Blood Chemistry and Renal function Flashcards

1
Q

What tests are part of the Basic Metabolic Panel (BMP) ?

A

sodium, potassium, chloride, carbon dioxide, BUN, creatinine, glucose, and calcium

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2
Q

What tests are part of the Comprehensive Metabolic Panel (CMP)?

A

BMP + most of the hepatic panel (albumin, alkaline phosphatase, AST, ALT, bilirubin, total protein)

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3
Q

Way to write notes for BMP

A
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4
Q

What is sodium used to evaluate? What are the normal and critical values?

A

Used to evaluate and monitor fluid and electrolyte balance and therapy

Normal = 136-145 mEq/L
Critical values are < 120 or > 160

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5
Q

Sodium is the major cation in what space?

A

extracellular space

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6
Q

Sodium content in the body is a balance between?

A

dietary sodium intake and renal excretion

Nonrenal losses (sweat) normally are minimal

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7
Q

What is sodium balance regulated by?

A

Aldosterone stimulates the kidneys to reabsorb sodium and decrease renal losses by conserving sodium

Natriuretic hormone is stimulated by increased sodium levels and decreases renal absorption and increases renal losses of sodium

Antidiuretic hormone (ADH), which controls reabsorption of water at the distal tubules of the kidneys, affects serum sodium levels by dilution or concentration

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8
Q

What happens to sodium if free body water is increased?

A

sodium is diluted and the concentration may decrease. The kidneys compensate by conserving sodium and excreting water.

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9
Q

What happens to sodium if free body water is decreased?

A

If free body water is decreased, sodium concentration will rise and the kidneys will compensate by conserving free water.

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10
Q

What daily intake of sodium is required to maintain balance?

A

Average dietary intake of 90-250 mEq/day is required to maintain sodium balance

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11
Q

What are the symptoms of decreased sodium and at what levels do they appear?

A

Symptoms of decreased sodium may begin when levels are < 125 mEq/L.
First symptom is weakness.

When level falls below 115, confusion and lethargy occur and may progress to stupor or coma.

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12
Q

What are the symptoms of increased sodium?

A

Symptoms of increased sodium include dry mucous membranes, thirst, agitation, restlessness, hyperreflexia, mania, and convulsions.

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13
Q

What are the interfering factors for sodium?

A

Recent trauma, surgery, or shock may cause increased levels because renal blood flow is decreased.

Aldosterone is secreted which stimulates increased renal absorption of sodium.

Drugs may increase levels – antibiotics, corticosteroids, estrogens, contraceptives, laxatives
Drugs may decrease levels – antihypertensives, loop diuretics, antipsychotics, antiepileptics, NSAIDs.

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14
Q

Causes of hypernatremia?

A

Increased sodium intake
Decreased sodium loss
Excessive free body water loss

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15
Q

Causes of decreased sodium loss?

A

Cushing syndrome – corticosteroids have effect like aldosterone
Hyperaldosteronism – aldosterone stimulates kidneys to absorb sodium

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16
Q

What can cause excessive free body water loss?

A

Gastrointestinal loss (without rehydration) – loss of free water concentrates sodium

Excessive sweating – most sweat is free water causing sodium to concentrate

Extensive thermal burns – serum and free water lost through open wounds causing sodium to concentrate

Diabetes insipidus – ADH deficiency and inability of kidneys to respond to ADH causes large free water losses

Osmotic diuresis – water lost at rate greater than sodium loss

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17
Q

What causes Hyponatremia?

A

Decreased Sodium Intake
Increased Sodium Loss
Increased Free Body Water

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18
Q

What causes increased sodium loss?

A

Addison disease – aldosterone and corticosteroid hormone levels are low so sodium is not reabsorbed by the kidneys and is lost in the urine

Diarrhea, vomiting, or nasogastric suctioning – sodium in the GI contents is lost with the fluid

Intraluminal bowel loss (ileus, mechanical obstruction) – large amount of extracellular fluids are third-spaced into the lumen of the dilated bowel. This fluid contains sodium

Diuretic administration – inhibit sodium reabsorption by the kidney

Chronic renal insufficiency – kidneys lose their ability to reabsorb sodium

Large volume aspiration of pleural or peritoneal fluid – aspiration of these fluids is compensated by secretion of ADH, which increases absorption of free water to dilute sodium

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19
Q

What causes increased free body water?

