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Diagnostic Medicine Exam 3 > Comprehensive Metabolic Panel > Flashcards

Comprehensive Metabolic Panel Flashcards

1
Q

Basic Metabolic Panel vs. CMP

A

Basic- everything except the liver enzymes (AST/ALT)

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2
Q

Total protein

A

Prealbumin (low= malnourished)

Albumin (60%)

Globulins:

–>Example are the immunoglobulins IgA, IgE, IgG, IgM

–> How you measure for these immunoglobulins: Serum Protein Electrophoresis (SPEP)

Proteins are how we transport things! Helps determine where the fluid in the body is located

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3
Q

When can the total protein be abnormal?

A
  1. Some cancers
  2. Protein-losing enteropathies
  3. Impaired nutrition
  4. Liver disease
  5. Edema
  6. Burns
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4
Q

Protein functions in the blood

A
  1. Makes up tissues, enzymes transport, hormones etc.
  2. Transport substances in the serum
  3. Creates osmotic pressure in the intravascular space :

–>Pulls fluids into or prevents fluid from leaving ex: if someone is edematous, usually protein levels are low, which allows the fluid to leave

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5
Q

What percent of total protein does Albumin make up?

A

60% of total protein

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6
Q

Functions of albumin

A
  • Osmotic pressure
  • Transport drugs, hormones, enzymes
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7
Q

What is Albumin an indicator of?

A
  • nutritional status (prealbumin more specific)
  • indicator of liver function b/c it is synthesized in the liver
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8
Q

What does decreased Albumin indicate?

A
  1. Malnutrition
  2. “Protein losing enteropathies” (ex: Crohn’s disease, Celiac disease)
  3. Nephrotic syndrome (Proteinuria, edema, hyperlipidemia)
  4. Liver disease
  5. Inflammatory disease
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9
Q

What can an increased albumin indicate?

A
  • Dehydration

** -some cancers

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10
Q

Total Body Water (TBW)

A

Specific places where water is harbored

  • women have less fluid in total body mass than men
  • We are 55-65% made up of water

ECF–> 75-80% interstitial and 15-20% plasma

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11
Q

Osmolality

A

Definition: the solute or particle concentration of a fluid

  • the concentration of a solution expressed as the total number of solute particles per kilogram.
  • main idea: osmolality drives what is inside the cell and what is outside of the cell

–>tells you if the patient is more diluted or concentrated

-Water will move between compartments until their osmolality is the same

Main solutes: sodium, glucose, and urea

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12
Q

What is the normal osmolality range?

A

Normal osmolality range is: 280 - 295 mOsm/kg

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13
Q

How do you calculate Osmolality?

A
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14
Q

What happens to the osmolality if glucose is elevated?

A

Osmolality would increase

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15
Q

What would happen to the osmolality value if sodium decreases?

A

Osmolality would decrease

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16
Q

How do you calculate Osmolality gap?

A
  • Osmolal gap = OSM (measured) – OSM (calculated)
  • If > 10mOsm/L consider exogenous substance
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17
Q

What are some other “Osmotically active” substances?

A
  • Mannitol and various proteins
  • Ethanol, methanol, ethylene glycol (antifreeze)
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18
Q

Normal values for an electrolyte panel

A

—Sodium (Na)- 135 - 145 mEq/L

—Potassium (K) - 3.5 - 5.0 mEq/L

—Chloride (Cl) - 98 - 106 mEq/L

Carbon dioxide (CO2) (“Bicarbonate”)- 22 - 32 mEq/L

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19
Q

Abnormal sodium levels on an electrolyte panel

A

In general, consider:

◦Abnormal Extracellular Fluid Volume (ECFV) is due to sodium control mechanisms

◦Abnormal Extracellular Fluid (ECF) sodium concentration is due to problems with water control

*both abnormalities can co-exist

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20
Q

Abnormal sodium levels on an electrolyte panel- ->Abnormal Extracellular fluid volume

A

This is due to sodium control mechanisms

◦too little sodium = Fluid Volume Deficit (FVD)

◦too much sodium = Fluid Volume Excess (FVE)

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21
Q

Abnormal sodium levels on an electrolyte panel–> abnormal extracellular fluid (ECF) sodium concentration

A

This is due to problems with water control

◦too much water = Hyponatremia

◦too little water = Hypernatremia

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22
Q

Osmolality’s role in interpreting sodium levels

A

Must R/O Pseudohyponatremia

◦serum Na <135, but normal osmolality

◦due to hypertriglyceridemia or hyperproteinemia (multiple myeloma)

◦

Must R/O Hyponatremia due to hyperosmolar state

•Increased glucose in ECF causes shift of water from ICF to ECF–> lowering serum Na

(glucose also attracts water, thus lowering water)

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23
Q

What is pseudohyponatremia due to?

