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SAM II > Acute Renal Failure > Flashcards

Acute Renal Failure Flashcards

1
Q

What is the definition of Acute Renal Failure?

A

Decreased GFR leading to the retention of nitrogenous wastes.

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2
Q

What is the definition of Acute Kidney Injury?

A

Encompasses mild damage, that does not cause azotemia to severe damage associated with complete anurira.

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3
Q

T/F AKI is reversible.

A

True!

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4
Q

T/F AKI can be pre renal, renal or post renal.

A

True!

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5
Q

What does the RIFLE acronym stand for?

A 
R: Risk
I: Injury
F: Failure
L: Loss 
E: End- stage kidney dz
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6
Q

What are some of the main pre renal etiologies of AKI?

A

Dehydration, hypoxia, ischemia, anesthesia (one of most common causes because it causes hypotension so decrease GFR so decreases O2 to kidney), Addison’s, trauma, shock, hypoALB ( oncotic pressure super low so decrease GFR).

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7
Q

What are some of the main aspects/causes of renal etiologies of AKI?

A
  1. prolonged renal hypoperfusion will lead to tubular hypoxia
  2. prolonged obstruction (> 1 week)
  3. excessive vasoconstriction
  4. thrombosis and DIC
  5. infectious causes (lepto, bacterial pyelonephritis)
  6. Immune mediated causes
  7. neoplasia
  8. secondary to systemic dz (sepsis, DIC, pancreatitis, snake envenomation)
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8
Q

What are some major nephrotoxins associated with renal AKI?

A

ethylene glycol, Nsaids, aminoglycosides, heavy metals, raisins

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9
Q

What are the post renal etiologies of AKI?

A

urine leakage or obstruction

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10
Q

What exactly goes wrong in post renal AKI?

A

Pressure on the collecting tubule will damage aquaporin 2 channels, disrupt normal hydrostatic and oncotic balance

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11
Q

What are the four phases of ARF?

A
  1. initial
  2. extension
  3. maintenance
  4. recovery
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12
Q

What is the first phase of ARF and how is it defined?

A

Initial ! Definable by a decrease in urine output or increase in creatinine.

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13
Q

T/F The initial phase of ARF present with major clinical signs.

A

False! Usually no clinical signs!

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14
Q

What triggers the initial phase of ARF?

A

usually an ischemic event triggers it

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15
Q

Is intervention necessary in the initial phase of ARF?

A

Absolutely !

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16
Q

What is the second phase of ARF and what is happening?

A

Extension phase ! The proximal tubule and loop of Henle receive 90% of the blood flow going to the kidney and are susceptible to toxic and ischemic damage.
Compromised Na:K pumps- leads to swelling and death :(
Increased cytosolic calcium
Loss of brush border or apical and basal cell surfaces
Continued hypoxia and inflammation

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17
Q

Tell me bout the third phase of ARF.

A

Maintenance phase
1-3 weeks duration
Urine output is increased OR decreased
Urine = ultrafiltrate

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18
Q

What is the fourth and final stage of ARF?

A

Recovery!
Polyuria!!!!
Extreme Na loss (ascending limb of Henle and AQP-2 loss)
Takes weeks to months to recover

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19
Q

T/F Intra -renal vasoconstriction deals with the imbalance between vasoconstrictors (endothelin) and vasodilators (NO).

A

True!

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20
Q

What are some of the major things that happen when intra renal vasoconstriction happens?

A
  1. decreased O2
  2. ATP cannot the formed to leads to energy deficit
  3. Mitochondrial damage
  4. Oxidant injury
  5. Intracellular acidosis
  6. Intracellular hypercalcemia
21
Q

What happens with tubular dysfunction?

A
  1. cytoskeletal injury with loss of polarity- cells don’t know where they are anymore
  2. loss of tight jxns btwn cells
  3. cell necrosis
22
Q

What are some of the preventative measures with regards to ARF?

A
  1. address BP: keep >80 mmHg (avg= 120 in cats and dogs)
  2. address circulatory volume: ensure CVP >0 and 30% SpO2 > 96% PaO2> 80mmHg
  3. ECG: avoid hyperkalemia induced bradyarrhythmias
23
Q

What fluids do we give to patients with ARF?