A

Excessive oral water intake – psychogenic polydipsia

Hyperglycemia – osmotic effect of glucose pulls in free water from the extracellular space and dilutes sodium

Excessive IV water intake

Congestive heart failure and peripheral edema – increased free water retention

Ascites, peripheral edema, pleural effusion, intraluminal bowel loss – third space losses of sodium

Syndrome of inappropriate or ectopic secretion of ADH – oversecretion of ADH stimulates kidneys to reabsorb free water.

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20
Q

Function of potassium in the body?

A

Major cation within the cell. Intracellular potassium concentration is about 150 mEq/l and normal serum potassium concentration is about 4. This ratio is the most important determinant in maintaining membrane electrical potential, especially in neuromuscular tissue.

Potassium is also involved in protein synthesis and contributes to the metabolic portion of acid base balance – kidneys can shift potassium ions for hydrogen to maintain a normal pH.

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21
Q

What is the function of Potassium test? What are the normal and critical values?

A

Part of all routine evaluations as well as in patients with any type of serious illness. Important to cardiac function with significant effects on heart rate and contractility.

Normal range: 3.5-5.0 mEq/L
Critical values < 2.5 or > 6.5

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22
Q

What does the serum potassium concentration depend on?

A

**Aldosterone **– increases renal losses of potassium

Sodium reabsorption – as sodium is reabsorbed, potassium is lost

Acid base balance – alkalotic states lower serum potassium levels by shifting potassium into the cell. Acidotic states raise the potassium by reversing the shift

Minor changes in serum concentration have significant consequences since the serum concentration is so small

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23
Q

What is the treatment for hyperkalemia?

A

Sodium bicarbonate administration and dieuretics.

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24
Q

How are potassium levels maintained in the body?

A

Potassium is excreted by the kidneys without any reabsorption, so potassium must be adequately supplied by the diet as levels can drop rapidly.

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25
Q

What are the symptoms of Hyperkalemia

A

Irritability
Nausea and vomiting
Intestinal colic
Diarrhea

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26
Q

Symptoms of hypokalemia?

A

Decreased contractility of smooth, skeletal, and cardiac muscles
Weakness
Paralysis
Hyporeflexia
Ileus
Dysrhythmias

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27
Q

When should potassium levels be closely monitored?

A

Follow potassium levels closely in uremia, Addison disease, vomiting and diarrhea, and in patients taking steroids, potassium depleting diuretics, and digoxin (hypokalemia can induce arrhythmias)

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28
Q

Can hypokalemia or hyperkalemia cause EKG changes?

A

YES

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29
Q

Serum potassium level interfering factors

A

Opening and closing hand with tourniquet in place may increase levels

Hemolysis of blood during the draw or in the lab causes increased levels – WHY?

Drugs may increase levels – antibiotics, some antihypertensives, lithium, potassium sparing diuretics, potassium supplements, and succinylcholine

Drugs may decrease levels – antibiotics, diuretics, insulin, laxatives, Kayexalate (sodium polystyrene sulfonate)

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30
Q

Causes of Hyperkalemia

A

**Excessive dietary intake or **Excessive IV intake

Acute or chronic renal failure – most common cause of hyperkalemia – due to decreased excretion

Addison disease, hypoaldosteronism, aldosterone inhibiting diuretics (spironolactone, triamterene) – Aldosterone enhances potassium excretion but is absent in these states

Crush injury to tissues, hemolysis, transfusion of hemolyzed blood, infection – cellular injury and lysis causes potassium within the cells to be released

Acidosis – hydrogen ions are driven from the blood and into the cells to maintain physiologic pH. To maintain electrical neutrality, potassium is released from the cell

Dehydration

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31
Q
A
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32
Q

Causes of Hypokalemia?

A

Deficient dietary intake, deficient IV intake – kidneys cannot reabsorb potassium to compensate for reduced potassium intake

Burns, GI disorders (vomiting, diarrhea) – potassium is lost due to ongoing fluid and electrolyte losses

Diuretics – increase renal excretion of potassium

Hyperaldosteronism – aldosterone enhances potassium excretion

Cushing syndrome – glucocorticosteroids have an aldosterone-like effect

Renal tubular acidosis – increased excretion

Licorice ingestion – licorice has an aldosterone-like effect

Alkalosis – to maintain physiologic pH during alkalosis, hydrogen ions are driven out of the cell and into the blood. Potassium is driven into the cell

Insulin administration – glucose and potassium are driven into the cell***

Glucose administration – causes insulin to be secreted***

Ascites – decreased renal blood flow from reduced intravascular volume from the collection of fluid. Reduced blood flow stimulates secretion of aldosterone which increases potassium excretion

Renal artery stenosis – reduced renal blood flow

Cystic fibrosis – increased potassium loss in secretions and sweat

Trauma/burns/surgery – body’s response mediated by aldosterone which increases potassium excretion

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33
Q

What is the function of Cholride in the body?