A

◦due to hypertriglyceridemia or hyperproteinemia (multiple myeloma)

This is when serum Na <135 but normal osmolality

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24
Q

Hyponatremia with HYPERvolemia- What are fluid overload conditions

A

◦Congestive heart failure (get backflow of fluid- drives sodium down because of dilution in extravascular space)

◦Renal failure (Kidney isnt able to let fluid and waste go like it should)

◦Nephrotic syndrome (disfunction of the kidney, have increased protein, which takes water with it resulting in dilution and hyponatremia)

◦Hepatic cirrhosis (low protein/low albumin in serum–>drives fluid out of the vessels)

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25
Q

Hyponatremia with HYPERvolemia- What are clinical findings of fluid overload conditions?

A

◦Pedal edema (seen in CHF), pulmonary crackles, JVD

◦Anemia, may be dilutional

◦Other signs of heart, liver, or renal disease

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26
Q

What causes Hyponatremia with HYPOvolemia?

A

◦Renal causes–> Diuretics- thiazides

◦Non-renal–> GI: vomiting and diarrhea

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27
Q

Hyponatremia with HYPOvolemia–> What are clinical characteristics of dehydration?

A

◦Reduced skin turgor; dry mucus membranes

◦Orthostatic BP and pulse changes (neck veins are flat)

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28
Q

Hyponatremia with Euvolemia

A

No evidence of fluid overload, volume depletion or dehydration

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29
Q

What is the differential diagnosis of someone that has hyponatremia with euvolemia?

A

◦Hypothyroidism

◦SIADH (syndrome of inappropriate ADH secretion)

–>The most common cause of euvolemic hyponatremia. Due to impaired renal free water excretion

–>Can see in lung cancer pts

◦Diuretic use (without volume depletion)

◦Adrenal Insufficiency

◦Primary (diabetes insipidus) or psychogenic polydipsia

◦Tea and toast diet (low solute or excessive beer drinking)

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30
Q

Overview of Hyponatremia–> differential diagnosis for hyponatremia

A
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31
Q

Serum potassium

A

Normal= 3.5-5.0

  • Potassium is the major intracellular cation
  • Renal excretion is the major route of elimination:
  • GFR < 20% = hyperkalemia
  • Aldosterone increase NA/K exchange–>Increased NA reabsorption/K secretion
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32
Q

What are potential sources of excess potassium?

A
  • Dietary intake
  • Breakdown of tissue (rhabdomyolysis, hemolysis)
  • Potassium supplements (Rx vs. OTC)
  • Potassium-sparing medications
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33
Q

What are the serum K levels in hypokalemia?

A

Serum K+ < 3.5 mEq/L

Potassium <3.0 is potentially dangerous

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34
Q

What are clinical manifestations of hypokalemia

A

◦Neuro: weakness, fatigue, paralysis (if severe enough)

◦GI: constipation, ileus

◦ECG changes (U waves, flattened T waves, ST segment changes)

◦Cardiac arrhythmias (A-fib most common)

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35
Q

When should a low K+ concentration be corrected?

A

Hypokalemia in the presence of alkalosis (more basic than acidic), a low K+ concentration needs to be corrected

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36
Q

Hypokalemia- How to correct serum potassium if pH > 7.45

A

If the pH > 7.45 there will be a–>

◦0.3mEq/L K decrease for each 0.1 increase in pH

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37
Q

Serum potassium levels in Hyperkalemia

A

Serum potassium > 5.0

K+ > 6.5 may cause serious problems

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38
Q

Clinical manifestations of hyperkalemia

A

◦Weakness, ascending paralysis

◦Respiratory failure

◦ECG changes: peaked T waves, flattened P waves, prolonged PR interval, widened QRS and ventricular fibrillation (would give calcium to help stabilize myocardium)

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39
Q

Hyperkalemia- elevated potassium correction in acidosis

A
  • Metabolic acidosis:
  • 0.7 mEq/L increase in K for every 0.1 decrease in pH
  • Respiratory acidosis:
  • 0.3 mEq/L increase in K for every 0.1 decrease in pH

