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NURS 412 Final Exam > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

CKD

A

Progressive, irreversible loss of kidney function

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2
Q

AKI

A
  • a potentially reversible, abrupt decline in kidney function leading to increased creatinine, decreased urine output or both
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3
Q

AKI is usually associated with…

A

other life-threatening conditions

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4
Q

AKI follows: (3)

A

Follows severe, prolonged hyptension, hypovolemia, or exposure to a nephrotoxic

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5
Q

How quickly do symptoms of AKI develop

A

Develops over hours to days

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6
Q

Onset of AKI

A

sudden

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7
Q

Most common cause of AKI

A

Acute tubular necrosis

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8
Q

Diagnostic criteria AKI

A

Acute reduction in urine output, elevation in serum creatinine, or both

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9
Q

Reversibility of AKI

A

potentially

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10
Q

Morality of AKI

A

High

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11
Q

Primary Cause of Death AKI

A

Infection

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12
Q

Onset of CKD

A

Gradual, often over many years

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13
Q

Most common cause of CKD

A

Diabetic nephropathy

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14
Q

Diagnostic Criteria of CKD

A

GFR<60 for >3 mo, kidney damage >3 mo or both

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15
Q

Reversibility of CKD

A

Progressive and irreversible

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16
Q

Primary cause of death in CKD

A

Cardiovascular disease

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17
Q

RIFLE Criteria

A

R - risk
I - Injury
F - Failure
L - loss
E - ESRD - end-stage renal disease

This is one of the most commonly used classification systems for AKI. uses serum creatinine, GFR, and urine output to identify these five criteria

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18
Q

Clinical Manifestations of AKI

A

Range from mildly elevated serum creatinine to anuric renal failure

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19
Q

Causes Leading to AKI: Prerenal

A
  • External to the kidneys (hypovolemia or meds) that impact renal blood flow.
  • Usually, reversible
    Although renal tubular and glomerular function is preserved, glomerular filtration is reduced as a result of decreased perfusion.
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20
Q

Prerenal Causes of AKI - Hypovolemia

A

Hypovolemia, decreased cardiac output, decreased peripheral vascular resistance, and vascular obstruction cal all decrease the effective circulating volume of the blood. With reduced circulation, autoregulatory mechanisms that increase aldosterone, angiotensin II, norepinephrine and AHD attempt to preserve blood flow to essential organs. Prerenal azotemia (or accumulation of nitrogenous waste products) result in reduced excretion of sodium, increased salt and water retention, and decrease urine output

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21
Q

Other cause of prerenal AKI: vasoactive medications

A
  • ACE inhibitors
  • ARBs
  • Epinephrine and/or dopamine that cause intrarenal vasoconstriction leading to hypoperfusion of the glomeruli.
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22
Q

Result of prolonged prerenal AKI

A

Prerenal AKI can lead to result in acute tubular necrosis, but if the prerenal cause is dealt with promptly, usually, renal function can be regained

23
Q

Causes Leading to AKI: Intrarenal

A
  • Conditions that cause direct damage to renal tissue (parenchyma) –> impaired nephron function (ATN due to ischemia, nephrotoxins, or sepsis)
  • Due to prolonged ischemia OR the presence of nephrotoxins (gentamycin or CT contrast). Hgb from hemolyzed RBC’s (sickle cell disease) or myoglobin released from necrotic muscle cells
  • infrarenal causes of AKI can be due to untreated prerenal causes OR they can begin with direct damage to the renal
  • SLE or acute glomerulonephritis may also cause AKI
24
Q

Causes Leading to AKI: Postrenal

A
  • mechanical obstruction of urine outflow (BPH, prostate Ca, renal calculi, tumors)
  • Usually reversible if identified before permanent kidney damage occurs
25
Q

Prerenal and postrenal AKI correctible

A

ADDRESS THE CAUSE
- If the AKI hasn’t caused intrarenal damage usually resolves quickly with correction of the cause.
if tissue damage HAS occurred from either cause or from intrarenal causes, acute tubular necrosis results and/or the course of AKI is prolonged

26
Q

Untreated prerenal and postrenal causes +/- or infrarenal causes leads to

A

Acute Tubular Necrosis

27
Q

ATN has three phases
- what happens if the pt doesnt recover?

