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NSCC 7320 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Abdominal compartment syndrome

A

from increased intra-abdominal pressure
(e.g. from intra-abdominal bleeding, ascites, or severe gut edema etc).

Perfusion to the organs can be critically reduced - leading to pre-
renal AKI. Pressure on the ureters etc can result in post-renal AKI.

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2
Q

AKIN criteria

A

define and classify the severity of acute kidney injury. Uses urine output and serum
creatinine levels as criteria.

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3
Q

Glomerular filtration rate

A

Compares the amount of creatinine excreted in the urine with the amount in the blood over 24 hours

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4
Q

Intra-renal AKI cause

A

Intra-renal AKI refers to AKI that affects the nephron function.
Factors contributing to intra-renal AKI include those that result in ischemia, and those that arise from nephrotoxins.

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5
Q

Myoglobinuria

A

Presence of myoglobulin in the urine; occurs when myoglobulin is released into the blood subsequent to muscle breakdown e.g. during crush injury, extensive trauma etc.
It contributes to intra-renal AKI because it is nephrotoxic

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6
Q

Nephrotoxic

A

cause damage to the tubular cells in the nephron. They include drugs (aminoglycoside antibiotics), furosemide, contrast

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7
Q

Post-renal AKI cause

A

occurs from causes ‘beyond’ the kidney

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8
Q

Pre-renal AKI cause

A

Pre-renal AKI is renal dysfunction that arises from inadequate blood flow to the kidney

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9
Q

Primary Function of the Kidney:7

A

o Maintain fluid and electrolyte balance
o Remove metabolic waste products
o Maintain acid-base balance
o Maintain endocrine functions
oHelp regulate blood pressure
o Release of erythropoietin for RBC production
o Produces active form of Vitamin D

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10
Q

Juxtaglomerular Cells (Granular Cells)

A

Located in the smooth muscle cells of the afferent arteriole

They store, produce and secrete renin.

Play critical role in RAAS

Autoregulation of renal blood flow.

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11
Q

RAAS system is a….

A

RAAS is one of the body’s compensatory mechanisms.

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12
Q

Renal Assessment

A 
Patient history
Monitoring volume status 
-Intake and output , 24 hour balance
-Hourly urine output
-Daily weights
-Color and consistency of urine

Monitoring hemodynamic parameters

  • Hourly blood pressure and heart rate
  • Frequent CVP (if available)

Monitoring oxygen supply/respiratory parameters (hourly)

Reviewing urine and serum lab values

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13
Q

Urine Volume

A
  • One of the first indicators of decreased renal perfusion
  • Subject to other conditions, so trends and full assessment required
  • Monitor on hourly basis
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14
Q

Urinalysis

A

Aids in locating site of damage

Guides management of renal dysfunction

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15
Q

Urine Sodium

A

Reflects renal perfusion

Decreased perfusion, RAAS, sodium retained, therefore urinary sodium concentration falls.

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16
Q

Urine Osmolality

A

Measure of the concentration of solutes in the urine (the ratio of urine density compared with water density). Provides information on the kidney’s ability to concentrate urine. It’s included as part of urinalysis

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17
Q

Creatinine

A

By product of muscle breakdown and cell metabolism

Produced and cleared at a constant rate

Filtered out by glomerulus- NOT reabsorbed

In patients with low perfusion states, a small rise in creatinine might occur as a result of decreased filtering at the glomerular level

May be falsely elevated in hypercatabolism seen in CC patients not properly fed.

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18
Q

Urea

A

By product of protein metabolism

Not a reliable indicator of renal function on its own (affected by protein intake, digestion of blood from UGIB).

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19
Q

BUN:Cr Ratio

A

Can help identify etiology of AKI

Urea-filtered out of the blood at glomerulus, significant percentage of it is reabsorbed as the filtrate passes through the renal tubules

Creatinine-filtered out of the blood at the glomerulus but is NOT reabsorbed in the renal tubules (so it’s peed out!)

In low perfusion states: Filtrate flow rate through tubules slows

Tubules still working normally therefore MORE BUN is reabsorbed = increased serum BUN levels

Creatinine not affected by slower flow rate as not reabsorbed = no/minimal increase in creatinine

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20
Q

Creatinine Clearance Test

A

•Compares the amount of creatinine excreted in the urine in 24 hours against the amount that has been reabsorbed into the blood

.The number that we get then provides us with an accurate GLOMERULAR FILTRATION RATE!

decreased creatinine clearance indicates decreased renal function!

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21
Q

Glomerular Filtration Rate (GFR)

A

Calculates how much blood passes through the glomerulus per minute

22
Q

Sodium and water

A

Responds to Aldosterone

23
Q

Water

A

Responds to ADH (vassopressin)

24
Q

Bicarbonate

A

Buffer

LOW IN AKI: Renal injury leads to poor reabsorption of HCO3

Contributes to metabolic acidosis

25
Q

Anion gap

A

An anion gap refers to the difference between the cations and the anions and is calculated using Na (the most abundant cation in the serum) and Cl & HCO3 (the most abundant anions in serum). The calculation looks like this:

“gap” reflecting all the
unmeasurable ions present in the extracellular fluid (sulfates, ketones & lactate)

Increased anion gap: either an over production of acids or decreased excretion of acids
•In Renal Failure, an increased anion gap reflects
the metabolic acidosis that arises when renal
tubule damage results in retention of acids and
poor reabsorption of bicarbonate

