Comprehensive Metabolic Panel Flashcards
Basic Metabolic Panel vs. CMP
Basic- everything except the liver enzymes (AST/ALT)
Total protein
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
When can the total protein be abnormal?
- Some cancers
- Protein-losing enteropathies
- Impaired nutrition
- Liver disease
- Edema
- Burns
Protein functions in the blood
- Makes up tissues, enzymes transport, hormones etc.
- Transport substances in the serum
- 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
What percent of total protein does Albumin make up?
60% of total protein
Functions of albumin
- Osmotic pressure
- Transport drugs, hormones, enzymes
What is Albumin an indicator of?
- nutritional status (prealbumin more specific)
- indicator of liver function b/c it is synthesized in the liver
What does decreased Albumin indicate?
- Malnutrition
- “Protein losing enteropathies” (ex: Crohn’s disease, Celiac disease)
- Nephrotic syndrome (Proteinuria, edema, hyperlipidemia)
- Liver disease
- Inflammatory disease
What can an increased albumin indicate?
- Dehydration
** -some cancers
Total Body Water (TBW)
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
Osmolality
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
What is the normal osmolality range?
Normal osmolality range is: 280 - 295 mOsm/kg
How do you calculate Osmolality?
What happens to the osmolality if glucose is elevated?
Osmolality would increase
What would happen to the osmolality value if sodium decreases?
Osmolality would decrease
How do you calculate Osmolality gap?
- Osmolal gap = OSM (measured) – OSM (calculated)
- If > 10mOsm/L consider exogenous substance
What are some other “Osmotically active” substances?
- Mannitol and various proteins
- Ethanol, methanol, ethylene glycol (antifreeze)
Normal values for an electrolyte panel
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
Abnormal sodium levels on an electrolyte panel
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
Abnormal sodium levels on an electrolyte panel- ->Abnormal Extracellular fluid volume
This is due to sodium control mechanisms
◦too little sodium = Fluid Volume Deficit (FVD)
◦too much sodium = Fluid Volume Excess (FVE)
Abnormal sodium levels on an electrolyte panel–> abnormal extracellular fluid (ECF) sodium concentration
This is due to problems with water control
◦too much water = Hyponatremia
◦too little water = Hypernatremia
Osmolality’s role in interpreting sodium levels
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)
What is pseudohyponatremia due to?
◦due to hypertriglyceridemia or hyperproteinemia (multiple myeloma)
This is when serum Na <135 but normal osmolality
Hyponatremia with HYPERvolemia- What are fluid overload conditions
◦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)
Hyponatremia with HYPERvolemia- What are clinical findings of fluid overload conditions?
◦Pedal edema (seen in CHF), pulmonary crackles, JVD
◦Anemia, may be dilutional
◦Other signs of heart, liver, or renal disease
What causes Hyponatremia with HYPOvolemia?
◦Renal causes–> Diuretics- thiazides
◦Non-renal–> GI: vomiting and diarrhea
Hyponatremia with HYPOvolemia–> What are clinical characteristics of dehydration?
◦Reduced skin turgor; dry mucus membranes
◦Orthostatic BP and pulse changes (neck veins are flat)
Hyponatremia with Euvolemia
No evidence of fluid overload, volume depletion or dehydration
What is the differential diagnosis of someone that has hyponatremia with euvolemia?
◦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)
Overview of Hyponatremia–> differential diagnosis for hyponatremia
Serum potassium
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
What are potential sources of excess potassium?
- Dietary intake
- Breakdown of tissue (rhabdomyolysis, hemolysis)
- Potassium supplements (Rx vs. OTC)
- Potassium-sparing medications
What are the serum K levels in hypokalemia?
Serum K+ < 3.5 mEq/L
Potassium <3.0 is potentially dangerous
What are clinical manifestations of hypokalemia
◦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)
When should a low K+ concentration be corrected?
