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MHD II Test 4 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

AKI and Critical Illness Sepsis

  1. How common is it?
  2. What is it often part of?
  3. What do 5% require?
A
  1. 5-20% of critically ill patients; sepsis pts
  2. Multi-System Organ Dysfunction Syndrome
    3.
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2
Q

Acute Kidney Injury Causes

  1. Prerenal
  2. Intrinsic Renal
  3. Postrenal
A
  1. Absolute drop in blood volume, relative drop in blood volume (ECV), renal artery stenosis of occlusion, NSAID/ACE-I/ARB mechanism
  2. Vascular, Acute Glomerular Disease, AIN, ATN
  3. Bladder outlet obstruction, bilateral ureteral obstruction, unilateraly ureteral obstruction (solitary kidney)
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3
Q

Common Causes of AKI

  1. Prerenal Azotemia and Ischemic ATN accounts for what % of AKI cases?
  2. Are these two totally different diseases?
  3. Define Prerenal Azotemia
  4. What can it complicate?
  5. How can pre-renal Azotemia be corrected?
  6. What can it progress to?
A
  1. 75%
  2. continuum of the same pathologic process
  3. appropriate physiological response to renal hypoperfusion
  4. true hypovolemia or low effective circulating volume (ECV)
  5. by reversing the cause;
  6. ischemic ATN
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4
Q

Normal Renal Autoregulation

  1. What is the overall goal?
  2. What 2 things does a drop in BP or ECV lead to? What mediates each?
  3. What antagonizes each?
A
  1. to keep GFR constant
  2. Vasodilatation of preglomerular arterioles via Prostaglandin I2, NO
  3. Vasoconstriciton of postglomerular arterioles via Angiotensin II
  4. COX I/II (NSAIDS) inhibit pre-glomerular vasodilatation
  5. ACE-Is/ARBs inhibit post-glomerular vasoconstriction
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5
Q

Post-renal Failure

  1. Risk Factors (3)
  2. What needs to occur to improve/recover renal function?
  3. Post-intervention sequelae?
  4. How is it diagnosed?
A
  1. Older men w/prostate disease, solitary kidney, intra-abdominal (pelvic) cancer
  2. prompt ID and intervention
  3. post obstructive diuresis (>4L/day); hyperkalemic, hyperchloremic Renal Tubular Acidosis (can be chronic)
  4. Phyiscal Exam, renal ultrasounds, measurement of post void residual volume (beside bladder scan or urinary catheterization)
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6
Q

What are the four categories of Intrinsic Renal Failure?

A
  1. Vascular (malignant HTN, other)
  2. Acute Glomerular Disease
  3. Acute interstitial necrosis
  4. Acute tubular necrosis
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7
Q

Causes of Acute Tubular Necrosis (ATN)

  1. most common
  2. second most common
  3. other causes
A
  1. sepsis
  2. surgery
  3. Nephrotoxic exposures: anti-microbial agents, anti-neoplastic agents, recreational drugs, tubular hemoglobinuria (massive hemolysis), tubular myoglobinuria (rhabdomyolysis), tubular proteins (myeloma), tubular crystals (urate, oxalate)
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8
Q

ATN

  1. Risk Factors
  2. Pathogenesis
A
  1. Advanced age, pre-existing chronic kidney disease, HTN, cardiac disease, liver disease, peripheral vascular disease, DM
  2. Injury to vascular/tubular components; then Repair:
    death/exfoliation of proximal tubular cells (–>epithelial cell casts)
    Appearance of poorly differentiated epithelial cells
    Proliferation of surviving proximal tubular cells
    Normal differentiation of tubular cells
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9
Q

Classic Clinical Features of ATN

  1. What happens to urine?
  2. 2 phases
A
  1. Dirty or Muddy brown urine
  2. Oliguric phase: HTN, volume overload, hyperkalemia, acidosis
  3. Polyuric phase: volume depletion, hypotension, hypernatremia,
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10
Q

Vascular Causes of AKI (5)

A
  1. Vasculitits
  2. Thromboembolic disease
  3. HUS/TTP
  4. Malignant HTN
  5. Scleroderma renal crisis
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11
Q