26
Q

3 Types of AKI

A

PRERENAL
INTRARENAL
POSTRENAL

27
Q

Pre renal AKI

A

Before the kidney, due to hypoperfusion
nephron is intact

Pre Renal Injury = Decreased GFR
•May lead to intra-renal AKI

28
Q

Intra renal AKI

A

Damage to renal parenchyma (nephron)

•Ischemic and nephrotoxic causes

29
Q

Post renal AKI

A

Any obstruction in the outflow of urine
Results from an obstruction which hinders the flow of urine from beyond the kidney through the remainder of the urinary tract

•May lead to intra-renal AKI

30
Q

Pre renal AKI LABS

A

Rise in BUN
CR relatively stable
urine output decreased and increased urine concentration

31
Q

Pre ranal AKI causes

A 
Poor perfusion to kidneys
hypotension/hypovolemia
Cardiac dysfunction leading to poor renal perfusion
sepsis
hemorrhage, 
post cardiac arrest

•Source of problem is not the kidneys but what happens before the kidneys (tubular function of the nephron is intact)

32
Q

Drugs that alter renal perfusion

A

NSAIDS

ACE inhibitors

33
Q

Subtypes of Intrarenal AKI

A

Ischemic and Nephrotoxic

34
Q

Ischemic Intrarenal Injury

A
  • Decreased renal perfusion = decreased oxygen supply to the tubules
  • Tubular cells are highly metabolic
  • When tubular epithelial cells become hypoxic, ATP production by renal cell mitochondria is impaired and the energy needed for active transport of solutes is not available
  • Ischemia compromises normal tubular function –swell and become necrotic
  • Necrotic cells slough off and obstruct the tubule lumen and cause “back leak” of tubular fluid which decreases GFR
35
Q

Nephrotoxic Intrarenal Injury

A

Is associated with a concentration of a toxin in the tubules which causes cellular necrosis
. Contrast dye, aminoglycosides, amphotericin B, myoglobin
•Cellular dysfunction and death results in loss of normal functions of the nephron (filtration, secretion and reabsorption)
•Cells slough off and cause obstruction of the tubular lumens and decrease GFR

36
Q

Nephrotoxic Drugs

A 
PCN
Cyclosporins
Furosemide
Corticosteroids
Contast dye
37
Q

Rhabdomylosis

A

Complication of skeletal muscle injury

  • Damaged muscle releases myoglobin into the blood where it gets filtered by the glomerulus and travels to the PCT.
  • Blocks PCT and overwhelms tubules ability to reabsorb metabolites resulting in toxic injury.
  • Myoglobinuriaresults: Dark, tea coloured urine. Decreased u/o.
38
Q

Prevention of AKI

A

•Recognition is key
•Monitor for signs of developing AKI
•Using effective preventative strategiessuch as:
-Early and aggressive IV fluid replacement (.9%NS)
-Maintain adequate MAP
-Limiting exposure to nephrotoxins
-Careful with BiPaP/CPAP-Monitoring for intra abdominal compartment syndrome

39
Q

Management of AKI

A 
Primary management is alleviating the precipitating causes
•Management of issues which arise as a result of AKI
○Fluid balance
○Electrolyte abnormalities
○Acid-base imbalance
○Relevant supportive care
•Renal Replacement Therapies 
○Hemodialysis
○Peritoneal dialysis
○Continuous dialysis (CRRT)
40
Q

Difference Between: Ischemic Intra Renal Injury and Nephrotoxic Intra-Renal Injury

A

In nephrotoxin Injury
•Basement membrane intact
•Necrotic areas usually more localised
•Healing process more rapid

41
Q

Decreased GFR results in 7

A 
Filtrate travels more slowly through the tubule
This causes
•Increased urea reabsorption
•Increased sodium reabsorption
•Increased water reabsorption
•Decreased urine volume
•Increased concentration of urine
•Low urine sodium levels
•Small increase in creatinine
42
Q

Intra renal AKI Causes

A
  • Rhabdo
  • nephrotoxic drugs,
  • persistent pre-renal AKI
  • A condition which produces damage to the site of the nephron itself and may involve the glomeruli and renal tubules.
43
Q

Post renal AKI causes

A 
trauma to ureters 
Enlarged prostate
kidney stones,
abdominal compartment syndrome,
tumours, 
strictures

Abdominal compartment syndrome creates excessive pressure on the ureters blocking out flow of urine

44
Q

increased anion gap

A

An increased anion gap
reflects either overproduction of acids or decreased excretion of acids. In renal dysfunction
it reflects a metabolic acidosis that arises when tubules dysfunction results in retention of
acids and poor reabsorption of bicarbonate

45
Q

Where does the concentration and dilution of the urine occur

A

In the juxtamedullary nephrons

46
Q

The function of aldosterone is primarily

A

Control of sodium and water

47
Q

After angiotensin I is converted to angiotensin II, the adrenal glands are stimulated to secrete:

A

Aldosterone

48
Q

Increased secretion of ADH results in

A

increased resorption of water in collecting duct

49
Q

Angiotensin 2 actions

A
  • potent vasoconstrictor (arterioles so increases afterload)
  • stimulates the release of aldosterone
  • Triggers production of Vassopressin (ADH)
  • enhances SNS activity
50
Q

aldosterone action

A

reabsorption of sodium and water

increasing circulating volume and preload

51
Q

Vassopressin

A

also known as ADH- antidiuretic hormone
increases reabsorption of water in kidneys
increasing circulating volume and preload

NSCC 7320 (9 decks)

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