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Renal Yr2 Exam 2 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Pre-renal failure

A

Renal hypoperfusion

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2
Q

2 major causes of hypoperfusion

A

1) True volume depletion

2) Decreased effective arterial blood volume (CHF, hepatic cirrhosis, sepsis)

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3
Q

GFR maintenance

A

Afferent arteriolar vasodilation
Efferent arteriolar vasoconstriction
*Increase in filtration fraction leads to an increase in oncotic pressure in post-glomerular capillaries with increase in salt and water absorption in pt.

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4
Q

NSAIDs

A

Block PG (block afferent arteriolar dilation) and ACE inhibitors/ARBs (block efferent>afferent arteriolar constriction) prevent proper homeostasis

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5
Q

CHF and cirrhosis

A

Can lead to decrease in effective arterial blood volume

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6
Q

**Cardinal feature of Pre-renal azotemia

A

Decrease in effective arterial blood volume (EABV)

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7
Q

Pre-renal azotemia may be a cause of acute or chronic kidney disease

A

Can vasoconstriction b/c activation of at II and sympathetics.

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8
Q

Pre-renal azotemia and AKI are NOT same thing

A

Pre-renal azotemia: Urine NaCl low, FENa 40, Uosm >500

AKI: >20 for urine NaCl and FENa >1% losing it all, U/P creatinine and urea <20 and isomolar Uosm.

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9
Q

Most common cause of pre-renal failure is extracellular fluid volume depletion from GI losses

A

Severe vomiting develops volume contraction.

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10
Q

Do NOT give ACE-Inhibitors or ARBs to patients with

A

Renal Artery Stenosis

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11
Q

NSAIDs cause

A

inhibition of PG synthesis which will lead to unopposed activity of these hormonal systems, resulting in exaggerated renal vasoconstriction and magnified antinatriuretic and anti-diuretic effects.

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12
Q

In pre-renal acute kidney injury

A

The same mechanism that ra’s Na is also responsible for ra of BUN.
Creatinine is NOT reabsorbed avidly by the proximal tubule and is secreted into the pt lumen from the blood.

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13
Q

In pre-renal case

A

BUN and Cr elevated b/c of DECREASE in GFR.
Urea high b/c avid proximal reabsorption.
URINE urea and creatinine concentrations are ELEVATED b/c of high concentration of urine due to ADH mediated water ra.

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14
Q

Pre-renal see HYPOkalemia

A

-renal K+ losses, aldosterone high
Na+ ra, K+ out.
Bicarb acts as a non-reabsorbable anion and also increases distal Na delivery.
Little K+ lost from vomiting b/c not much in gastric secretions.

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15
Q

Pre-renal see HYPOchloremia

A

1) loss b/c HCl in vomiting

2) Dilution with water, same reason why see hyponatremia

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16
Q

Pre-renal see total CO2 elevated b/c of loss of HCl

A

CO2 is about equal to plasma bicarb concentration

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17
Q

Summary pre-renal failure

A

Decrease in EABV triggers kidney to conserve sodium and water at expense of retaining excesses of nitrogenous wastes, creatine.
Kidney is working fine.
Reversible with restoration of effective circulatory volume.
Restore EABV allows kidney to regulate volume and electrolytes at normal levels once again.

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18
Q

Oliguric ATN flow less than 400 ml/day

A

Progressive rise in phosphorus, BUN, creatinine, and potassium as muscle breakdown due to hypercatabolism takes place in absence of renal excretory function.
Serum Ca2+ falls in consequence to the rise of serum phosphorus (due to solubility effect) and a sharp fall in 1,25 (OH)2 vitamin D levels and skeletal resistance to PTH levels.
Life threatening acidosis and hyperkalemia may develop.

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19
Q

ATN

A

most common form of intrinsic renal failure. Occurs after period of sustained period of ischemia or exposure to nephrotoxic agents.
Typically reversible form of renal failure.

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20
Q

Common causes nephrotoxic injury:

A

Aminoglycoside antibiotics
Radiocontrast agents
Myoglobin (rhabdomyolysis)
ATN associated with 4-6 fold increase in mortality.

