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Renal > SM_195a: AKI: Pre, Post, and Intrinsic > Flashcards

SM_195a: AKI: Pre, Post, and Intrinsic Flashcards

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1
Q

AKI is _______

A

AKI is deterioration of renal function over hours to days resulting in the kidney’s inability to excrete nitrogenous waste products, maintain fluid balance, and maintain electrolyte balance

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2
Q

AKI occurs due to _____ in developing nations

A

AKI occurs due to hypovolemic shock from diarrhea in developing nations

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3
Q

AKI occurs due to _____ in industrialized nations

A

AKI occurs due to bypass cardiac surgery in industrialized nations

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4
Q

There is a higher risk of AKI if ________

A

There is a higher risk of AKI if pre-existing chronic kidney disease

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5
Q

Prognosis of AKI is worse if _____ or _____

A

Prognosis of AKI is worse if elderly or pre-existing CKD

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6
Q

AKI is observed clinically as ______ or ______

A

AKI is observed clinically as rise in creatinine or reduction in urine output

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7
Q

Oliguria is 24 hour urine output ______

A

Oliguria is 24 hour urine output < 500 mL

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8
Q

Anuria is 24 hour urine output _____

A

Anuria is 24 hour urine output < 50 mL

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9
Q

Describe the systemic manifestations of AKI

A

Systemic manifestations of AKI

  • Extracellular volume expansion manifesting as HTN, CHF, pulm or peripheral edema
  • Hyperkalemia
  • Metabolic acidosis
  • Hyperphosphatemia
  • Anemia due to a decrease in the production of erythropoietin
  • Uremia (toxic metabolic state)
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10
Q

Describe the natural history of AKI

A
  • Full recovery (best)
  • AKI to CKD
  • Acute-on-chronic kidney disease
  • AKI to ESRD (worst)
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11
Q

Types of AKI are _____, _____, and _____

A

Types of AKI are pre-renal, intrinsic, and post-renal

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12
Q

Describe the etiology of pre-renal AKI

A

Pre-renal AKI

  • Occurs when kidney hypoperfusion
  • Due to true volume depletion or ineffective arterial blood volume
  • No structural injury to kidney
  • Generally prompt recovery of glomerular filtration when hemodynamics are restored
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13
Q

Describe causes of pre-renal AKI

A

Causes of pre-renal AKI

  • Hypovolemia: intravascular volume depletion, third spacing, decreased cardiac output
  • Hypotension
  • Pharmacologic
  • Large vessel compromise
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14
Q

Pre-renal AKI is most common in ______

A

Pre-renal AKI is most common in outpatients

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15
Q

Glomerular filtration depends on sufficient _____ to provide adequate blood flow to glomerulus and adequate filtration pressure

A

Glomerular filtration depends on sufficient effective circulating blood volume to provide adequate blood flow to glomerulus and adequate filtration pressure

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16
Q

Normally, autoregulation of GFR ____ over a wide range of systemic blood pressures

A

Normally, autoregulation of GFR is constant over a wide range of systemic blood pressures

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17
Q

As blood pressure falls, _____ progressively dilates due to ______, while ______ progressively constricts due to ______

A

As blood pressure falls, afferent arteriole progressively dilates due to prostaglandins, while efferent arteriole progressively constricts due to angiotesin II

  • Prostaglandins preferentially vasodilate afferent arteriole to increase blood flow into glomerulus
  • Angiotesin II causes greater constriction of efferent than afferent arteriole to preserve ultrafiltration pressure
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18
Q

When effective circulating blood volume decreases, GFR ______ due to ______ and ______

A

When effective circulating blood volume decreases, GFR stays constant due to afferent arteriole vasodilation via prostaglandins and efferent arteriole vasoconstriction via angiotensin II

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19
Q

When effective circulating blood volume decreases and person takes NSAIDs, GFR ______ because ______

A

When effective circulating blood volume decreases and person takes NSAIDs, GFR decreases because vasodilatory effect of prostaglandins on afferent arteriole is blocked

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20
Q

When effective circulating blood volume decreases and person takes an ACE-i/ARB, GFR ______ because ______

A

When effective circulating blood volume decreases and person takes an ACE-i/ARB, GFR decreases because ACE-i/ARB inhibit vasoconstrictive effect of angiotensin II on efferent arteriole

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21
Q

In pre-renal AKI, what occurs when glomerular filtration is reduced?

