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MOHD Keystone Exam 2 > #31 - Acute Kidney Injury > Flashcards

#31 - Acute Kidney Injury Flashcards

1
Q

Patient comes in with acute kidney injury. The dipstick is 3+ for RBCs / heme, but when you look under the microscope, there are only 1 or 2. What is on your differential?

A

It must be either myoglobin or hemoglobin damaging the kidney. They both react with dipstick.

myoglobinuria = rhabdomyolysis
hemoglobinuria - hemolytic anemia

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2
Q

Kidney injury with muddy brown granular casts in urine. Diagnosis?

A

acute tubular necrosis.

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3
Q

elevated BUN/ Creatinine

  • WBCs in urine
  • WBC casts
  • no evidence of infection

Diagnosis?

A

acute interstitial nephritis.

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4
Q

Etiology of acute interstitial nephritis

A

most often drug induced.

can be infection related

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5
Q

kidney injury with RBC casts in urine. Diagnosis?

A

Glomerulonephritis.

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6
Q

Kidney injury with White blood cell casts. Diagnosis?

A

Interstitial nephritis (usually drug induced)

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7
Q

azotemia

A

accumulation of nitrogenous waste (BUN / creatinine )

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8
Q

BUN =

A

blood urea nitrogen

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9
Q

uremia =

A

symptomatic renal failure

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10
Q

oliguria =

A

urine output

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11
Q

anuria =

A

urine output

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12
Q

Define Acute Kidney injury (AKI)

A

sudden loss of renal function over hours to day.
Characterized by a rise in creatinine or BUN,

Decreased urine output may or may not be present.

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13
Q

Difference between Azotemia and uremia

A

uremia = azotemia + symptoms (nausea, vomiting, decreases in appetite, fatigue)

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14
Q

What are the symptoms of Acute Kidney Injury? (6)

A
  • Azotemia
  • Hyperkalemia
  • Metabolic Acidosis
  • hyperphophatemia
  • volume overload
  • accumulation of medications
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15
Q

What happens to the following labs in Acute Kidney Injury?

  • BUN/ Creatinine
  • K+
  • Bicarb
  • PO4 (phosphate)
A
  • BUN / Creatinine go up
  • K+ up hyperkalemia
  • bicarb down(metabolic acidosis)
  • phosphate goes up

The kidney normally gets rid of potassium, phosphorus, and acid (and nitrogen). When it fails, it can’t. And you see the above labs.

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16
Q

Why does volume overload occur in acute kidnay injury?

A

Kidney can’t get rid of Na and Water.

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17
Q

What causes Postrenal Acute Kidney injury?

A

Obstructions in the urinary tract.

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18
Q

Most common location of obstruction for postrenal AKI.

A

below bladder, often due to prostate growth. (stones have to block both ureters if it is to cause AKI)

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19
Q

If you suspect postrenal AKI, what should you ask in your history?

A

History of??

  • pelvic malignancy
  • radiation therapy
  • prostate disease
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20
Q

What is the best diagnostic study for postrenal acute Kidney Injury?

A

Have them pee then do an ultrasound of the bladder right after - it should have less than 100mL, if more - voiding defect.

If you’re bold, you can stick a foley catheter up there and see if fluid comes gushing out.

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21
Q

T/F - If you suspect postrenal AKI, urine sediment will help in diagnosis.

A

False.

In postrenal, urine sediment, and urine / plasma chemistries, are both unhelpful in diagnosis. Physical exam much more important.

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22
Q

Whenever you are volume depleted (or your baroreceptors think you are due to low Cardiac output, etc), three systems get activated. What are they?

A

1- Renin/Angiotensin/aldosterone
2-ADH (antidiuretic hormone)
3- Sympathetic system (increased contractility, heart rate, constricts blood vessels to raise pressure)

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23
Q

What happens to the afferent arteriole and efferent arteriole in dehydration?

A

Afferent dilates, Efferent constricts, raising pressure to maintain GFR

24
Q

What is the single most important mechanism which maintains GFR in dehydration?

A

angiotensin/aldosterone system.
Angiotensin2 constricts the efferent arteriole. At the afferent arteriole, it also tries to constricts but it cancelled by prostaglandin?

25
Q

Why do diabetic, hypertensive patients get acute kidney injuries at lower levels of dehydration than normal?? interferes with afferent dilation/ efferent constriction to improve GFR in dehydration?

A

Atherosclerosis in the vessels interferes with afferent dilation/ efferent constriction, which normally improves GFR in dehydration states (think diabetes/ hypertension)

26
Q

Which drugs should you avoid in volume depleted patients (risk of kidney injury) - 4 classes

A
  • NSAIDS
  • Cyclosporine (immunosuppressive)
  • ACE inhibitors
  • ARBs
27
Q

NSAIDs in kidney injury

A

potentiate prerenal AKI. inhibit prostaglandins, which normally mediate vasodilation of afferent arteriole in hypovolemic states.

28
Q

Cyclosporine in kidney injury.

A

potentiate prerenal AKI.

inhibit prostaglandins, which normally mediate vasodilation of afferent arteriole in hypovolemic state

29
Q

ACE inhibitors, ARBs role in acute kidney injury

A

potentiate prerenal AKI.

By decreasing action of angiotensin II on the efferent arteriole (constriction / maintenence of GFR)

30
Q

3 categories of etiology for prerenal Acute Kidney Injury

A

1- Hypovolemia (vomiting / diarrhea)
2- Low “Effective blood volume” (cardiac failure, cirrhosis, sepsis) - blood doesn’t reach kidneys.

