Grin AKI & CKD Flashcards

1
Q

what is AKI

A

abrupt decline in renal function, it is a clinical syndrome with many causes not just one disease

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2
Q

What defines AKI?

A

Any of these:

  • increase in serum creatinine by >0.3 w/n 48 hrs
  • Increase in serum creatinine to >1.5 times baseline w/n 7 days
  • Urine vvolume <0.5 for six hrs
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3
Q

What is creatinine?

A

metabolite of creatine phosphate from muscle used to estimate GFR

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4
Q

Anuria?

A

urine less than 50-100 ml per day

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5
Q

oliguria

A

urine outuput less than 400-500 ml/day

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6
Q

Azotemia

A

elevated BUN no sx

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7
Q

Pre renal azotemia

A

elevaton in BUN out of proportion to serum creatinine due to poor renal perfusion

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8
Q

Uremia

A

elevated serum BUN with sx such as N/V confusion metallic tase in mouth, fatigue, anorexia

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9
Q

What happens if the kidney cant maintain normal volume status?

A

Volume overlaoad occurs

  • dyspnea
  • edema
  • pulmonary edema
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10
Q

What happens if kidney cant maintain electrolyte homeostasis?

A
  • hypertension
  • hyperkalemia
  • asx

Severe consequences

  • hypertensive emergency
  • arrhythmia
  • sudden cardiac death
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11
Q

What happens if kidney cant maintain acid base balance?

A
  • metabolic acidosis
  • Dyspnea due to respiratory compensation

Serious consequences

  • arrhythmia
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12
Q

What happens when the kidney cant eliminate waste

A
  • increased urea
  • uremia
    • N/V, altered taste, fatigue confusion

severe:

  • encephalopathy
  • uremic paericarditis
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13
Q

What does prerenal AKI mean?

A
  • hypovolemia
  • hypervolemia
  • systemic vasodilation
  • drugs causing impaired renal function

things not directly involving the kidney

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14
Q

What is an intrinsic renal AKI?

A
  • Acute tubular necrosis
  • Acute interstitial nephritis
  • Glomerular disease
  • Vascular

processes occuring inside the kidney

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15
Q

What is a post renal AKI

A
  • bladder outloest obstruction
  • ureteral obstruction

occurs after the kidney

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16
Q

What is the most common type of pre renal AKI?

A

hypovolemia due to bleeding, vomiting, diarrhea, overdiuresis, dehydration

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17
Q

What causes hypervolemia in prerenal aki?

A

congestive heart failure

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18
Q

what causes systemic vasodilation in a pre renal aki

A
  • Sepsis
  • SIRS
  • Cirrhosis
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19
Q

What drugs cause pre renal aki>

A
  • NSAIDs and ACEi
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20
Q

How does tubular necrosis cause intrinsic renal AKI?

A

most common cause of intrinsic AKI

  • prolonged pre renal, kidneys lack blood flow for too long (sepsis is common cause)
  • toxins such as myoglobin, uric acid, myeloma light chains, and IV contrast can cause tubular damage
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21
Q

How does acute interstitial nephritis cause intrinsic AKI

A

infiltration of immune cells into the interstitium of the kidneys commonly caused by PPIs, NSAIDs, and some abx

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21
Q

How does acute interstitial nephritis cause intrinsic AKI

A
  • infiltration of immune cells into the interstitium of the kidneys commonly caused by PPIs, NSAIDs, and some abx
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22
Q

In an intnrisic AKI, the kidney has damage to the glomerulus, tubules, or interstitium which leads to two problems. what are they? what will labs show?

A
  • problems with filtration
  • problems with reabsorption and secretion
  • Urine Na >40
  • BUN/Cr <15:1
  • Urine osm <350
23
Q

What are the two types of bladder outlet obstruction that can cause post renal AKI?

A
  • BPH is most common cause of bladder outlet obstruction
  • blood clots can also cause this
24
Q

How does uretereal obstruction cause post renal AKI?

A

stones or external compression from a malignancy, but it has to be bilateral ureteral obstruction to cause this

25
Q

What history should be asked for a patient with suspected AKI?

A
  • volume status
  • urine volume color changes
  • sx of urinary obstruction
  • recent infection, dysuria
  • Recent IV contrast
  • complete medication hx
26
Q

What PE should be doen with suspected AKI?