A

Major extracellular anion, it maintains electrical neutrality, mainly as a salt with sodium.

Water moves with sodium and chloride, so chloride also affects water balance.

Chloride acts as a buffer to assist in acid base balance. As carbon dioxide and hydrogen increase, bicarbonate must move from the intracellular space to the extracellular space. To maintain neutrality, chloride shifts back into the cell

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34
Q

What do chloride values indicate? What are the normal and critical values?

A

With other electrolytes, chloride gives an indication of acid base status and hydration status

Normal: 98-106 mEq/L
Critical values: < 80 or > 115

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35
Q

Signs of hyperchloremia?

A

lethargy

weakness

deep breathing.

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36
Q

Signs of hypochloremia?

A

Hyperexcitability of the nervous system and muscles

shallow breathing

hypotension

tetany

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37
Q

Serum Chloride interfering factors?

A

Excessive infusions of saline can increase chloride levels
Drugs may increase or decrease levels

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38
Q

Causes of Hyperchloremia?

A

Dehydration

Excessive infusion of normal saline

Metabolic acidosis, renal tubular acidosis, Cushing syndrome, kidney dysfunction, hyperparathyroidism, eclampsia –urinary excretion of chloride is decreased

Respiratory alkalosis – chloride is driven out of cells in place of bicarbonate

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39
Q

Causes of Hypochloremia?

A

Overhydration, Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH) – chloride is diluted

Congestive heart failure – chloride is diluted by excess total body water

Vomiting or prolonged gastric suction, chronic diarrhea or high output GI fistula – chloride cation is high in the stomach and GI tract due to HCl acid produced

Chronic respiratory acidosis, metabolic alkalosis – chloride is driven into the cell to compensate for the bicarbonate that leaves the cell – this maintains pH neutrality

Salt losing nephritis, Addison disease, diuretic therapy, hypokalemia, aldosteronism – chloride excretion increased

Burns – sodium and chloride losses

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40
Q

What is CO2 Bicarbonate measure used for? What are the normal and critical ranges?

A

It is used to assist in evaluating the pH status of the patient and to assist in electrolyte evaluation

Normal = 23-30 mEq/L
Critical values < 6

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41
Q

What does the CO2 + Bicarbonate measure?

A

Measures the H2CO3 (carbonic acid), dissolved CO2, and the bicarbonate ion (HCO3-) that exists in the serum. The amounts of the first two are small, so CO2 content is an indirect measure of the HCO3- anion, which is second in importance to the chloride ion in electrical neutrality of extracellular and intracellular fluid

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42
Q

In what organ are CO2 and Bicarbonate levels regulated?

A

Levels are regulated by the kidney. Levels are increased with alkalosis and decreased with acidosis

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43
Q

What is the role of CO2 and Bicarbonate in the body?

A

Plays a major role in acid base balance

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44
Q

What are the CO2 and Bicarbonate interfering factors?

A

Underfilling the tube allows carbon dioxide to escape and may reduce values

Drugs may increase levels – aldosterone, barbiturates, bicarbonates, loop diuretics, steroids

Drugs may decrease levels – some antibiotics, thiazide diuretics

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45
Q

What causes increased levels of CO2 and Bicarbonate?

A

Severe vomiting, high volume gastric secretion, aldosteronism, use of mercurial diuretics – hydrogen ions are lost

Chronic obstructive pulmonary disease – ions are increased to compensate for chronic hypoventilation – compensation for respiratory alkalosis

Metabolic alkalosis – defined by an increased number of anions in the blood

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46
Q

What causes decreased levels of CO2 and Bicarbonate?

A

Chronic diarrhea, chronic use of loop diuretics – persistent loss of base ions

Renal failure, diabetic ketoacidosis, starvation – ketoacids and other anions build up, neutralizing the acids and causing levels to drop

Metabolic acidosis – defined by a decreased amount of anions in the blood

Shock – lactic acid builds up and is buffered, causing levels to drop

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47
Q

What is Anion gap used for?

A

Assists in the evaluation of patients with acid base disorders. It is used to attempt to identify the potential cause of the disorder and can be used to monitor therapy for acid base abnormalities

Helpful in identifying the cause of metabolic acidosis

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48
Q

What is the anion gap? What are the normal ranges? What is the formula?

A

Anion gap is the difference between the cations and anions in the extracellular space.