**dont need to know exact numbers–> just know that if patient is acidodic, their serum potassium will be falsely high

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40
Q

What does the lab measure when it measures “calcium”

A
  • Lab value is a measure of BOTH free & protein bound Ca++
  • About 40% of Ca++ in the ECF is bound to albumin; about 50% is free (aka ionized Ca++)–> *dont memorize numbers
  • Used as a measure of parathyroid function
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41
Q

When to monitor calcium levels

A

-Monitor in patients with: renal failure, hyperparathyroidism & malignancies (~ 10-20% of pt w malignancy have elevated Ca++)

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42
Q

Calcium physiology

A

Enters body → through GI tract

Absorbed from → the intestine under the influence of Vitamin D

Stored in → bone

Excreted by → the kidney

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43
Q

Regulation of blood calcium level

A

Serum calcium regulated by: PTH, vit D

–>A decrease in serum Ca triggers: PTH secretion = ↑ in serum Ca

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44
Q

Regulation of Calcium- role of PTH

A

↑ vit. D activation (calcitriol)= ↑Calcium absorption from gut

  • Promotes Ca release from bone
  • Promotes conservation of Ca by kidneys

*PTH= parathyroid hormone

45
Q

Role of Free (ionized) Ca++

A
  • Helps regulate neuromuscular activity (eg. cardiac contractility)
  • Enzymatic reactions
  • Blood clotting
46
Q

What EKG abnormality may be observed in HYPERcalcemia?

A

Short QT

47
Q

What are the most common causes of hypercalcemia

A

Hypercalcermia= >10.5

Hyperparathyroidism (#1)

Malignancy (bone destruction or stimulation of osteoclast activity)

48
Q

What are the less common causes of hypercalcemia

A
  • Paget’s disease of the bone
  • Prolonged immobilization
  • Hyperthyroidism
  • Acromegaly
  • Addison’s disease
  • Excess Vit D or Ca++ intake
  • Granulomatous disease
  • Drugs (thiazide diuretics, others)

**All related to endocrine system

49
Q

Hyperparathyroidism as a cause of hypercalcemia

A

Etiology: usually parathyroid adenoma F>M; > 60 yo

Signs and symptoms=

-Typically asymptomatic

“Stones (kidney stones), bones, abdominal groans and psychiatric overtones (can make you crazy)”

50
Q

How to diagnose hyperparathyroidism?

A

Hypercalcemia

Hypophosphatemia

Elevated PTH

Parathyroid scan (nuclear medicine test); parathyroid bx & surgical removal

51
Q

What is the second leading cause of hypercalcemia?

A

**Malignancy

Solid tumors: Lung, Kidney, Breast

Hematologic malignancies: Multiple myeloma, Lymphoma, Leukemia

52
Q

Main causes of HYPOcalcemia

A

hypocalcemia= <9

  1. Decreased ability to mobilize bone stores
  2. Excess loss of Ca from kidneys
  3. Increased protein binding
53
Q

Cause of hypocalcemia- Decreased ability to mobilize bone stores

A

Hypoparathyroidism

Mg deficiency (causes inhibition of PTH)

54
Q

Cause of hypocalcemia- Excess loss of Ca from kidneys

A

Renal failure causes phosphate retention, & reciprocal loss of Ca

55
Q

Cause of hypocalcemia- increased protein binding

A

Less free Ca (eg: alkalosis )

56
Q
A
57
Q

What are less common causes of hypocalcemia

A

Hypoparathyroidism

Vit D deficiency

Renal failure

Hypomagnesemia

58
Q

Hypocalcemia and albumin

A

Hypoalbuminemia = most common cause of reported hypocalcemia (pseudohypocalcemia)

**If serum albumin is low, Ca measurement must be corrected:

Adjusted Ca = Serum Ca – Ser. Alb + 4.0

59
Q

Symptoms of hypocalcemia

A

Neuromuscular (↑excitability):

◦Paresthesias; muscle cramps

◦Hyperactive reflexes; carpopedal spasms–> Positive Chvostek and Trousseau signs

◦Tetany- sustained mm spasm

CV Effects:

◦Hypotension; EKG changes (prolonged QT interval); arrhythmias

60
Q

Hypocalcemia- testing for carpopedal spasms: Chvostek’s sign

A

Tapping facial nerve against the bone just anterior to the ear results in contraction of facial muscles

61
Q

Hypocalcemia- testing for carpopedal spasms: Trousseau’s sign

A

occluding brachial artery for 3 minutes with BP cuff induces carpal spasms

62
Q

Relationship b/w calcium and phosphorus

A

as calcium increases, phosphorus decreases

As calcium decreases, phosphorus increases

63
Q

Use of phosphate labs

A

Used to investigate parathyroid and calcium abnormalities

**Inverse relationship w Ca++

64
Q

What can decrease phosphate levels?