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A

In pre-renal AKI, when glomerular filtration is reduced

  • Aldosterone release increased -> increased distal nephron Na+ reabsorption
  • ADH increased -> decreased free water clearance

Leads to concentrated urine with low urine sodium

22
Q

Describe diagnosis of pre-renal AKI

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A

Diagnosis of pre-renal AKI

  • Diarrhea, diuretic use, dizziness
  • Signs of dehydration or heart failure
  • Lab: urinalysis, urine sodium (FENA < 1% suggestive but not exclusive), BUN/creatinine (> 20:1)
23
Q

Describe management of pre-renal AKI

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A

Management of pre-renal AKI

  • Rapid and reversal of underlying process
  • Volume expansion of hypovolemic
  • Blood pressure support (vasopressors, inotropes)
24
Q

Pre-renal AKI is _____ to volume repletion, while hepatorenal syndrome is _____ to volume repletion

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A

Pre-renal AKI is responsive to volume repletion, while hepatorenal syndrome is NOT responsive to volume repletion

25
Post-renal AKI is \_\_\_\_\_\_\_
Post-renal AKI is obstruction anywhere in urinary tract, causing AKI (increase in hydrostatic pressure -\> decrease in GFR)
26
Post-renal causes of AKI are \_\_\_\_\_, \_\_\_\_\_, and \_\_\_\_\_
Post-renal causes of AKI are ureteral (bilateral in setting of 2 functional kidneys), bladder neck, and urethral
27
In post-renal AKI, severe or complete obstruction causes increased ______ in renal pelvis, leading to \_\_\_\_\_\_
In post-renal AKI, severe or complete obstruction causes increased hydrostatic pressure in renal pelvis, leading to decreased GFR
28
Describe diagnosis of post-renal AKI
Diagnosis of post-renal AKI * Physical exam: distended bladder, enlarged prostate * BUN/Cr \> 20:1 - enhanced urea reabsorption in decreased urine flow state * Post-void residual bladder volume (lower tract obstruction) * Renal ultrasound (upper tract obstruction) * Foley catheter placement * Non-contrast CT
29
Management of post-renal AKI necessitates _____ and _____ to preserve kidney function
Management of post-renal AKI necessitates rapid diagnosis and relief of obstruction to preserve kidney function
30
In intrinsic renal AKI, \_\_\_\_\_, \_\_\_\_\_, \_\_\_\_\_, and _____ are affected
In intrinsic renal AKI, tubules (acute tubular necrosis), interstitium (interstitial nephritis), glomeruli (glomerulonephritis), and vasculature (vascular disorders) are affected
31
Causes of acute renal AKI are \_\_\_\_\_, \_\_\_\_\_, \_\_\_\_\_, and \_\_\_\_\_
Causes of acute renal AKI are tubules, interstitium, glomeruli, and vascular (small vessels)
32
Describe diagnosis of intrinsic AKI
Diagnosis of intrinsic AKI * Medications (can cause interstitial or tubular damage) * Labs: urinalysis (proteinuria, hematuria), urine sediment * Renal ultrasound (vascular)
33
Urine sediment of intrinsic AKI would reveal \_\_\_\_\_, \_\_\_\_\_, \_\_\_\_\_, or \_\_\_\_\_
Urine sediment of intrinsic AKI would reveal renal tubular epithelial cells, muddy brown casts, RBC casts, or WBC casts
34
The tubular etiology of intrinsic AKI is \_\_\_\_\_\_
The tubular etiology of intrinsic AKI is acute tubular necrosis (ATN) * Most common cause of hospital AKI * Etiology: ischemic (pre-renal, sepsis), nephrotoxic (exogenous, endogenous), intra-tubular obstruction (myeloma, tumor lysis syndrome, drugs) * Does not resolve immediately after restoration of renal blood flow
35
Describe acute tubular necrosis