Malignant HTN

  1. Causes what?
  2. BP?
  3. What can happen?
A
  1. AKI
  2. > =180/120
  3. impending/progressive organ dysfunction: HTN encephalopathy
    Intracerebral hemorrhage
    ACS (acute MI, unstable angina)
    Acute LV dysfunction w/ pulmonary edema (new S4, rales)
    Dissecting aortic aneurysm
    Eclampsia
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12
Q

Acute Glomerular Disease

  1. Causes
  2. When is it commonly seen?
A
  1. neoplastic disorders, infections, autoimmunity, drugs, genetic abnormalities, idiopathic
  2. uncommon acutely, more commonly seen in subacute and chronic kidney disease
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13
Q

Glomerular Diseases: Nephritic pattern

  1. Histo
  2. Urinary sediment
  3. Proteinuria
A
  1. inflammatory changes
  2. active sediment (cells/casts)
  3. variable
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14
Q

Glomerular Diseases: Nephrotic pattern

  1. Histo
  2. Urinary sediment
  3. Proteinuria
A
  1. cooler findings, far less inflammation
  2. inactive urine sediment
  3. severe proteinuria
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15
Q

Acute Interstitial Nephritis

  1. Most common cause?
  2. Classic triad
  3. What helps make the diagnosis?
A
  1. medications (70%)- PPIs, NSAIDs, antimicrobials (PCNs, cephalosporins); also due to Autoimmune disorders (SLE), infections
  2. fever, peripheral eosinophilia, rash; all 3 only seen 10% of time; usually at least 1 present
  3. may help make diagnosis, PPV and NPV are low though
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16
Q

AKI Workup: What questions are important in the history?

A 
antecedent illness/trauma?
changes in oral intake?
vomiting and/or diarrhea?
suspicion on insensible water loss (high fevers, rapid breathing, excess sweating)?
New medications/dosage changes?
Recent medical procedures/IV dye use?
Rash, joint pain, pulmonary symptoms?
17
Q

AKI Workup: What needs to be looked for in a chart review?

A 
weight trends
intake/output trends
BP trends
O2 sat trends
Operative/anesthesia notes (labile BP/HR/O2 during case, estimated blood loss, urine output, IV fluids given)
18
Q

AKI Workup: Physical Exam

  1. Too wet? signs
  2. Too dry? signs
  3. urine color
  4. Assessment for urinary retention
  5. Signs of vasculitic process
A
  1. abdominojugular reflux, S3 gallop, ascites, peripheral edema and rales are TOUGH to interpret
  2. dry mucuous membranes, skin tenting (only useful if positive in adults), neck veins flat at 0 degrees, signs of shock (orthostatic or frank
    hypotension)
  3. bloody, dirty/muddy, dark yellow/concentrated
  4. fullness/dullness on suprapubic exam, enlarged prostate on digital rectal exam
  5. characteristic rash, synovitis, pulmonary findings
19
Q

AKI Workup: Lab Review

  1. 3 important tests
  2. Others
A
  1. Renal indices (BUN/Creatinine)
  2. Urinalysis (critically important)
  3. Urine indices(electrolytes/creatinine)
  4. infectious labs (CBC, cultures, serologies), complement levels, autoimmune serologies, urine eosinphils
20
Q

AKI Workup: Imaging Review

  1. What is most helpful?
  2. What else can be done? Why?
A
  1. renal ultrasound

2. CXR, CT, MRI: evidence of infection, volume overloaded state, postrenal obstruction

21
Q

Pre-renal Azotemia

  1. Urinalysis
  2. Urine Specific Gravity
  3. Urine Osmolality
  4. Urine Sodium
  5. Fractional Excretion of Na
  6. Fractional Excretion of Urea
A
  1. Hyaline casts
  2. 1.020
  3. > 500
  4. <35%
22
Q

Acute Tubular Necrosis

  1. Urinalysis
  2. Urine Specific Gravity
  3. Urine Osmolality
  4. Urine Sodium
  5. Fractional Excretion of Na
  6. Fractional Excretion of Urea
A
  1. 1.010
  2. > 300
  3. > 40
  4. > 2%
  5. > 35%
23
Q

Why is Creatinine a poor indication of function in AKI?