A
  • VS
  • Volume status
    • mucous membranes, JVP, cardio-pulm
  • Prostate exam
  • Examine bladder and kidneys
  • Skin exam
27
Q

Labs for suspected AKI

A
  • BMP look at BUN/Cr
  • UA with microscopy
  • Urine electrolytes
  • Urine microalbumine/Cr ratio or Urine protein/Cr ratio

ALL patients with AKI need a BMP and UA

28
Q

On UA if you see hyaline casts what can that suggest

A

non specific pre renal axotemia

29
Q

Renal tubular epithelial cells and granular casts (muddy brown) on UA suggests what kind of kidney disease?

A

ATN

30
Q

What type of kidney disesase does WBC, WBC casts, or urine eosiniphils on a UA suggest?

A

Acute interstitial nephritis

31
Q

What kind of kidney disease does Proteinuria (<3.5), hematuria, dysmorphic RBC and RBC casts suggest?

A

Nephritic syndrome

32
Q

What kidney disase does heavy protein >3.5g/day, fatty casts, oval fat bodies, and minimal hematuria suggest?

A

Nephrotic syndrome

33
Q

What is Fractional excretion of Sodium (FENa) used for?

A
  • used to differentiate between pre renal AKI and ATN
  • FENa <1% suggests pre renal AKI
  • FENa >2% suggests ATN
34
Q

When would you use FEUrea instead of FENa?

A

If a patient is on diuretics as you are inducing excretion of Na

35
Q

When does FEUrea suggest AKI vs ATN?

A
  • FEUrea <35% is prerenal AKI
  • FEUrea >50% ATN
36
Q

What is a post void residulal used for?

A

Used if suspecting bladder outlet obstruction, looks at volume of urine left in bladder after urination

37
Q

What is a renal US used for?

A

Concern for ureteral obstruction or other post renal processes

38
Q

What does a urine eosinophil assess for?

A

Historically used to look for AIN, but has poor sensitivity and specificity, not used

39
Q

When is a renal bx done

A

Severe AKI rapidly progressive unclear etiology

40
Q

How do you treat AKI generally?

A
  • Depends on cause
  • Avoid nephrotoxins
  • renally dose all medications
    • dialysis if needed
41
Q

How do you treat pre renal AKI?

A
  • correct hemodynamics
  • low preeload give fluids
  • high preload give diuretics
42
Q

Intrinsic AKI treatment

A
  • ATN is supportive care
  • AIN stop medications consider steroids
  • Glomerular depends on cause
43
Q

Post renal AKI tx

A
  • remove obstruction
  • Bypass obsruction
  • Catheter
44
Q

Outcomes of AKI?

A
  • likelihood of recovery depends on severity of injury and their baseline renal function
45
Q

Indications for dialysys?

A
  • AEIOU
  • Acidosis (pH <7.2)
  • Electrolytes
  • Intoxication
  • Overload
  • Uremia
46
Q

CKD definition?

A
  • If it’s less than 3 months wit hGFR <60 and or markers of kidney damage patient has AKI
  • After three months then it is CKD
47
Q

Top causes of CKD

A

Diabetes and Htn

48
Q

How does the lack of EPO production in CKD impact the body?

A
  • Anemia
49
Q

how does the kidneys inability to regulate calcium and phosphours metbaolism in CKD impact the body?

A
  • secondary hyperparathyroididsm
  • bone pain and fragility
  • fractures
50
Q

What labs are seen with secondary hyperparathyroidism cased by CKD?

A
  • Calcium is decreased
  • PTH is increased
  • Phosphorus is increased
51
Q

What is the pathophysiology of tertiary hyperparathyroidism with CKD?

A
  • prolonged secondary hyperparathyroiodism
  • Parathyroid gland hyperplasia
  • autonomously functioning parathyroid gland and loss of function of calcium sensing receptors
52
Q

Labs for tertiary hyperparathyroidism?

A
  • Calcium is increased
  • PTH is increased
  • Phosphorus is increased
53
Q

What is osteitis fibrosi cystica?

A
  • excess PTH due to ossteoclast activation leading to bony breakdown
  • leads to subperiosteal bone reabsorption
  • Bone cyst formation
  • brown tumors due to microhemorrhages

Pathologic fractures common in patients with advanced CKD due to renal osteodystrophy

54
Q

Labs and tests for CKD?

A
  • BMP looking at serum creatinine
  • Estimate GFR
  • UA with microscopy
  • UA microalbumin/creatinine ratio
  • Urine protein/Cr ratio
  • Renal US
  • Renal Bx
55
Q

Treatement for CKD?

A
  • Diuretics and fluid restrictiono to maintain volume
  • Low K diet
  • Bicarb supplement to correct acidosis
  • Monitor for encephalopathy due to lack of waste elimination
  • iron repletion and EPO agents
  • Calcitrol and phosphorus binders