Acute tubular necrosis * Most common cause of hospital AKI * Etiology: ischemic (pre-renal, sepsis), nephrotoxic (exogenous, endogenous), intra-tubular obstruction (myeloma, tumor lysis syndrome, drugs) * Does not resolve immediately after restoration of renal blood flow
36
The interstitial etiology of intrinsic AKI is \_\_\_\_\_\_
The interstitial etiology of intrinsic AKI is acute interstitial nephritis * Drug-induced, infection, autoimmune disease, malignancy, sarcoidosis, idiopathic
37
The glomerular etiology of intrinsic AKI is \_\_\_\_\_\_
The glomerular etiology of intrinsic AKI is glomerulonephritis * RPGN, IgA nephropathy, post-infectious glomerulonephritis, MPGN, FSGS, MCD, MGN
38
The vascular etiology of intrinsic AKI is ______ or \_\_\_\_\_\_
The vascular etiology of intrinsic AKI is small/medium vssel inflammation resulting in vasculitis or vascular obstruction/occlusion * Prinicipal vessels: bilateral renal artery thrombosis or embolism * Bilateral renal vein thrombosis * Small vessels
39
Describe the urinalysis and urine chemistry findings in different types of AKI
40
Pre-renal AKI has urine osmolality \_\_\_\_\_
Pre-renal AKI has urine osmolality \> 500
41
Describe AKI in tropical countries
AKI in tropical countries * Bimodal pattern: spike during rainy season and after rainy season * Lots of infectious, insect, obstetric causes
42
Post-renal AKI has urine osmolality \_\_\_\_\_
Post-renal AKI has urine osmolality \< 350
43
Describe conservative and immediate management for AKI
Conservative and immediate management for AKI * Adjust fluids: volume depletion, volume overload * Adjust dose and frequency of meds at minimum daily * Review electrolytes, BUN, creatinine, urine output closely
44
Risk factors for developing AKI include \_\_\_\_\_, \_\_\_\_\_, and \_\_\_\_\_
Risk factors for developing AKI include hypovolemia, older age, and underlying chronic kidney disease
45
Urine sodium / fractional excretion of sodium is low in pre-renal AKI because \_\_\_\_\_\_
Urine sodium / fractional excretion of sodium is low in pre-renal AKI because there is decreased kidney perfusion, which results in reduction in GFR, prompting reabsorption of nearly all the filtered sodium
46
Diagnostic tests/maneuvers used to rule out post-renal problems as the cause of AKI include _____ and \_\_\_\_\_
Diagnostic tests/maneuvers used to rule out post-renal problems as the cause of AKI include renal ultrasound and Foley catheter placement
47
All of the following findings would be suggestive of pre-renal AKI EXCEPT A. orthostatic hypotension B. urine sodium of 75 C. BUN/Cr ratio of 30 D. urine osmolality of 500
All of the following findings would be suggestive of pre-renal AKI EXCEPT A. orthostatic hypotension **B. urine sodium of 75 - should be \< 20 in pre-renal** C. BUN/Cr ratio of 30 D. urine osmolality of 500
48
There is a mismatch between ____ and \_\_\_\_
There is a mismatch between GFR and urinary flow rate
49
What should you do? A. start IV fluids (e.g. normal saline) B. stop ACE inhibitor C. stop ibuprofen D. check for post-void residual urine, place catheter in bladder E. all of the above
What should you do? A. start IV fluids (e.g. normal saline) B. stop ACE inhibitor C. stop ibuprofen D. check for post-void residual urine, place catheter in bladder **E. all of the above**
50
Describe common causes of AKI
51
AKI is defined as ______ or \_\_\_\_\_\_\_
AKI is defined as rise in serum creatinine or decreased urine output (oliguria) * Creatinine increase by \>0.3 mg/dL in 48 hours or rise to above 1.5x baseline in preceding 7 days * Urine output of \<0.5 mL/kg/hr for ≥6 hours

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