A
  1. AKI is not a steady state condition
  2. Depends on clearance rate, rate of production, volume of distribution, all of which change in AKI
  3. Bottom line: poor estimate of GFR
24
Q
  1. Causes of High (>10:1) BUN:Creatinine Ratios
  2. Causes of Normal (10:1) BUN:Creatinine Ratios
  3. Causes of Low (<10:1) BUN:Creatinine Ratios
A
  1. Prerenal Azotemia, Decreased Urea load, Obstructive uropathy, ureteroenterostomy, decreased muscle mass
  2. Normal, CKD, ATN
  3. Decreased urea load,inhibition of creatinine secretion, increased creatinine load, interference with creatinine measurement, increased muscle mass
25
Q

BUN: Creatinine Ratio >10:1

  1. What causes Prerenal Azotemia?
  2. What causes an increased urea load?
  3. Other cause?
  4. Why does decreased muscule mass cause it?
  5. Which causes lead to increased urea?
A
  1. true hypovolemia or decreased ECV
  2. GI bleeding (protein load, inc urea abs), glucocorticoids (lead to catabolic state), tetracycline, hypercatabolic states, high protein diet
  3. Ureteroenterostomy
  4. drops creatinine due to muscular atrophy
  5. Prerenal azotemia, increased urea load, ureteroenterostomy
26
Q

BUN: Creatinine Ratio

A
  1. low protein diet, liver failure
  2. cimetidine, probenecid, trimethoprim (common)
  3. ingesting cooked meat, rhabdomyolysis
  4. ketosis, isopropyl alcohol ingestion (metabolized to acetone), cefoxitin, flucytosine
  5. anabolic steroids, muscular development
27
Q

AKI Management: 3 things

A
  1. search for and correct cause of prerenal azotemia or postrenal obstruction (improve ECV when possible)
  2. stop/avoid nephrotoxic agents
  3. adjust dosages of medications in relation to renal clearance
  4. Watch intake/output, daily weight, volume status closely
  5. Manage complications (electrolyte derangement-high K, low Na, high Phos, metabolic acidosis, pulmonary edema)
  6. Nutritional support (ensure adequate carb (prevents protein breakdown) and protein (not too much)
  7. Aggressively manage infections (skin care, catheter care)
  8. Hemodialysis when needed
28
Q

Hemodialysis in AKI

  1. When should it be done?
  2. Indications (there’s a mnemonic)
A
  1. controversial, too early better than too late
  2. AEIOU: Acidosis (severe/refractory)
  3. Electrolyte derangement (usually severe hyperkalmemia)
  4. Intoxication syndrome (severe, dialyzable cause)
  5. Overload (significant pulm edema)
  6. Uremia (significantly symptomatic)
29
Q

AKI Prognosis

  1. What happens to most pts?
  2. What happens 5-16% of time?
  3. What can be seen following AKI?
  4. When is mortality highest?
A
  1. most recover, complete recovery not always the cacse
  2. progresses to irreversible condition
  3. progressive chronic kidney disease
  4. if they require RRT +/- Multi System Organ Dysfunction; mortality >= 50%
30
Q

Prevention of AKI

  1. What needs to be promoted?
  2. What should be avoided?
  3. What should be given with IV contrast?
  4. What is Tumor Lysis Syndrome?
  5. How should it be managed?
A
  1. adequate volume status, cardiac output
  2. nephrotoxic agents in at risk pts (ex use NSAIDs, ACE-Is, ARBs cautiously)
  3. prophylactic care: saline infusion, bicarbonate infusion, N-acetylcysteine (antioxidant)
  4. large lymphoid or solid tumor burden; death of tumor cells delivers large uric acid load to kidneys
  5. prevention with allopurino, rasburicase, alkaline diuresis (reduces likelihood of urate cystal formation)

MHD II Test 4 (4 decks)

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