Normal = 12 +/- 4 mEq/L

AG = Sodium – (Chloride + Bicarbonate)

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49
Q

What creates the anion gap?

A

Gap is created by small amounts of anions in the blood (lactate, phosphates, sulfates, organic anions, and proteins) that are not measured

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50
Q
A
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51
Q

How does bicarbonate affect the anion gap (AG)?

A

As acids accumulate in the bloodstream (lactic acid or ketoacids), bicarbonate neutralizes them to maintain normal pH in the blood.

When bicarbonate decreases, AG increases

52
Q

How does albumin affect the anion gap?

A

As albumin (negatively charged) increases, the AG will increase. If albumin is normal, a high AG is usually due to an increase in non-chloride-containing acids or organic acids.

53
Q

Most metabolic acidotic states have increased or decreased AG?

A

increased

54
Q

What causes a decreased AG?

A

A decreased AG is rare and is due to an increase in unmeasured cations (calcium or magnesium).

A reduction in anionic proteins (nephrotic syndrome) will also decrease AG. If proteins are lost, the bicarbonate increases to maintain electrical neutrality

Increases in cationic proteins (some immunoglobulins) will also decrease AG.

Hyperaldosteronism – lose large amounts of potassium and hydrogen ions causing a metabolic alkalosis with a decreased AG

Hypoproteinemia – loss of anionic proteins directly causes decrease in AG

Lithium toxicity – increase in inorganic cations decreases the measured cations to decrease the AG

Excess alkali ingestion (antacids) – increases bicarbonate to decrease the AG

Multiple myeloma – proteins produced by neoplastic cells are cationic, causing a compensatory decrease in measured cations and increase in measured anions to maintain electrical neutrality

Chronic vomiting or gastric suction – loss of hydrochloric acid causes a decrease in chloride and an increase in bicarbonate to decrease the AG

55
Q

What causes an increased AG?

A

An increased AG, despite a normal pH, will indicate an acidotic component to the metabolic picture

Lactic acidosis, diabetic ketoacidosis, alcoholic ketoacidosis, alcohol intoxication, starvation – increased acid ions such as lactate, hydroxybutyrate, or acetoacetate are formed

Renal failure – uremic organic acids (phosphate, sulfates) accumulate in the blood due to poor excretion. Hydrogen combines with the bicarbonate to maintain a normal pH, so bicarbonate levels decrease and AG rises.

Increased GI losses of bicarbonate (diarrhea or fistula) – bicarbonate and other base losses can occur, increasing the AG

Hypoaldosteronism – aldosterone stimulates acid secretion in the distal renal tubule in exchange for sodium. Acid can build up and combine with bicarbonate, which decreases to increase the AG

56
Q

AG interfering factors?

A

Hyperlipidemia – may cause under measurement of sodium to falsely decrease AG

Drugs may increase AG – diuretics, ethanol, methanol, salicylate, some antibiotics

Drugs may decrease AG – lithium, spironolactone

57
Q

What is BUN and what does it measure?

A

Blood Urea Nitrogen

Rough measurement of renal function and glomerular filtration rate. Also a measurement of liver function.

Measures the amount of urea nitrogen in the blood

58
Q

What are the normal and critical ranges for BUN?

A

Normal range : 10-20 mg/dL
Critical value > 100 mg/dL indicates serious impairment of renal function

An elevated BUN alone does not indicate that renal function is inadequate.

59
Q

Explain how Urea is formed.

A

Urea is formed in the liver as the end product of protein metabolism and digestion.
Protein is broken down into amino acids which are catabolized in the liver to form free ammonia.
Ammonia molecules are combined to form urea, which enters the blood and is transported to the kidneys for excretion

60
Q

What is azotemia?

A

Patients with elevated BUN are said to have azotemia.

61
Q

What affect does renal disease have on BUN?

A

Renal diseases cause an inadequate excretion of urea, which causes blood concentration to rise.
If only one kidney is diseased, the unaffected kidney can compensate for the diseased kidney, and the BUN may stay normal

An elevated BUN alone does not indicate that renal function is inadequate.

62
Q

What is Prerenal Azotemia?

A

Elevation of BUN due to pathologic conditions that affect urea nitrogen accumulation before it gets to the kidney

Shock, dehydration, CHF, excessive protein catabolism
GI bleeding causes blood in the intestinal tract – the proteins in the blood and blood cells are digested to urea and get absorbed, causing BUN to increase

63
Q

What is Postrenal Azotemia?

A

Elevation of BUN due to pathologic conditions that affect BUN after it gets to the kidney

What would cause this??????
Ureteral and urethral obstruction

64
Q

How will liver disease affect the BUN?

