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NSCC 7320 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

(51 cards)

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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)

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A

Calculates how much blood passes through the glomerulus per minute

22
Q

Sodium and water

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A

Responds to Aldosterone

23
Q

Water

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A

Responds to ADH (vassopressin)

24
Q

Bicarbonate

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A

Buffer

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

Contributes to metabolic acidosis

25
Anion gap
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
3 Types of AKI
PRERENAL INTRARENAL POSTRENAL
27
Pre renal AKI
Before the kidney, due to hypoperfusion nephron is intact Pre Renal Injury = Decreased GFR •May lead to intra-renal AKI
28
Intra renal AKI
Damage to renal parenchyma (nephron) | •Ischemic and nephrotoxic causes
29
Post renal AKI
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
Pre renal AKI LABS
Rise in BUN CR relatively stable urine output decreased and increased urine concentration
31
Pre ranal AKI causes
``` 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
Drugs that alter renal perfusion
NSAIDS | ACE inhibitors
33
Subtypes of Intrarenal AKI
Ischemic and Nephrotoxic
34
Ischemic Intrarenal Injury
* 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
Nephrotoxic Intrarenal Injury
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
Nephrotoxic Drugs
``` PCN Cyclosporins Furosemide Corticosteroids Contast dye ```
37
Rhabdomylosis
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
Prevention of AKI
•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
Management of AKI
``` 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
Difference Between: Ischemic Intra Renal Injury and Nephrotoxic Intra-Renal Injury
In nephrotoxin Injury •Basement membrane intact •Necrotic areas usually more localised •Healing process more rapid
41
Decreased GFR results in 7
``` 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
Intra renal AKI Causes
* 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
Post renal AKI causes
``` 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
increased anion gap
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
Where does the concentration and dilution of the urine occur
In the juxtamedullary nephrons
46
The function of aldosterone is primarily
Control of sodium and water
47
After angiotensin I is converted to angiotensin II, the adrenal glands are stimulated to secrete:
Aldosterone
48
Increased secretion of ADH results in
increased resorption of water in collecting duct
49
Angiotensin 2 actions
* potent vasoconstrictor (arterioles so increases afterload) * stimulates the release of aldosterone * Triggers production of Vassopressin (ADH) * enhances SNS activity
50
aldosterone action
reabsorption of sodium and water | increasing circulating volume and preload
51
Vassopressin
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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