Hypokalemia in the presence of alkalosis (more basic than acidic), a low K+ concentration needs to be corrected
Hypokalemia- How to correct serum potassium if pH > 7.45
If the pH > 7.45 there will be a–>
◦0.3mEq/L K decrease for each 0.1 increase in pH
Serum potassium levels in Hyperkalemia
Serum potassium > 5.0
K+ > 6.5 may cause serious problems
Clinical manifestations of hyperkalemia
◦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)
Hyperkalemia- elevated potassium correction in acidosis
- 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
What does the lab measure when it measures “calcium”
- 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
When to monitor calcium levels
-Monitor in patients with: renal failure, hyperparathyroidism & malignancies (~ 10-20% of pt w malignancy have elevated Ca++)
Calcium physiology
Enters body → through GI tract
Absorbed from → the intestine under the influence of Vitamin D
Stored in → bone
Excreted by → the kidney
Regulation of blood calcium level
Serum calcium regulated by: PTH, vit D
–>A decrease in serum Ca triggers: PTH secretion = ↑ in serum Ca
Regulation of Calcium- role of PTH
↑ vit. D activation (calcitriol)= ↑Calcium absorption from gut
- Promotes Ca release from bone
- Promotes conservation of Ca by kidneys
*PTH= parathyroid hormone
Role of Free (ionized) Ca++
- Helps regulate neuromuscular activity (eg. cardiac contractility)
- Enzymatic reactions
- Blood clotting
What EKG abnormality may be observed in HYPERcalcemia?
Short QT
What are the most common causes of hypercalcemia
Hypercalcermia= >10.5
Hyperparathyroidism (#1)
Malignancy (bone destruction or stimulation of osteoclast activity)
What are the less common causes of hypercalcemia
- 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
Hyperparathyroidism as a cause of hypercalcemia
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)”
How to diagnose hyperparathyroidism?
Hypercalcemia
Hypophosphatemia
Elevated PTH
Parathyroid scan (nuclear medicine test); parathyroid bx & surgical removal
What is the second leading cause of hypercalcemia?
**Malignancy
Solid tumors: Lung, Kidney, Breast
Hematologic malignancies: Multiple myeloma, Lymphoma, Leukemia
Main causes of HYPOcalcemia
hypocalcemia= <9
- Decreased ability to mobilize bone stores
- Excess loss of Ca from kidneys
- Increased protein binding
Cause of hypocalcemia- Decreased ability to mobilize bone stores
Hypoparathyroidism
Mg deficiency (causes inhibition of PTH)
Cause of hypocalcemia- Excess loss of Ca from kidneys
Renal failure causes phosphate retention, & reciprocal loss of Ca
Cause of hypocalcemia- increased protein binding
Less free Ca (eg: alkalosis )
What are less common causes of hypocalcemia
Hypoparathyroidism
Vit D deficiency
Renal failure
Hypomagnesemia
Hypocalcemia and albumin
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
Symptoms of hypocalcemia
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
Hypocalcemia- testing for carpopedal spasms: Chvostek’s sign
Tapping facial nerve against the bone just anterior to the ear results in contraction of facial muscles
Hypocalcemia- testing for carpopedal spasms: Trousseau’s sign
occluding brachial artery for 3 minutes with BP cuff induces carpal spasms
Relationship b/w calcium and phosphorus
as calcium increases, phosphorus decreases
As calcium decreases, phosphorus increases
Use of phosphate labs
Used to investigate parathyroid and calcium abnormalities
**Inverse relationship w Ca++
What can decrease phosphate levels?
- 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
Conditions associated with increased phosphate
Magnesium
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)
K, Mg and Ca relationship
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
What is the kidneys role in control of magnesium levels?
Eliminated primarily through the kidney
Increased serum Mg? –> Kidney excretes Mg (urine)
Increased serum Ca?–> Kidney excretes Mg (urine)
How can Mg excretion be increased?
Mg excretion INCREASED by loop diuretics (eg. furosemide)
What types of food is Magnesium present in?
green veggies, grains, nuts, meats, & seafood
Hypomagnesemia
Serum Mg < 1.3 mg/dl
Often seen in sick (ICU ) patients & ED
Common in CHF b/c of diuretics
-More common than hypermagnesemia
What is Hypomagnesemia usually caused by
Usually caused by conditions that:
◦Limit GI intake of Mg (feeding problems, EtOH abuse)
◦Increase GI or Renal losses of Mg (diarrhea, DKA)
Hypomagnesemia- neuromuscular effects
similar to low Ca
Hyperactive reflexes, paresthesias, muscle weakness & tremors
Tetany with +Chvostek & +Trousseau signs
Hypomagnesemia- CV effects
HTN
Tachycardia and arrhythmias
What can hypomagnesemia cause
hypocalcemia & hypokalemia.