A

Synthesis of urea also depends on the liver, so severe liver disease will have decreased BUN

65
Q

What is hepatorenal syndrome?

A

Combined liver and renal disease.

May have a normal BUN because of poor hepatic function resulting in decreased urea formation. A normal BUN is not an indicator that renal function is adequate

66
Q

What is interpreted with BUN for a good measurement of kidney and liver function?

A

BUN is interpreted with the creatinine. These are referred to as renal functions.

The BUN/creatinine ratio is a good measurement of kidney and liver function.

Normal range is 6-25 with 15.5 being optimal

67
Q

Name the interfering factors for BUN.

A

Changes in protein intake – low protein diets will decrease BUN if caloric intake is maintained with carbohydrates. High protein diets will elevate BUN.

Muscle mass has an effect on BUN levels

Advanced pregnancy may increase BUN due to high protein metabolism

GI bleeding can increase BUN

Overhydration dilutes BUN and causes lower levels.

** Dehydration** concentrates BUN and raises levels.

Many drugs can increase BUN

68
Q

List the Prerenal causes for increased BUN

A

Hypovolemia, shock, burns, dehydration – reduced blood volume decreases renal blood flow, so excretion of BUN is decreased and levels rise

CHF, MI – decreased cardiac function decreases renal blood flow

**GI bleeding, excessive protein ingestion ** – gut is overloaded with protein so urea is formed at a higher rate and BUN accumulates

Excessive protein catabolism, starvation – increased rate of protein breakdown leads to increased urea formation

Sepsis – renal blood flow and renal function are reduced, so BUN rises

69
Q

What are the Renal causes for an increased BUN?

A

Renal disease (glomerulonephritis, pyelonephritis, acute tubular necrosis), renal failure, nephrotoxic drugs – primary renal diseases all have reduced excretion of BUN

70
Q

What are the Postrenal causes of an increased BUN?

A

Ureteral obstruction from stones, tumor, congenital abnormalities, bladder outlet obstruction from prostatic hypertrophy or cancer or bladder/urethral congenital abnormalities – obstruction of urinary flow reduces excretion and BUN rises

71
Q

What are the causes of decreased levels of BUN?

A

Liver failure – BUN is made in the liver, so reduced liver function causes reduced BUN levels.

Overhydration due to fluid overload from SIADH – BUN is diluted by fluid overload

Negative nitrogen balance (malnutrition, malabsorption) – protein depletion causes reduced urea production to reduce BUN

Pregnancy – early pregnancy has increased water retention and BUN dilution

Nephrotic syndrome – protein loss in urine. With protein depletion, BUN is reduced.

72
Q

Creatine is used to diagnose? What are the normal and critical ranges?

A

Used to diagnose impaired renal function

Normal ranges:
Females: 0.5-1.1 mg/dL
Males: 0.6-1.2 mg/dL

Critical values > 4 mg/dL indicates serious impairment in renal function

73
Q

Creatine is excreted by?

A

the kidneys

74
Q

Creatine levels are directly proportional to?

A

Renal excretory function. It is an approximation of glomerular filtration rate

With normal renal function the creatinine level should remain normal and constant

75
Q

Where is creatine used in the body?

A

Creatinine is a catabolic product of creatine phosphate, which is used in skeletal muscle contraction.

Daily production depends on muscle mass

76
Q

What do eleveations in creatine suggest?

A

Tends to rise later than the BUN, so elevations in creatinine suggest the disease process is chronic.

Doubling of the creatinine indicates a 50% reduction in GFR.

In unstable critically ill patients, acute changes in renal function may not initially be reflected by serum creatinine.

77
Q

Is creatine affected by hepatic function?

A

Minimally affected by hepatic function

78
Q

Interfering factors of Creatine?

A
  • *Diet high in meats** may cause transient elevation in creatinine
  • *Drugs** may increase creatinine – ACE inhibitors, nephrotoxic drugs
79
Q

Causes of increased Creatine levels?

A

Diseases affecting renal function (glomerulonephritis, pyelonephritis, acute tubular necrosis, urinary tract obstruction, reduced renal blood flow due to shock, dehydration, CHF, atherosclerosis, diabetic neuropathy, nephritis) – renal function is impaired and creatinine rises

Rhabdomyolysis – skeletal muscle injury causes myoglobin to be released into the bloodstream. Large amounts are nephrotoxic and creatinine levels rise.

Acromegaly, gigantism – increased muscle mass causes “normal” creatinine level to be high

Dehydration

80
Q

Causes of decreased Creatine?