A

Fluid Bolus: 10-15ml/kg crystalloids (oliguric patients) OR 2-5 ml/kg colloid

24
Q

How do we diagnose AKI/ARF?

A
  1. Identify predisposing cause (shock, nephrotoxin)
  2. Reduce urine output: normal= 1-2 ml/kg/hr; abnormal (OLIGURIA): 1%
  3. Renal tubular biomarkers (relative to creatinine as a ratio): GGT = creatinine; NAG= creatinine . . . helps localize the region of the tubular structure, multiple enzymes will provide a great diagnostic accuracy
25
Q

How do we treat ARF?

A

FLUIDS FLUIDS FLUIDS. Hydrate these mofos

26
Q

How do we correct shock?

A

60-90 ml/kg = canine
45 ml/kg= feline

over 60 mins, 15 min interval boluses

27
Q

What is the formula to correct dehydration ?

A

% dehydration x 10 x BW in kg = ___ ml (over 6-12 hrs)

28
Q

What is the definition of oliguria?

29
Q

How do we know if the oliguria is pre renal?

A

Give fluid and if the dog starts urinating then we know there wasn’t enough volume in the dog so this is a physiological aka a pre renal cause.

30
Q

What is the prognosis for pre renal oliguria?

A

Not good. Animal is pretty fucked.

31
Q

We already know the main treatment for ARF is to give fluids but what kinda drugz do we give?

A

Mannitol, Furosemide, Dopamine, Calcium channel blockers

32
Q

How does Mannitol work?

A

Osmotic diuretic
Increase circulatory volume: flushes through tubules
Decreases cell swelling
Blunts the influx of calcium intracellularly
Contraindications:
-anuria, dehydration

33
Q

How does Furosemide work?

A

Loop diuretic
Inhibits the Na-K-Cl symporter in thick ascending loop of Henle
increased urine production WITHOUT increasing GFR
Renoprotective!
Output should increase within 2-60 mins
Contraindications:
-dehydration, lethargy, tachycardia, ototoxity

34
Q

What’s up with Calcium Channel Blockers?

A

MOA: preglomerular vasodilation
Prevents Ca moving intracellularly
used in post transplant as renoprotective agent
Standard of care in Lepto!

35
Q

What is the definitive treatment of ARF?

A

Extracorporal renal replacement therapy ak dialysis!

36
Q

What are the indications for dialysis?

A
  1. fluid overload with pulmonary edema
  2. hyperkalemia
  3. progressive azotemia
  4. acute toxicity
37
Q

What’s the specific tx for ethylene glycol toxicity?

A

4-methylpyrazole within 8 hours of ingestion

38
Q

What’s the specific tx for Nsaids?

A

Misoprostal

39
Q

What’s the specific tx for Lepto?

A

Penicillins and doxy- immediately use!

40
Q

What’s the specific tx for pyelonephritis?

A

Culture, fluoroquinilones or TMS

41
Q

What is the specific tx for amino glycoside toxicity?

A

Ticarcillin IV: binds to gentamycin

42
Q

What is the specific tx for TMS toxicity?

A

Urinary alkalinization

43
Q

Why does hyperkalemia develop in ARF?

A

inability to excrete k so acidosis bc H+ exchanged for K+

complications include bradycardia/sinus arrest, muscle weakness and ileus

44
Q

How do we correct the hyperkalemia that develops in ARF?

A

Insulin followed by dextrose then calcium gluconate and correct metabolic acidosis by giving HCO3

45
Q

Why does acidosis develop in ARF?

A

the failing kidney is unable to absorb HCO3- or excrete H+

46
Q

How do we tx the acidosis that develops?

A

HCO3- administration IV

Contraindications:
-when CO2 elevated

47
Q

How do we tx the hypercalcemia that develops?

A 
Diuresis or ERRT 
Furosemide/ GC's
Calcitonin
Biphosphonates 
Bad prognosis :(
48
Q

Why does hypertension develop in ARF?

A

secondary to RAAS activation and fluid overload

Avoid ACE inhibitors in ARF b of arterial vasoconstriction!

49
Q

What circumstances have a good prognosis?

A

Dialysis, Lepto, obstructive and infective

SAM II (20 decks)

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