A
  • Dietary phosphate absorbed in small intestine
  • Decreased with antacids (opposite of Ca)
  • PTH decreases phosphate reabsorption by the kidneys–> Incr. urinary PO4 excretion; Incr. Ca absorption
65
Q

Conditions associated with increased phosphate

A
66
Q

Magnesium

A

Normal= 1.5-2.3

2nd most common intracellular cation (mainly in bone (50-60%) and body cells(40-50%) but a small amount in ECF(1%))

~1/3 is protein-bound (mainly to albumin)

67
Q

K, Mg and Ca relationship

A

K, Mg & Ca are closely related–> absorption and excretion are interdependent

Common to see hypocalcemia with hypomagnesemia

Neuromuscular and cardiac function depend on K, Mg and Ca

68
Q

What is the kidneys role in control of magnesium levels?

A

Eliminated primarily through the kidney

Increased serum Mg? –> Kidney excretes Mg (urine)

Increased serum Ca?–> Kidney excretes Mg (urine)

69
Q

How can Mg excretion be increased?

A

Mg excretion INCREASED by loop diuretics (eg. furosemide)

70
Q

What types of food is Magnesium present in?

A

green veggies, grains, nuts, meats, & seafood

71
Q

Hypomagnesemia

A

Serum Mg < 1.3 mg/dl

Often seen in sick (ICU ) patients & ED

Common in CHF b/c of diuretics

-More common than hypermagnesemia

72
Q

What is Hypomagnesemia usually caused by

A

Usually caused by conditions that:

◦Limit GI intake of Mg (feeding problems, EtOH abuse)

◦Increase GI or Renal losses of Mg (diarrhea, DKA)

73
Q

Hypomagnesemia- neuromuscular effects

A

similar to low Ca

Hyperactive reflexes, paresthesias, muscle weakness & tremors

Tetany with +Chvostek & +Trousseau signs

74
Q

Hypomagnesemia- CV effects

A

HTN

Tachycardia and arrhythmias

75
Q

What can hypomagnesemia cause

A

hypocalcemia & hypokalemia.

  • impairs ability of the kidney to conserve K+–> Need to correct Mg deficit to fix K level
76
Q

Severe hypomagnesemia

A

severe hypomagnesemia–>hypocalcemia

Probably related to low PTH levels

Need to correct Mg deficit to fix Ca level

77
Q

Hypermagnesemia

A

Serum Mg > 2.1 mg/dl

↑Mg is rare b/c Kidney is usually able to excrete excess Mg

***Renal insufficiency is most likely cause of ↑Mg

Beware using Mg-containing medications such as Milk of Magnesia, Maalox, Mylanta, etc. → can lead to ↑Mg

78
Q
A
79
Q

Neuromuscular effects of hypermagnesemia

A

Hyporeflexia

Muscle weakness; respiratory paralysis

Confusion

80
Q

CV effects of hypermagnesemia

A

Hypotension

Cardiac arrhythmias

81
Q

BUN

A

BUN= Blood Urea Nitrogen

RR( adult)= 10-20

-Rough measurement of renal function and glomerular filtration

82
Q

BUN- what happens if urea is poorly excreted by kidneys?

A

Urea is a by-product of protein metabolism –> If urea poorly excreted by kidneys = ↑BUN …..which is “AZOTEMIA”

83
Q

What are the bodily functions of Magnesium?

A
  1. Regulates Calcium (strong bones and teeth, helps excete excess calcium)
  2. Relaxes skeletal muscle (helps relieve muscle cramping and pain)
  3. Energy Production (Require by over 300 energy producing reactions)
  4. Regulates heart contractility (Blocks calcium from heart muscle, heart has 20x greater concentration)
  5. Cleans the bowel (Unabsorbed Magnesium causes laxitive effect)
  6. Relaxes smooth muscle (relaxes bronchioles and arterioles, relaxes uterine muscle)
84
Q
A
85
Q

What is something that almost all renal diseases cause?

A

Inadequate excretion of urea–> causes BUN to rise

86
Q

What is urea?

A

Substance formed in liver when body breaks down protein

Liver disease= decreased BUN

87
Q

What happens to BUN with liver disease?