A

Debilitation, decreased muscle mass (muscular dystrophy, myasthenia gravis) – decreased muscle mass causes “normal” creatinine to be low

81
Q

What is the Creatinine Clearance (CrCl) used for?

A

A measure of the GFR (the number of milliliters of filtrate made by the kidneys per minute).

82
Q

What does the amount of filtrate made in the kidneys depen on?

A

the amount of blood to be filtered and on the ability of the glomeruli to act as a filter

83
Q

Can a bilateral obrstruction to urinary flow affect CrCl?

A

Bilateral obstruction to urinary outflow affects CrCl only after the obstruction is longstanding

84
Q

What are the normal values for CrCl?

A

Adult < 40 years

Male: 107-139 mL/min

Female: 87-107 ml/min

Values decrease 6.5 mL/min/ per decade of life after age 20.

85
Q

Urine collections are timed in CrCl measurements, how will incomplete collections affect the CrCl?

A

incomplete collections will falsely decrease CrCl

86
Q

When measuring CrCl what is the time period for urine collection and what is formula for calculating it?

A

Test requires a 24-hour urine collection and a serum creatinine level.

CrCl = [(Cr excreted in urine over 24 hrs in mg/dl) X (vol of urine in mL/min)] / (serum creatinine in mg/dL)

87
Q

What is the estimated GFR?

A

Difficult to collect 24 hour urine collections, so a new measure is the estimated GFR, which uses the serum creatinine, age, and numbers that vary depending on gender and ethnicity to calculate the GFR.

88
Q

Average values of the estimated GFR?

A
89
Q

CrCl interfering factors?

A

Exercise may increase creatinine

Incomplete urine collection may lower value

Pregnancy increases CrCl – increased load on kidneys by the fetus

Diet high in meat may transiently elevate creatinine and CrCl. When creatinine is high, its clearance is increased and GFR is overestimated

Estimated GFR may be inaccurate in extremes of age and in patients with malnutrition or obesity, paraplegia or quadriplegia, and in pregnancy

Drugs may increase levels – same as creatinine

Drugs that may cause a decrease in estimated GFR interfere with creatinine secretion (cimetidine or trimethoprim) or creatinine assay (cephalosporins) – may need a 24 hour creatinine clearance.

90
Q

Causes of Increased levels of CrCl?

A

Exercise, pregnancy, high cardiac output syndromes – blood flow increases to the kidney causing GFR and CrCl to increase

91
Q

Causes of decreased level of CrCl?

A

Impaired kidney function (renal artery atherosclerosis, glomerulonephritis, acute tubular necrosis), decreased GFR (CHF, cirrhosis with ascites, shock, dehydration) – decreased renal blood flow will decrease GFR

Decreased muscle mass

92
Q

What is the Cockcroft Gault equation?

A

Cockcroft and Gault equation:
CrCl = (140 - age) x BM(kg) / (Plasma creatine x 72) (x 0.85 for females)

Estimated Creatining Clearance

93
Q

What is the glucose measurement commonly used for? What are the normal and critical ranges?

A

Most commonly used in the evaluation of diabetic patients

Normal range: Fasting adult – 70-110 mg/dL
Critical values: < 40 and > 400 mg/dL

94
Q

What are glucose levels controlled by?

A

Levels controlled by insulin and glucagon

Levels must be evaluated according to the time of day they are obtained.

95
Q

What is the function of glucagon?

A

In the fasting state, glucose levels are low, so glucagon is secreted.

Glucagon breaks down glycogen to glucose in the liver so glucose levels rise

If fasting persists, protein and fatty acids are broken down due to glucagon stimulation so glucose levels continue to rise.

96
Q

Where is glucagon made?

A

made in the alpha cells of the pancreatic islets of Langerhans.

97
Q

Where is insulin made?

A

made in the beta cells of the pancreatic islets of Langerhans

98
Q

What is the function of insulin?

A

Glucose levels rise after eating.

Insulin is secreted and attaches to insulin receptors in muscle, liver, and fatty cells.

This drives glucose into these cells to be metabolized to glycogen, amino acids, and fatty acids and causes glucose levels to decrease.

99
Q

What is the most common cause of hypoglycemia?

A

Inadvertent insulin overdose

100
Q

In new diabetic patients what must be monitored regularly?

A

Glucose measurements must be performed frequently in new diabetic patients to monitor insulin dosage – finger stick measurements are often performed before meals and at bedtime.

101
Q

List the interfering factors of Glucose measurements?

