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MS_Primers for Exam 3 Content > Acute & Chronic Kidney Failure (Disease) Primer > Flashcards

Acute & Chronic Kidney Failure (Disease) Primer Flashcards

1
Q

Renal failure results in the inability of the body to…

A

• Excrete metabolic waste

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2
Q

Compare the onset of acute vs chronic kidney failure.

A
  • Acute: Sudden onset

* Chronic: Insidious onset over many years

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3
Q

Compare the most common causes of acute vs chronic kidney failure.

A
  • Acute: acute tubular necrosis

* Chronic: Diabetic nephropathy

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4
Q

What is acute tubular necrosis?

A

• A kidney disorder involving damage to the tubule cells of the kidneys, which can lead to acute kidney failure

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5
Q

What are some causes of acute tubular necrosis?

A

• Heart attacks, strokes, and clots that cut off blood flow to your kidneys

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6
Q

What is diabetic nephropathy?

A
  • a common complication of type 1 and type 2 diabetes.
  • Over time, poorly controlled diabetes can cause damage to blood vessel glomeruli of the kidneys.
  • This will impair filtration, cause high blood pressure, and other issues, ultimately leading to kidney failure.
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7
Q

Compare dx criteria of acute vs chronic kidney failure.

A
  • Acute: Urine OP reduction, rise in serum creatinine, progressive elevation of BUN levels
  • Chronic: GFR < 60mL/min for 3 months
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8
Q

Compare reversibility of damage in acute vs chronic kidney failure.

A
  • Acute: damage reversible if caught early, though it has a high mortality rate
  • Chronic: irreversible and progressive
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9
Q

Compare primary cause of death in acute vs chronic kidney failure.

A
  • Acute: Infection

* Chronic: Cardiovascular disease

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10
Q

Acute Kidney Injury (AKI): Explain pre-renal etiology.

A
  • Source of damage is to circulation BEFORE the blood hits the kidney.
  • This causes a reduction in glomerular perfusion and overall filtration of kidneys
  • This reduction in glomerulus pressure causes autoregulatory mechanisms to be triggered
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11
Q

What are some examples of pre-renal conditions that can cause AKI?

A
  • Dehydration
  • Burns
  • Any condition that lowers BP
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12
Q

Why do pre-renal conditions trigger the autoregulatory mechanisms?

A
  • The body perceives low glomerular pressure as low body fluids
  • The autoregulatory mechanisms are triggered to try and reverse this by retaining fluids to raise pressure back up and restore glomerular/renal function
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13
Q

What autoregulatory mechanisms are triggered by a decreased glomerular pressure?

A

• ↑ ADH, ↑ Renin, ↑ Aldosterone → Na and H2O retention and ↓ urine OP

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14
Q

Acute Kidney Injury (AKI): Explain intrarenal etiology.

A

• Direct damage to the parenchyma (functional tissue) impairs nephron functioning

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15
Q

What are some conditions that cause intrarenal AKI?

A
  • Prolonged renal ischemia
  • Nephrotoxins (aminoglycosides)
  • ↑ Hgb from hemolyzed RBCs
  • ↑ Myoglobin from necrotic muscle cells
  • Acute tubular necrosis
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16
Q

Acute Kidney Injury (AKI): Explain post-renal etiology.

A

• This occurs when there is a mechanical obstruction that can cause reflux

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17
Q

What are some causes of post-renal AKI?

A
  • BPH
  • Prostate cancer
  • Calculi (stones)
  • Trauma
  • Extra renal tumors
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18
Q

True or False

Urine OP is useful in determining etiology of renal failure

A

• True

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19
Q

Anuria may indicate what condition?

A

• UTI obstruction

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20
Q

Oliguria may indicate what etiology of AKI?

A

• Pre-renal

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21
Q

What specific gravity value indicates renal failure?

A

• 1.007-1.010

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22
Q

What is the normal WBC range in urine?

A

• 0-5

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23
Q

Elevated WBCs in urine indicates…

A

• Infection

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24
Q

What is the normal RBC range in urine?

A

• 0-4

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25
Q

Is it normal to have WBCs or RBCs in urine?

A

• Trace amounts can be ok, otherwise there should be none

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26
Q

True or False
Urine osmolality is used to measure the number of dissolved particles per unit of water in the urine. As a measure of urine concentration, it is more accurate than specific gravity.