A
  • initiation
  • maintenance
  • recovery
    In some situations, the patient does not recover from AKI and CKD develops
28
Q

Initiation Phase: characterized by (2)

A
  • increased serum creatinine + BUN
  • decreased urine output
29
Q

Maintenance Phase: how long does it last?

A

days to weeks

30
Q

Maintenance Phase: Nonoliguric

A

Dilute urine but uremic toxins present (low specific gracity) kidneys are unable to filter out urea toxins into the urine

30
Q

Urine output in Maintenance Phase

A

May be anuric: RARE, oliguric, or nonoliguric

31
Q

Maintenance Phase: Oliguric
- manifestations (3)
- how long does this phase last?

A
  • less than 400ml/day or 20ml/hr
  • lasts 10-14 days usually. the longer it is prolonged, the poorer to outcome
  • changes in urinary output
  • fluid and electrolyte abnormalities
  • uremia
32
Q

Maintenance Phase - Oliguric: Urinary Changes

A

Decreased U/O to <400mL/24h.

33
Q

Maintenance Phase - Oliguric: Fluid volume excess (5)

A
  • JVD
  • edema
  • hypertension
  • pulmonary edema
  • pericardial and.or pleural effusions
34
Q

Maintenance Phase - Oliguric: Metabolic Acidosis

A
  • Kussmaul’s resps (deep rapid) to increase blowing off Co2
  • lethargy/stupor (if prolonged)
  • kidneys can’t synthesize ammonia, which is needed for hydrogen ion excretion or to excrete acid products of metabolism. Serum bicarb levels decrease b/c bicarb is used up buffering H+ ions
35
Q

Maintenance Phase - Oliguric: Sodium Balance

A

Hyponatremia
Damaged tubules cannot conserve sodium, therefore, the urinary excretion of sodium may increase resulting in hyponatremia

36
Q

Maintenance Phase - Oliguric: Potassium Excess

A

hyperkalemia -> tall, peaked T waves
occus b/c the normal ability of the kidneys to regulate and excrete potassium is impaired. May be precipitated by a number of causes: massive tissue trauma; bleeding and blood transfusion may cause cellular destruction; acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells into the extracellular fluid.
Prompt treatment is essential

37
Q

Maintenance Phase - Oliguric: Hematological Disorders

A

Anemia, increased bleeding, decreased WBC
- anemia r/t impaired erythropoietin production. Uremia reduces platelt adhesiveness, leading to bleeding.
WBCs are altered leading to immune deficiency. Infection in association with AKI is associated with double the mortality rate

38
Q

Maintenance Phase - Oliguric: Calcium and Phosphate

A
  • hypocalcemia
  • hyperphosphatemia
    Activated Vit D must be present for GI absorption of calcium. Only functioning kidney’s can activate Vitamin D, therefore, in damaged kidneys, serum calcium decreases in response the parathyroid gland releases PTH, stimulating bone demineralization. Phosphate is released as well, leading to hyperphosphatemia, worsened by the reduced excretion of PO4 by the kidneys
39
Q

Maintenance Phase - Oliguric: Waste Product Accumulation

A
  • increased creatinine
  • increased BUN
  • decreased eGFR
    Kidneys are the primary exretors for urea, the end product of protein metabolism and creatinine, and end product of endogenous muscle metabolims. BUN results have to be interpreted carefully because other things can increased BUN.
40
Q

Maintenance Phase - Oliguric: Neurological Disorders

A

Fatigue/difficulty concentrating –> seizures, stupor, coma

41
Q

Recovery Phase

A

Marked by return of BUN, Creatinine and GFR towards normal states
Diuresis –> fluid & electrolyte abnormalities
- patients acid-base, electrolyte and waste product values begin to normalize
- Renal function may take up to 12 months to stabilize