A

BUN decreases

88
Q

What happens to BUN when someone eats a low protein diet?

A

Low protein diets reduce BUN

89
Q

What happens to BUN when someone eats a high protein diet?

A

High protein diets increase BUN

90
Q

How does hydration status affect BUN?

A

Overhydration dilutes BUN, causing it to decrease

Dehydration concentrates BUN–> BUN incerases

91
Q

What is creatinine used to assess?

A

In conjunction with BUN, it is useed to assess renal function

***Creatinine is the best assessment of GFR

92
Q

What happens to creatinine levels in children and the elderly?

A

Elderly and children typically have lower levels due to decreased muscle mass (creatinine is a byproduct of creatinine phosphate which is used in skeletal muscle contraction

93
Q

What is the normal range and critical value of Creatinine?

A

RR (adult) female= 0.5-1.1

RR (adult) male= 0.6-1.2

Critical value= >4= kidney failure

94
Q

What is the normal BUN:Creatinine ratio?

A

~10-20/1

Typical: BUN 10-20; Creat 0.5-1.2

95
Q

What are the Azotemia disease states?

A

Azotemia= increased BUN

Prerenal Azotemia= >20/1 BUN: Creatinine ratio

Renal Azotemia= ~10-15/1

Postrenal Azotemia: variable BUN: Creatinine ratio

96
Q

PRErenal Azotemia

A

*Elevated BUN/Cr ratio: > 20/1

-No inherent kidney disease

Common cause: Hypovolemia (intravascular vol. depletion):

◦Trauma, hemorrhage, burns, shock

◦Dehydration (GI losses or decreased intake, Diuretic therapy)

Infection (sepsis)

Low cardiac output (eg. CHF)

97
Q

PRErenal Azotemia–> main idea

A

Physiologic effects occuring BEFORE the kidney

Prerenal Azotemia is a sign of Intravascular volume depletion or hypotension (reduced renal perfusion pressure)

98
Q

What is the treatment of PRErenal Azotemia?

A
  • Restore intravascular volume–> GIVE FLUIDS (oral or IV)
  • Reduce or discontinue diuretics
  • Follow clinical fluid status, watch BUN/Cr closely when changes in meds are made
99
Q

Renal Azotemia

A

BUN/Cr ratio ~ 10-15/1

The Problem is the Kidney Itself!

Causes:

  1. Acute tubular necrosis
    - Most common cause of renal azotemia
    - Renal insufficiency due to tubular damage
    - 2° to low perfusion, nephrotoxic drugs (vancomycin, acyclovir)
  2. Chronic renal disease
  3. Acute glomerulonephritis (Not as common, Can follow endocarditis or strep infection)
100
Q

Treatment of renal azotemia

A

When BUN and Cr both increase, suspect intrinsic renal disease :

◦Medical management helpful, consider hemodialysis if not effective

Optimize fluid management:

◦Follow intake, output closely – minimizes likelihood of fluid overload

101
Q

POSTrenal azotemis

A

Physiologic effects AFTER kidney

BUN/Cr ratio is variable and non-diagnostic

**Obstruction to urine flow is the cause:

  • Stones or tumor in Ureter/renal pelvis (Stones, tumor)
  • Obstruction in Bladder–> Prostatic hypertrophy, tumor, Neurogenic bladder with urinary retention, Blood clot
  • Urethral stricture
102
Q

What is the treatment of POSTrenal azotemia

A
  • Identify location of obstruction
  • If urethral or bladder outlet obstruction, a Foley catheter may correct problem (temporarily)
  • If obstruction is higher (ureter, renal pelvis)–>consult urologist
103
Q

What are normal values of magnesium?

A

RR 1.5-2.3

104
Q

What are the normal values for phosphate?

A

RR 3.0-4.5

105
Q

What is the normal range for calcium?

A

RR 9.0-10.5

106
Q

What part of the CMP are the renal labs?

A

BUN

Creatinine

Calculated BUN/creat

107
Q

Which part of the CMP are the electrolytes?

A

Sodium

Potassium

Chloride

Carbon Dioxide

108
Q

Which part of the CMP has to do with the liver?

A

Alkaline phophatase

AST

ALT

109
Q

What may or may not be included in a CMP depending on the standards of the lab and whether or not you want to order them?

A

Calcium

Phosphorus

Magnesium

Anion gap

Diagnostic Medicine Exam 3 (1 decks)

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