A

• True

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27
Q

What is urine osmolality?

A
  • an index of the concentration of osmotically active particles, particularly chloride, sodium, urea, and potassium
  • glucose can also add significantly to the osmolality when it is abundant in urine.
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28
Q

True or False

In a healthy state, the specific gravity of the urine corresponds to the urine osmolality

A

• True

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29
Q

A urine osmolality of 300 is indicative of…

A

• Osmotic diuresis

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30
Q

What is osmotic diuresis?

A

• When the body is unable to reabsorb water and sodium

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31
Q

What are some s/s of acute AKI?

A
  • (OX SOUP FACT)
  • Oliguria or anuria (decreased or absent urine OP)
  • Xerostomia (dry mouth), thirst
  • Swelling
  • Orthostatic BP
  • Uremic frost
  • Pale skin
  • Fatigue
  • Asterixis (low calcium)
  • Confusion
  • Tachycardia
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32
Q

What is the nursing management for AKI?

A
  • Strict I/Os
  • Vitals
  • Fluids
  • Urinary assessment
  • Treat underlying infection (fluids/abx)
  • Rest
  • Daily weight
  • Observe skin and manage edema
33
Q

What are the two main causes of chronic kidney disease?

A
  • Diabetes Mellitus

* Hypertension

34
Q

True or False

CKD is frequently asymptomatic until 80% of nephrons are damaged

A

• True

35
Q

What is normal GFR of a healthy kidney?

A

• 125mL/min

36
Q

A GFR of < 15mL/min indicates…

A

• The pt will need dialysis

37
Q

GFR of < 10mL/Min will result in…

A

• Uremia

38
Q

What is uremia?

A

• a raised level in the blood of urea and other nitrogenous waste compounds that are normally eliminated by the kidneys.

39
Q

What are the urinary s/s of CKD?

A
  • Uremia
  • Polyuria
  • Fluid retention
  • Anuria
40
Q

What causes CKD metabolic disturbances?

A

• Waste product accumulation in the blood as a result of kidney dysfunction

41
Q

How does a decreased GFR affect BUN and Creatinine levels?

A

• Both will be elevated

42
Q

What are the s/s of ↑ BUN?

A
  • N/V
  • Lethargy, impaired thought
  • Fatigue
43
Q

True or False

BUN levels are more accurate indicators of kidney function than Serum creatinine and creatinine clearance tests.

A

• False, Serum creatinine and creatinine clearance tests are more accurate

44
Q

CKD impairs carbohydrate metabolism. How does this affect glucose and insulin?

A
  • Cells become insensitive to insulin, thus cellular glucose uptake will be reduced.
  • This reduction results in glucose and insulin circulating in the blood (hyperglycemia and hyperinsulinemia)
45
Q

Why do diabetic CKD pts that become uremic require less insulin?

A

• Kidney excretion is impaired causing it to stay in the system longer

46
Q

What are triglycerides?

A
  • A type of fat (lipid) found in your blood.

* When you eat, your body converts any calories it doesn’t need to use right away into triglycerides.

47
Q

What is dyslipidemia?

A

• Elevation of plasma cholesterol, triglycerides (TGs), or both, or a low high-density lipoprotein cholesterol level that contributes to the development of atherosclerosis

48
Q

Explain how hyperinsulinemia leads to cardiovascular disease.

A
  • High levels of insulin in the blood triggers the hepatic production of triglycerides that leads to dyslipidemia
  • Without correction, dyslipidemia will cause atherosclerosis and cardiovascular disease.
  • Cardiovascular disease is the leading cause of death for pts w/ CKD
49
Q

Calcium and phosphate have what kind of relationship?

A

• Inverse, if one goes up, the other goes down

50
Q

Normal serum calcium range?

A

• 8.5-10.2

51
Q

Normal serum phosphorus range?

A

• 3-4.5

52
Q

Normal serum magnesium range?

A

• 1.3-2.1

53
Q

Normal serum potassium range?

A

• 3.5-5.5

54
Q

How does CKD cause anemia?

A
  • ↓ renal production of erythropoietin results in ↓ bone marrow RBC production
  • ↑ parathyroid hormone also inhibits erythropoiesis, shortening life of RBC and causes bone marrow fibrosis
55
Q

CKD patients need to take what supplements to assist erythropoiesis?

