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Flashcards in Acute kidney injury Deck (35)
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1
Q

a sudden decrease in kidney function, resulting in an inability to maintain acid-base, fluid and electrolyte balance and to excrete nitrogenous wastes

A

acute kidney injury (AKI) or acute renal failure

2
Q

A condition occuring in AKI where urea and other nitrogenous waste products are not excreted properly in urine and levels become elevated in the blood.

A

Uremia

3
Q

What are the 3 categories of AKI? Give one cause for each.

A

1) Pre-renal (hypovolemia leads to low kidney perfusion, HF, dehydration, diuresis, etc) Pre-renal is most common*
2) Intrinsic (kidney disease)
3) Post-renal (urinary obstruction like BPH)

4
Q

What happens to the kidney on an ACEI?

A

its efferent arteriole cannot constrict to maintain high pressure in the glomerulus thus decreasing GFR.

5
Q

When GFR decreases what happens to BUN and creatinine concentrations in blood?

A

They will both increase

6
Q

Does a decrease in GRF affect BUN and creatinine levels evenly? Why?

A

No! BUN is both filtered AND re-absorbed in the kidney. So a slower rate will 1) not filter as much BUN out of the blood and 2) gives the kidneys more time to reabsorb BUN back into the blood. So a slow GFR affects BUN much more significantly. (Creatinine is just excreted, no re-absorption)

7
Q

AKI result in a ___________to the GFR

A

decrease

8
Q

In a low flow state (ie low GFR) the kidney thinks there is hypovolemia. So besides having extra time to reabsorb BUN, what else is the kidney doing?

A

low volume triggers kidney to reabsorb Na and therefore H20. So low GFR often results in low Na and low H20 in urine….urine becomes concentrated (high osmolality = high specific gravity).

9
Q

What if there is an intrinsic problem with the kidney, for example a problem with the prox convoluted tubule. What would you expect to happen?

A

Reabsorption would not happen. So BUN would not be reabsorbed. Neither would Na (and H20). So BUN would only increase proportionately to creatinine and urine would have tons of Na and H20. Dilute urine = low concentration = low specific gravity

10
Q

What is the normal BUN:creat ratio?

A

15:1

11
Q

If you see a BUN:creat ratio of 20:1, where do you think your AKI is coming from?

A

Pre-renal.

12
Q

If you see a BUN creat ratio of 15:1 but the GFR is low, where is your AKI?

A

Intrinsic renal problem

13
Q

What is the specific gravity of plasma?

A

1.010

14
Q

What is the FENa?

A

Fractional Excretion of Na. It is equal to (urine sodium/plasma sodium) over (urine creat/plasma creat) Algebraically, if your urine sodium is high…we know the FENa will be high. Urine sodium is high when it cannot be reabsorbed…so it is a renal-renal problem. HIGH FENa = RENAL RENAL. (>2%)

15
Q

If you have low perfusion (pre-renal) problem for hours…what do you expect will happen?

A

Ischemia leads to tissue death of the kidney…aka acute tubular necrosis (ATN)

16
Q

What is another cause of ATN?

A

Nephrotoxins like aminoglycosides, cephalosporins, contrast dye, NSAIDS, ACEIs

17
Q

How could increased destruction of RBCs affect kidneys?

A

hemolysis from anemia, transfusion reaction, GI bleeds cause increase of RBC metabolism. RBC’s have proteins so this will lead to increased ammonia. IF the liver can convert to BUN you’ll have increased BUN

18
Q

In ATN, what’s commonly seen in the urine?

A

sediment, pigmented casts

19
Q

What is the goal in treating ATN?

A

Avoid buildup of excess fluid and waste. Restrict fluid intake, give diuretics, control potassium–Furosemide does both. Tubular cells will typically regenerate. Dialysis used if necessary

20
Q

An interstitial inflammatory response with edema and possible tubular cell damage is the typical pathologic finding

A

Interstitial Nephritis.
(So basically, the interstitium of kidneys becomes inflammed as an immune response. Causes are either drug related or AI disorder) FYI: prognosis is good

21
Q

What is a classic finding for Interstitial Nephritis?

A

Eosinophils present in immune responses

22
Q

How do you treat interstitial nephritis?

A

steroids

23
Q

Your patient has suddenly become hypertensive and edematous. You look at his urine and detect WBC’s, dysmorphic RBC’s and RBC casts. There is also some proteinuria. GFR is decreased. What do you suspect?

A

glomerulonephritis

24
Q

What causes glomerulonephritis?

A

Inflammation caused by either immune response (lupus, Berger’s) or infection (post strep, hepatitis)

25
Q

What is the treatment of glomerulonephritis?

A

steroids

26
Q

Post-renal kidney failure will likely result in the back-up of urine. It can back up in the urethra, bladder, ureters, and then the renal pelvis of kidneys. This is called__________________

A

hydronephrosis

27
Q

How would you diagnose hydronephrosis?

A

Hx, flank pain, suprapubic pain, UA, imaging (IVP, US, CT)

28
Q

How do you treat hydronephrosis?

A

remove obstruction! (Catheter, cholinergics to dilate ureters/urethra and promote micturation, surgery for structural problem, BPH meds, etc)

29
Q

What is considered “elevated proteinuria”?

A

> 150mg/day

30
Q

How much protein is excreted in the urine to make a dx of nephrotic syndrome?

A

> 3.5GRAMS/day

31
Q

What is the osmolality of normal urine?

A

250-300Osm

32
Q

When you have a pre-renal kidney failure, what will the osmolality be? intrinsic kidney failure?

A

> 500Osm–pre renal and Normal for intrinsic (250-300)

33
Q

On a UA dipstick, in reference to protein, what does trace, +1, +2, +3, +4 mean?

A
trace = 150mg/day (normal)
\+1 = up to 500mg/day
\+2 = up to 1.5mg/day
\+3 = up to 5mg/day
\+4 = >5mg/day
34
Q

on UA dipstick, what does +ketones indicate?

A

DKA, starvation

35
Q

What does +nitrites on UA indicate?

A

bacterial infection