3-renal hypoperfusion - NSAIDs, ACEi’, ARBs

31
Q

Physical exam for prerenal AKI

A
  • orthostatic hypotension!
  • peripheral edema?
  • cardiac exam - heart failure
  • neck veins won’t be present in true hypovolemia
32
Q

Labs to look for in prerenal AKI?

A
  • BUN: Creatinine >20:1
  • Elevated urine concentration (high osmolality /specific gravity)
  • increased renal and urea absorption (low urine sodium, low Fractional Exretion of sodium/urea)
33
Q

Normal specific gravity of urine, what is high?

A

normal = 1.015,

High = >1.020

34
Q

How does the kidney interact with creatinine.

A

Creatinine is produced at a constant rate by muscle tissues in the body.
It is freely filtered at the glomerulus, and minimally secreted/ absorbed in the tubules.
Therefore, creatinine is essentially a proxy measure for GFR (glomerular filtration rate). Creatinine refers to SERUM creatinine (importantly, it is measured in the blood). When serum creatinine rises, it means that it is not getting filtered at the kidney (low GFR). If it drops, that means that the kidney GFR is high.

Serum Creatinine will be high in pre-renal kidney injury, since the GFR will be low (prerenal kidney injury = hypoperfusion of the kidney.)

It will not be as high in intrinsic AKI

35
Q

List the differences between Prerenal and Intrinsic Acute kidney injury, in terms of:

  • BUN: Creatinine ratio
  • Urine osmolality
  • Specific gravity of urine
  • Urine [Na=]
  • FE.Na (fractional excretion of Na)
  • FE.urea
  • urine microscopy
A

BUN:Creatinine = >20:1 in prerenal, 40).

In prerenal, FENa 2%, FE.urea >55%

In prerenal, nothing on urine micro. In intrinsic, often has cellular casts (muddy brown, granular)

36
Q

Treatment of pre-renal AKI - 3 things

A
  • correct fluids
  • discontinue meds that interfere with renal perfusion (NSAIDS, ACEi’s, ARBs, and diuretics)
  • optimize cardiac function in the case of heart failurel
37
Q

4 categories of intrinsic acute kidney injury

A
  • acute tubular necrosis
  • acute interstitial nephritis
  • acute glomerulonephritis
  • acute vascular syndromes.
38
Q

Most common category of intrinsic AKI

A

ATN - acute tubular necrosis.

39
Q

T/F. Prerenal injury can result in acute tubular necrosis.

A

True. This is a common cause of ATN.

40
Q

2 categories of causes of acute tubular necrosis

A
  • Ischemic (from untreated prerenal)

- Nephrotoxic (endogenous / exogenous)

41
Q

Free myoglobin or hemoglobin can cause which type of kidney injury?

A

Acute Tubular Necrosis (ATN) - they are toxic to the kidney.

42
Q

What causes free myoglobin?

A

Rhabdomyalysis - take a good history (did you work out like crazy yesterday?)

43
Q

What causes free hemoglobin? How do you figure out/confirm the cause?

A 
intravascular hemolysis (hemolytic anemia)
take some labs,
44
Q

T/F Acute Tubular Necrosis form of Acute Kidney injury is most often caused by drugs.

A

True.

45
Q

What will you find in labs for hemolytic anemia/ intravascular hemolysis? GIve me: LDH,

A
  • high LDH
  • low haptoglobin
  • high indirect bilirubin,
  • blood smear = schistocytes
46
Q

What labs should you order if you suspect hemolytic anemia/ intravascular hemolysis?

A

LDH, haptoglobin, indirect bilirubin, peripheral blood smear

47
Q

Treatment for toxic Acute tubular necrosis

A

Agressive hydration to wash out myoglobin/hemoglobin

48
Q

What kind of cells compose the brown muddy casts in ATN?

A

-necrotic tubule cells that have sloughed off.

49
Q

Treatment of acute tubular necrosis

A

Supportive therapy. - fluids/bicarb if acidosis, etc.

Dialysis if medical management doesn’t improve symptoms.

50
Q

Why are the fractional excretions of sodium and urea high in acute tubular necrosis?

A

Angiotensin and aldosterone normally act on the tubules to absorb sodium and water (urea follows water) - the tubules are necrotic and non-functioning!

51
Q

Define Acute interstitial nephritis

A

acute renal failure due to lymphocytic infiltration of the interstitium

52
Q

What is the most common cause of acute interstitial nephritis?

A

Drugs!!

53
Q

2 causes of acute interstitial nephritis..

A

DRUGs - #1

inflammation (infection / inflammatory conditions) - #2

54
Q

Classic triad for acute interstitial nephritis

A
  • fever
  • rash
  • eosinophilia
55
Q

Drugs that can cause acute interstitial nephritis - 4 - these aren’t tested though

A

penicillin
allopurinol (gout)
-NSAIDs
-Proton Pump Inhibitor (PPI)

56
Q

Treatment for acute interstitial nephritis

A

remove the drug causing the condition

57
Q

T/F - if a patient is on diuretics and you suspect ATN, you should check the FE.urea instead of the FE.Na.

A

True - diuretics alter sodium excretion - Fractional excretion will be altered. Check FE urea instead - this will be unchanged..

MOHD Keystone Exam 2 (14 decks)

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