Pathoma Acute Renal Failure Flashcards Preview

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Flashcards in Pathoma Acute Renal Failure Deck (32)
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1
Q

There are three divisions we make for acute renal failure. What are they?

A

Prerenal, postrenal, and intrarenal azotemia based on etiology

2
Q

What is azotemia?

A

Increase in nitrogenous waste products in the blood.

3
Q

What lab values indicate Azotemia

A

Elevated BUN and Cr

4
Q

Azotemia and ____ are hallmarks of acute renal failure

A

Oliguria

5
Q

Oliguria?

A

Decreased production of urine

6
Q

_______ is related to a prerenal azotemia etiology for renal failure

A

Decreased blood flow (think of this as a pre-kidney problem!)

7
Q

This would be an example of a post renal azotemia

A

Blockage in the ureter, caused backwards issues on the kindey

8
Q

Understandably, a decrease in blood flow to the kidney would also decrease this

A

GFR (less blood to glomerulus = less filtration)

9
Q

Azotemia will result in increased BUN and Cr no matter what. However, how can we distinguish between the three types?

A

The ratio.

BUN:CR>15 = prerenal, early postrenal
BUN:Cr<15 = Long standing post renal, Acute tubular necrosis
10
Q

Effect of prerenal azotemia on tubular function and how we can measure this

A

None.

FENa (Excretion) < 1%
Urine osm > 500

11
Q

Explain why in particular the ratio of BUN:Cr is >15 in a patient with prerenal acute renal failure

A

So you have your tube going to the kidney and it enters the glomerulus for filtration. BUN and Cr are both filtered. Normally, BUN is filtered by the blood, so it is taken out of the glomerulus, while the Cr will remain. This gives us a normal ration B:C of 15.

In pre-renal issues, the renin-angiotensin system will be activated, leading to aldosterone which will cause sodium to be reabsorbed, along with water, which results in further increases the BUN being taken out, causing the B:C to go > 15

12
Q

How does a post-renal obstruction cause a problem in the kidney and what do we see as a result?

A

Causes back pressure = reduced filtering = decreased GFR

13
Q

Wait…so in post renal we also have an increase in BUN:Cr…but aldosterone is not active. Why do we see this?

A

Back pressure forces more BUN out

14
Q

Early stage vs. Long-Standing Post-renal azotemia

A

Early: Exactly like prerenal with a B:Cr > 15 and a normal tubular function

Long-Standing: B:Cr < 15 along with opposite tubular values of FENa > 2% since you can’t reabsorb sodium and an inability to concentrate the urine leading to a urine osm < 500.

15
Q

Intrarenal causes of Acute Renal failure

A
  1. Acute Tubular Necrosis

2. Acute interstitial Nephritis

16
Q

What is acute tubular necrosis and what does it do? How common is this?

A

Injury and necrosis of tubular epithelial cells, most common cause of ARF.

Necrotic epithelial cells then sluff off and plug tubules, obstruction decreases GFR.

17
Q

What kind of urine do we see with Acute Tubular Necrosis?

A

Brown, granular casts (meaning in the shape of the tubule since they built up first and hardened in the tubule before dislodging) in the urine because the dead sluffed off cells are coming out

18
Q

We see these tubular findings with ATN

A

Since we have a dysfunctional tube we will see a desreased reabsorption of sodium leading to an FENa > 2% as well as an inability to concentrate the urine, leading to a urine osm < 500

19
Q

Discuss the two etiologies of Acute Tubular Necrosis

A

Ischemic - Decreased blood supply leads to death of tubule epithelial

Nephrotoxic - Toxins cause the death of the cells

20
Q

In ischemic acute tubular necrosis, what portions are particularly susceptible?

A

Proximal tubule and medullary segment of thick ascending limb

21
Q

In nephrotoxic acute tubular necrosis, what portions are particularly susceptible?

A

Proximal tubule

22
Q

Causes of nephrotoxic issues

A

Aminoglycosides
Heavy metals
myoglobinuria in crush injuries
Ethylene glycol in antifreeze (we wil see oxylate crystals in the urine)
radiocontrast dye
Urate, which we see in tumor lysis syndrome

23
Q

So we know that with ATN we will see oliguria, brown granular casts and elevated BUN and Cr as expected of all of these conditions.

What is special about ATN?

A

Hyperkalemia with metabolic acidosis.

This is due to less excretion of K out of the tube as well as acid

24
Q

How do we deal with ATN?

A

Supportive dialysis to help electrolyte imbalances which can be fatal

25
Q

During ATN, we see this type of recovery pattern

A

2-3 weeks of oliguria before recovery because the tubular cells take time to reenter the cell cycle and regenerate

26
Q

What are the causes and what is the general problem with acute interstitial nephritis

A

Drug induced Hypersensitivity reaction of interstitium and tubules that results in intrarenal ARF.

Causes include NSAIDs, PCN and diuretics

27
Q

Just to clarify, when we say interstitial inflammation, what will we see on histology?

A

The space between the tubules will have inflammatory process

28
Q

Typical presentation of acute interstitial nephritis

A

Oliguria as usual, but also fever, rash days to weeks after starting the drug. Obviously will resolve when you stop taking the drug

29
Q

Acute interstitial nephritis can progress to this

A

Renal papillary necrosis

30
Q

____ are seen in the urine with acute interstitial nephritis

A

Eosinophils

31
Q

How does renal papillary necrosis present?

A

Gross hematuria and flank pain

32
Q

Causes of renal papillary necrosis

A
  1. Chronic analgesic abuse
  2. Diabetes Mellitus
  3. SCT or SCD
  4. Severe Acute pyelonephritis