraindications of furosemide?

A

Dehydration, lethargy, tachycardia, ototoxicity

47
Q

Is dopamine an effective treatment for oliguria in cats?

A

No

48
Q

When is dopamine beneficial as a pressor?

A

When ARF is secondary to cardiac output failure or severe hypotension

49
Q

What does fenoldopan do?

A

Increase urine output

50
Q

What is the MOA of calcium channel blocker in oliguric patients?

A

Pre-glomerular vasodilation by preventing Ca from moving intracellularly

51
Q

When are calcium channel blockers usually used in kidney patients?

A

Post-transplant as a renoprotective agent or in standard care of lepto patients

52
Q

What are definitive treatments for acute renal failure?

A

Extracorporal renal replacement therapy (dialysis), peritoneal dialysis

53
Q

What is dialysis?

A

Use of artificial membranes with created hydrostatic and solute concentrations designed to mimic kidney function

54
Q

What are some indications for ERRT/dialysis?

A
  • Fluid overload with pulmonary edema
  • Hyperkalemia
  • Progressive azotemia
  • Acute toxicity
55
Q

Is peritoneal dialysis a simple useful procedure?

A

No, only used in ICU situations and has short survival times

56
Q

What is the most common complication of peritoneal dialysis?

A

Acute uremia

57
Q

What are some other complications of peritoneal dialysis?

A

Dialysis disequilibrium syndrome and blockage of the drain

58
Q

What is the specific therapy for ethylene glycol toxicity?

A

4-methylpyrazole within 8 hours of ingestion

Ethanol can work as well

59
Q

What is the specific therapy for NSAID toxicity?

A

Misoprostal

60
Q

What is the specific therapy for lepto patients?

A

Penicillins and doxycycline

61
Q

What is the specific therapy for pyelonephritis patients?

A

Culture/Sensitivity, fluoroquinolones or TMS for 4-6wks

62
Q

What is the specific therapy for aminoglycoside toxicity?

A

Ticarcillin IV (binding agent)

63
Q

What is the specific therapy for TMS toxicity?

A

Urinary alkalinization

64
Q

Why do acute kidney patients develop hyperkalemia?

A

Inability to excrete potassium due to damage to pumps

65
Q

What can result from hyperkalemia?

A

Acidosis, bradycardia, sinus arrest, muscle weakness, ileus

66
Q

How is hyperkalemia treated?

A

Insulin and dextrose infusion
Calcium gluconate
Correction of metabolic acidosis

67
Q

Why do acute kidney patients develop acidosis?

A

Failure to absorb bicarb or excrete hydogen

68
Q

How do you correct acidosis?

A

IV bicarb

69
Q

T/F: Hypocalcemia is a common complication of acute kidney patients.

A

False- rare complication

70
Q

What is hypocalcemia associated with in kidney patients?

A

Deficiency of calcitriol

71
Q

How is hypercalcemia corrected?

A

Diuresis or ERRT, calcitonin, biophosphates

72
Q

Is there a specific therapy for hyperphosphatemia?

A

No, reduce phosphorus intake or use binders in food

73
Q

Why do kidney patients develop hypertension?

A

RAAS activation and fluid overload

74
Q

What drugs should be avoided in ARF patients?

A

Ace inhibitors

75
Q

Which drugs should be considered to correct hypertension in acute kidney patients?

A

Amlodipine and hydralazine

76
Q

What are some aspects of GI supportive care in the acute renal patient?

A

Control of anorexia, nausea, and vomiting

Contorl uremic gastopathy

77
Q

What are some strategies for dietary supplementation in renal patients?

A

Enteral feeding device, renal prescription diet

78
Q

What acute kidney conditions have a good outcome usually?

A

Dialysis, leptospirosis, obstructive and infectice issues

79
Q

What acute kidney conditions have a poor outcome usually?

A

No ECRR when indicated, decreased urine production, hypothermia, hyperkalemia, toxins (especially ethylene glycol)

SAM 2 (21 decks)

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