42
Q

Recovery Phase: Diuresis

A
  • Begins 1-3L/24 h –> 3-5L/24h
  • pts must be monitored for hyponatremia, hypokalemia and dehydration
  • may last 1-3 weeks
    The high urine output occurs d/t osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. In this phase, the kidneys have recovered their ability to excrete wastes but not to concentrate the urine. Hypovolemia and hypotension can occur form massive fluid losses
43
Q

AKI - Diagnostic Studies (5)

A
  • Urinalysis - sediment WITH casts, cells, or proteins -> intrarenal disorders
  • urine specific gravity, sodium content, osmolality –> helps differentiate different types of AKI
  • renal ultrasound: anatmy and function
  • Renal CT: can identify causes of obstruction, but exposure to radiation and nephrotoxic contrast is greater risk
  • MRI and MRA are NOT recommended
44
Q

Goals of care AKI (3)

A

1) eliminate the cause
2) manage signs and symptoms
3) prevent complications

45
Q

IMPORTANT CONSIDERATIONS IN AKI COLLABORATIVE CARE

A
  • Is there sufficient intravascular volume and cardiac output to perfuse the kidneys?
46
Q

Collaborative Care: Diuretic Therapy

A
  • Loop diuretics (Lasix)
  • Osmotic diuretic (mannitol)
    Diuretics will not help the prerenal or postrenal
    Sometimes they can be helpful for the infrarenal causes.
47
Q

Collaborative Care

A
  • Fluid restriction: 600mL (insensible losses) + previous 24h losses
  • treatment of electrolyte imbalances
  • Renal Replacement Therapy - hemodialysis
48
Q

What is AKI is already established?

A

Fluids and diuretics will not be effective and may be harmful. Generally, begin early RRT to minimize symptoms and prevent complications

49
Q

Nutritional Therapy

A
  • main challenge –> balancing adequate calories to prevent catabolism despite restriction required to prevent electrolyte and fluid disorders
  • energy from fat and carb sources prioritized to prevent ketosis
  • 25-35kCal/kg
  • Electrolyte replacement in accordance with serum levels
  • sodium is restricted
  • hyperphosphatemia, hypermagnasemia and hypocalceia
    Enteral or parenteral feeding may be required (though parenteral would be done ++ cautiously if pt on RRT)
50
Q

AKI - Nursing Managenent: Health Promotion (VERY IMPORTANT)

A
  • ID high-risk populations for AKI (hypovolemic, dehdyrated, shockym poor cardiac output, advanced liver disease with low albumin- be thinking about renal perfusion)
  • Control nephrotoxic drugs (IV contrast, gentamicin, NSAIDS, ACE inhibitors and ARBs, PipTaz and Vanco have special dosing for renal patients)
  • Prevent prolonged episodes of hypovolemia or hypotension (treat low BP where it is warranted, the earlier the better)
51
Q

Prevention and AKI

A
  • essential d/t high morality rates associated with AKI. For patients with ANY level of renal insufficiency (esp those with diabetes or older adults), special attention must be given to prevent nephrotoxic events secondary to contrast dye.
  • Adequate hydration before and after the test is critical
  • Preventing prolonged episodes of hypovolemia INCLUDES monitoring output (esp when pts receiving ++ diuretic therapy, or in those with excessive diarrhea/NG/vomiting)
52
Q

AKI Acute Nursing Interventions (6)

A
  • Managing fluid and electrolyte balance
  • Monitoring AND recording accurate intake and output
  • Daily weights (at the same time; same scale) 1kg = 1L of fluid
  • Reducing risk of infection: blunted febrile response (infection is the leading cause of death in AKI, meticulous aseptic technique required)
  • Correct dosing of antibiotics for renal impairment
  • Skin care and month care (edema and decreased muscle tone, mouth care d/t ammonia in saliva causing breakdown of mucous membranes)

NURS 412 Final Exam (12 decks)

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