A

Stressors (trauma, general anesthesia, infection, burns, MI) can increase glucose levels

Caffeine may cause increased levels

Pregnancy may cause glucose intolerance – gestational diabetes

IV fluids containing dextrose, which gets converted to glucose to raise levels

Drugs may increase (TCAs, corticosteroids, diuretics, epinephrine, glucagon, lithium, salicylates) or decrease (alcohol, anabolic steroids, insulin, propranolol, oral hypoglycemics) levels

102
Q

Causes of Hyperglycemia?

A
  • *Diabetes mellitus** – glucose intolerance and hyperglycemia
  • *Acute stress response** – infections, burns, and surgery stimulate catecholamine release to stimulate glucagon secretion to cause hyperglycemia

Cushing syndrome – cortisol levels are high, leading to hyperglycemia

Pheochromocytoma – catecholamine stimulates glucagon secretion

Chronic renal failure – glucagon is metabolized by the kidney, so impaired renal function causes glucagon and glucose levels to rise.

Glucagonoma – glucagon autonomously secreted to cause hyperglycemia

Acute pancreatitis – glucagon spilled into the bloodstream as the cells of the pancreas are injured – glucagon causes hyperglycemia

Diuretic therapy

Corticosteroid therapy – cortisol causes hyperglycemia

Acromegaly – growth hormone stimulates glucagon

103
Q

Causes of Hypoglycemia?

A

Insulinoma – insulin autonomously produced

Hypothyroidism – thyroid hormones affect glucose metabolism – decreased levels cause glucose levels to fall

Hypopituitarism – ACTH and growth hormone, both secreted from the pituitary gland, affect glucose metabolism. Decreased hormone levels cause glucose levels to fall

Addison disease – diminished cortisol levels cause glucose levels to fall

Extensive liver disease – decreased liver function causes glucose levels to decrease

Insulin overdose – most common cause of hypoglycemia

Starvation – decreased carbohydrate ingestion causes glucose levels to fall.

104
Q

What are calcium levels used to evaluate?

A

Evaluates parathyroid function and calcium metabolism.

Used to monitor patients with renal failure or transplant, hyperparathyroidism, and various malignancies as well as calcium levels during and after large volume blood transfusions.

105
Q

What are the normal and critical values of calcium?

A

Normal:
Total calcium 9.0-10.5 mg/dL
Ionized calcium 4.5-5.6 mg/dL or 1.05-1.30 mmol/L

Critical values:
Total calcium < 6 or > 13 mg/dL
Ionized calcium < 2.3 or > 7 mg/dL or < 0.78 or
> 1.58 mmol/L

106
Q

In what forms does Calcium exist in the blood?

A

About half of the total calcium exists in blood in its free ionized form and half exists in protein bound form (mostly to albumin)

107
Q

What form of Calcium is measured in the blood

A

Serum calcium level is a measure of both free ionized and protein bound calcium. So if albumin is low the calcium level will also be low.

Total serum calcium decreases by 0.8 mg for every 1 gm decrease in albumin
The ionized form is not affected by changes in albumin levels

A normal calcium with reduced albumin (calcium should be reduced)– patient may have hypercalcemia

108
Q

When calcium levels drop what hormone is released to stimulate production and uptake? Where does the uptake occur?

A

Parathyroid Hormone (PTH) is released from the parathyroid gland when calcium levels drop.

This hormone stimulates realease of calcium from the bones.

It also stimulates Ca2+ uptake in the kidneys and along with Vitamind D stimulates uptake in the intestines

109
Q

What is the most common cause of hypercalcemia?

A

hyperparathyroidism – causes increased GI absorption, decreased urinary excretion, and increased bone resorption.

110
Q

What are the symptoms of elevated hypercalcemia?

A

Elevated levels cause anorexia, nausea, vomiting, somnolence, and coma.

111
Q

How can malginancies affect calcium levels?

A

Malignancy can elevate calcium due to metastasis (myeloma, lung, breast, renal cell) to the bone which then destroys the bone and pushes calcium into the blood.

Some cancers (lung, breast, renal cell) can also produce a parathyroid hormone like substance that increases calcium.

112
Q

What is secondary hyperparathyroidism?

A

Renal failure patients have high phosphate levels and other anions that chronically lower serum calcium, so parathyroid hormone is persistently stimulated to increase calcium levels. Calcium levels return to normal in time, but that level actually represents a “high” level as it should be low in these patients

113
Q

Interfering factors for Calcium?