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21
Q

Risk factors:

A
  • Volume depletion
  • Underlying chronic kidney disease
  • Use of NSAIDs
  • Diabetes mellitus
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22
Q

In ATN, tubular cells are damaged and cannot reabsorb Na+ and Cl- causing an

A

increase in Cl- delivery to MD and cause renal afferent arteriolar vasoconstriction to reduce intraglomerular hydraulic pressure and filtration. (good)

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23
Q

ATN patients are predisposed to

A

Development of volume overload since salt and water intake now easily exceeds the kidneys excretory capacity.
Low Na, Ca, higher K and P.

24
Q

Ischemia

A

Low BP or prolonged volume depletion, sepsis

25
Q

Toxins:

A

-Radiocontrast media (decline in renal function mild and transient, function back 3-5 days)
Help decrease severity with volume expansion and either isotonic saline or sodium bicarbonate.

26
Q

Drugs: tend to be non-oliguric >500 mL urine/24 hr

A

Aminoglycosides
Amphotericin B
Cisplatin

27
Q

Heme pigments

A

Suspect in pt with serum creatinine kinase level above 5,000 U/L who demonstrate heme positivity on urine dipstick in absence of hematuria.

28
Q

Muscle tenderness for

A

Rhabdomyolysis

29
Q

BUN: Creatinine

A

10-15: 1 tubules aren’t working so do not ra as much urea at pt

30
Q

Urine Na+ and Cl >20 mEq/L

A

not reabsorbing

31
Q

FENa >1%

A

In contrast nephropathy, rhabdomyolysis and edema forming states the FeNa maybe <1%

32
Q

Urine osmolality may be low <450 mosm/Kg

A

May have low grade proteinuria, due to impaired ra of protein at pt

33
Q

Urine sediment shows pigmented granular casts or free floating tubular epithelial cells

A

Intrinsic renal failure

34
Q

Acute Interstitial Nephritis (AIN)

A

Immune response mediated

35
Q

Drugs that cause AIN

A

NSAIDs, Penicillins, cephalosporins, sulfonamides (Trimethoprim-sulfamathoxazole), furosemide, rifampin, ciprofloxacin, PPI’s.

36
Q

AIN autoimmune diseases:

A

Sjogren’s syndrome, sarcoidosis

37
Q

AIN: infection

A

Legionella, Leptospira, CMV

38
Q

Drug induced AIN

A

3-5 days after 2nd exposure

Classic triad: rash, fever, eosinophilia

39
Q

NSAIDs induced AIN is associated with

A

Proteinuria.

40
Q

Dry eyes, dry mouth

A

Sjogren’s syndrome

41
Q

Renal biopsy is needed for

A

definitive diagnosis.

42
Q

Acute Tubular Obstruction: volume depletion and acidic urine favors precipitation of material

A
  • Cast nephropathy (multiple myeloma)

- Tumor lysis syndrome: after chemo, lots uric acid and phosphate

43
Q

Phosphorus containing enemas

A

bowel prep for colonoscopy

44
Q

ATO drugs

A

IV acyclovir
Methotrexate
Sulfonamide antibiotics (Trimetheprim-sulfamathoxazole)**Can also cause AIN

45
Q

High uric acid, phosphorus

A

Tumor lysis syndrome

46
Q

High phosphorus, low Calcium in serum

A

Phosphate nephropathy (bowel prep)

47
Q

Elevated free light chains in serum

A

Cast nephropathy

48
Q

Oliguria <500 mL urine output/24 h

A

low urine output

49
Q

Urine analysis

A

Demonstrates crystals of precipitated substance

50
Q

Cholesterol Crystal embolization

A

Can cause AKI in pts with diffuse atherosclerotic disease. Develops after coronary angiography or aortic surgery. See livedo reticularis and retinal artery emboli. Rising serum creatinine concentration. Increase in sedimentation rate, peripheral eosinophilia and hypocomplimentemia.

51
Q

Renal vasculitis

A

inflammation and necrosis of small arteries and arterioles

52
Q

Thrombotic microangiopathies TMA

A

endothelial injury with formation of platelet thrombi occluding small vessels (ischemia). HUS, TTP, malignant HTN, typically associated with low platelets.

53
Q

Low serum complements and peripheral eosinophilia

A

cholesterol emboli

54
Q

Thrombocytopenia (low platelets)

55
Q

Schistocytes

A

RBC fragments on peripheral smears-TTP/HUS

56
Q

Urine analysis

A

Bland sediment in cholesterol emboli, may have dysmorphic red blood cells in sediment in TTP/HUS

Renal Yr2 Exam 2 (5 decks)

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