A

• Iron and folic acid

56
Q

True or False

There is a greater bleeding tendency for CKD pts due to defects in platelet function.

A

• True

57
Q

CKD may manifest what cardiovascular complications?

A
  • Heart failure
  • Left ventricular hypertrophy
  • Peripheral edema
  • Dysrhythmias
  • Uremic pericarditis
58
Q

What are some respiratory manifestations of CKD?

A
  • Dyspnea, Kussmaul’s respirations (Deep, rapid breathing)
  • Pulmonary edema
  • Uremic pleuritis
  • Pleural effusion (build-up of excess fluid between the layers of the pleura outside the lungs)
  • Predisposition to respiratory infections
59
Q

What are some GI system clinical manifestations of CKD?

A
  • Stomatitis (swollen oral mucosa)
  • Uremic fetor (piss breath)
  • GI bleeding
  • Anorexia, N/V
60
Q

What aspects of CKD cause neurological issues?

A
  • ↑ Nitrogenous waste products
  • Electrolyte imbalances
  • Metabolic acidosis
61
Q

What specific damage does CKD cause to neurological tissues?

A
  • Axonal atrophy

* Demyelination of nerve fibers

62
Q

What are the neurological s/s of CKD?

A
  • Depression
  • Lethargy/apathy/fatigue
  • Irritability/lack of concentration
  • Seizure/twitching/asterixis
  • Parathesias
  • Peripheral neuropathy
63
Q

What is peripheral neuropathy?

A

• conditions that result when nerves that carry messages to and from the brain and spinal cord from and to the rest of the body are damaged or diseased.

64
Q

What is the diagnostic testing done for CKD?

A
  • GFR
  • Renal ultrasound
  • Renal biopsy
  • CT scan
  • 24hr urine collection
65
Q

What are the parameters around proteinuria to keep in mind?

A

• Persistent proteinuria (positive ≥2 times in a 3 month period) will need further assessment

66
Q

Why may a CKD pt develop hyperkalemia?

A
  • When insulin effect wears off, K+ leaves the cells and serum levels rise
  • As glucose/insulin management is more precarious w/ the CKD pt, we need to keep a close eye on s/s of hyperkalemia
67
Q

How is hyperkalemia treated w/ CKD pts?

A
  • Keep pt on a potassium restricted diet.
  • Admin sodium bicarbonate (to reduce K+ levels)
  • Admin Kayexalate (to reduce K+ levels)
68
Q

How does kayexalate get rid of potassium?

A
  • Increases fecal potassium excretion through binding of potassium in the lumen of the gastrointestinal tract.
  • Binding of potassium reduces the concentration of free potassium in the gastrointestinal lumen, resulting in a reduction of serum potassium levels.
69
Q

Hyperphosphatemia is associated with what cardiac condition (other than HTN)?

A

• cardiac hypertrophy, which may worsen cardiac contractility and heart failure.

70
Q

How may Hyperphosphatemia be treated to lower HTN?

A

• w/ calcium-based phosphate binders that will bind w/ phosphate in the bowels and be excreted

71
Q

When are calcium-based phosphate binders administered?

A

• w/ meals

72
Q

If iron and folic acid supplements aren’t working to stimulate erythropoiesis, how else may CKD induced anemia be treated?

A

• Via exogenous erythropoietin (IV or SubQ)

73
Q

Why should iron supplements NOT be taken at the same TIME as phosphate binders?

A

• Calcium binds w/ iron and will prevent absorption

74
Q

What are our LDL and Trigliceride level goals when treating the CKD pt?

A
  • LDLs <100

* Triglycerides <200

75
Q

CKD patients should have a diet low in ____, _____ and _____.

A
  • Sodium
  • Potassium
  • Phosphate
76
Q

What are some examples of dietary sodium to be avoided?

A
  • Salt
  • DASH diet items
  • Cured meats, hot dogs, cold cuts
  • Pickled foods
  • Canned food
  • Soy sauce and salad dressings
77
Q

What are some examples of dietary potassium to be avoided?

A

• Oranges, bananas, melons, tomatoes, prunes, raisins, deep green and yellow vegetables, beans, and legumes

78
Q

What are some examples of dietary phosphate to be avoided?

A

• Dairy products

MS_Primers for Exam 3 Content (13 decks)

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