- impairs ability of the kidney to conserve K+–> Need to correct Mg deficit to fix K level
Severe hypomagnesemia
severe hypomagnesemia–>hypocalcemia
Probably related to low PTH levels
Need to correct Mg deficit to fix Ca level
Hypermagnesemia
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
Neuromuscular effects of hypermagnesemia
Hyporeflexia
Muscle weakness; respiratory paralysis
Confusion
CV effects of hypermagnesemia
Hypotension
Cardiac arrhythmias
BUN
BUN= Blood Urea Nitrogen
RR( adult)= 10-20
-Rough measurement of renal function and glomerular filtration
BUN- what happens if urea is poorly excreted by kidneys?
Urea is a by-product of protein metabolism –> If urea poorly excreted by kidneys = ↑BUN …..which is “AZOTEMIA”
What are the bodily functions of Magnesium?
- Regulates Calcium (strong bones and teeth, helps excete excess calcium)
- Relaxes skeletal muscle (helps relieve muscle cramping and pain)
- Energy Production (Require by over 300 energy producing reactions)
- Regulates heart contractility (Blocks calcium from heart muscle, heart has 20x greater concentration)
- Cleans the bowel (Unabsorbed Magnesium causes laxitive effect)
- Relaxes smooth muscle (relaxes bronchioles and arterioles, relaxes uterine muscle)
What is something that almost all renal diseases cause?
Inadequate excretion of urea–> causes BUN to rise
What is urea?
Substance formed in liver when body breaks down protein
Liver disease= decreased BUN
What happens to BUN with liver disease?
BUN decreases
What happens to BUN when someone eats a low protein diet?
Low protein diets reduce BUN
What happens to BUN when someone eats a high protein diet?
High protein diets increase BUN
How does hydration status affect BUN?
Overhydration dilutes BUN, causing it to decrease
Dehydration concentrates BUN–> BUN incerases
What is creatinine used to assess?
In conjunction with BUN, it is useed to assess renal function
***Creatinine is the best assessment of GFR
What happens to creatinine levels in children and the elderly?
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
What is the normal range and critical value of Creatinine?
RR (adult) female= 0.5-1.1
RR (adult) male= 0.6-1.2
Critical value= >4= kidney failure
What is the normal BUN:Creatinine ratio?
~10-20/1
Typical: BUN 10-20; Creat 0.5-1.2
What are the Azotemia disease states?
Azotemia= increased BUN
Prerenal Azotemia= >20/1 BUN: Creatinine ratio
Renal Azotemia= ~10-15/1
Postrenal Azotemia: variable BUN: Creatinine ratio
PRErenal Azotemia
*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)
PRErenal Azotemia–> main idea
Physiologic effects occuring BEFORE the kidney
Prerenal Azotemia is a sign of Intravascular volume depletion or hypotension (reduced renal perfusion pressure)
What is the treatment of PRErenal Azotemia?
- 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
Renal Azotemia
BUN/Cr ratio ~ 10-15/1
The Problem is the Kidney Itself!
Causes:
- Acute tubular necrosis
- Most common cause of renal azotemia
- Renal insufficiency due to tubular damage
- 2° to low perfusion, nephrotoxic drugs (vancomycin, acyclovir) - Chronic renal disease
- Acute glomerulonephritis (Not as common, Can follow endocarditis or strep infection)
Treatment of renal azotemia
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
POSTrenal azotemis
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
What is the treatment of POSTrenal azotemia
- 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
What are normal values of magnesium?
RR 1.5-2.3
What are the normal values for phosphate?
RR 3.0-4.5
What is the normal range for calcium?
RR 9.0-10.5
What part of the CMP are the renal labs?
BUN
Creatinine
Calculated BUN/creat
Which part of the CMP are the electrolytes?
Sodium
Potassium
Chloride
Carbon Dioxide
Which part of the CMP has to do with the liver?
Alkaline phophatase
AST
ALT
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?
Calcium
Phosphorus
Magnesium
Anion gap