A

Vitamin D intoxication can increase calcium

Excessive milk ingestion can increase calcium

Serum pH – a decrease in pH causes increased calcium levels

Prolonged tourniquet time lowers pH and factitiously increases calcium levels

Hypoalbuminemia associated with decreased levels of total calcium

Drugs may increase levels (alkaline antacids, calcium salts, lithium, thiazide diuretics, and vitamin D) or decrease levels (albuterol, anticonvulsants, aspirin, corticosteroids, estrogens, heparin, laxatives, loop diuretics, magnesium salts, and oral contraceptives.

114
Q

What causes Hypercalcemia?

A

Hyperparathyroidism, nonparathyroid PTH producing tumor (lung or renal) – PTH mobilizes calcium stores from bone to blood

Metastatic tumor to bone, Paget disease of bone, prolonged immobilization – bone destruction or thinning pushes calcium from bone into blood

Milk-alkali syndrome – increased ingestion of milk products or antacids (which contain calcium) causes elevation

Vitamin D intoxication – vitamin D works with PTH to increase levels

Lymphoma, granulomatous infections (sarcoidosis and tuberculosis) – have enhanced vitamin D levels

Addison disease – glucocorticosteroids inhibit vitamin D activity – when steroid activity is decreased, vitamin D action is increased

  • *Acromegaly**
  • *Hyperthyroidism**
115
Q

What are some causes of Hypocalcemia?

A

Hypoparathyroidism –Reduced PTH causes decreased calcium

Renal failure, hyperphosphatemia due to renal failure – excess anions present in renal failure patients bind calcium

Rickets, vitamin D deficiency
Osteomalacia, hypoalbuminemia, malabsorption
– less calcium available to the blood

Pancreatitis, fat embolism – saponification (binding of calcium to fats) of the peripancreatic tissue

Alkalosis – high pH in blood drives calcium intracellularly.

116
Q

What are the normal and critical values of magnesium?

A

Normal: 1.3-2.1 mEq/L
Critical values < 0.5 or > 3 mEq/L

117
Q

Where is magnesium found in the body?

A

Most is found intracellularly with half in bone.

Most is bound to ATP molecule and is important in phosphorylation of ATP , so it is critical in the metabolic process

118
Q

What is the function of Magnesium?

A

Carbohydrate, protein, and nucleic acid synthesis and metabolism depends on magnesium.

Also is a cofactor that modifies enzyme activity

Most organ functions depend on magnesium
Low magnesium levels may increase cardiac irritability and aggravate arrhythmias

High magnesium levels retard neuromuscular conduction to slow cardiac conduction, diminish deep tendon reflexes, and cause respiratory depression.

119
Q

In what way is magensium important in calcium metabolism?

A

hypocalcemia may respond to magnesium replacement

120
Q

What are the common causes of hypomagnesemia?

A

Magnesium deficiency occurs in malnourished patients due to malabsorption or maldigestion or lack of food intake.

Important in postop patients who don’t eat for several days and whose metabolism is accelerated.

Alcohol abuse increases magnesium loss in the urine

Low magnesium occurs in diabetes mellitus, hypoparathyroidism, hyperthyroidism, hyperaldosteronism, and toxemia of pregnancy.

Chronic renal tubular disease – magnesium is reabsorbed in renal tubule. Diseases affecting this area of the kidney or drugs toxic to this area of the kidney allow increased losses of magnesium in the urine

Diabetic acidosis – magnesium levels fall with treatment of diabetic ketoacidosis. Insulin drives glucose into the cells and magnesium follows.

121
Q

What are the symptoms of hypomagnesemia

A

Symptoms of decreased magnesium are mostly neuromuscular (weakness, irritability, tetany, EKG changes, delirium, and convulsions

122
Q

What are the most common causes of Hypermagnesemia?

A

Increased magnesium levels usually are associated with ingestion of magnesium containing antacids

Most magnesium is excreted by the kidneys, so chronic renal diseases may elevate magnesium.

Hemolysis of a blood sample will create a falsely elevated magnesium since it is an intracellular cation.

Hyperparathyroidism – calcium levels are high so magnesium levels increase

Hypothyroidism

Addison disease – aldosterone enhances magnesium excretion. With reduced aldosterone, magnesium excretion is reduced

123
Q

Symptoms of hypermagnesemia?

A

Symptoms of elevated magnesium are lethargy, nausea and vomiting, and slurred speech.

124
Q

Interfering factors of Magnesium?

A

Hemolysis causes falsely elevated results
Drugs may increase levels (antacids, calcium containing meds, laxatives, lithium, loop diuretics, thyroid meds) or decrease levels (some antibiotics, diuretics, and insulin)

125
Q
A