Comprehensive Metabolic Panel (CMP) Flashcards
1
Q
What is included in a “Comprehensive” Metabolic Panel (BMP)?
A
- Renal labs
- Electrolytes
- Liver
2
Q
What is included in a “Basic” Metabolic Panel (BMP)?
A
everything except the liver enzymes (AST/ALT)
3
Q
What are the different proteins in the body?
A
- Prealbumin
- Albumin (60%)
- Globulins: Immunoglobulins IgA, IgE, IgG, IgM (1st responce to infection)
4
Q
What are protein levels used to diagnose?
A
Used to diagnose, evaluate, monitor patients with:
- Cancer
- immune disorders
- protein-losing enteropathies
- impaired nutrition
- Liver disease
- Edema
- burns
5
Q
What are protein functions?
A
- Makes up tissues, enzymes, hormones
- Transport substances in the serum
- Creates osmotic pressure in the intravascular space
- Pulls fluids into or prevents fluid from leaving
6
Q
What are the Functions of Albumen?
A
- Osmotic pressure
- Transport drugs, hormones, enzymes
Indicator of liver function –> Synthesized in the liver
7
Q
What would decrease/increase albumin?
A
Decreased albumin:
- Malnourishment
- “Protein losing enteropathies”: Crohn’s disease + Celiac disease
- Nephrotic syndrome: Proteinuria, edema, hyperlipidemia
- Liver disease
- Inflammatory disease
Increased Albumin: Dehydration
8
Q
Describe Globulins & Serum Protein Electrophoresis (SPEP)
A
- Immunoglobulins…IgA, IgE, IgG etc.
- Separates serum proteins based on electrical charge
- Specific patterns may be indicative of disease states
- Eg. Multiple Myeloma = Cancer of the plasma cells (usu. presents in 6th decade, initial findings incl. back or rib pain & anemia)
- SPEP demonstrates characteristic “Mspike” (spike in beta or gamma globulin)
- “monoclonal gammopathy”
- Bence-Jones proteins in urine
9
Q
What is the breakdown of fluid in the body?
A
60% water –> 2/3 ICF (K+) + 1/3 ECF
ECF –> 3/4 Intersticial fluid (Na+ Cl-) + 1/4 Plasma (Na+ Cl-)
10
Q
What is the percent of water in a fetus, baby, adult, and elderly person.
A
Fetus: 100%
Baby: 80%
Adult: 70%
Elderly: 50%
11
Q
Define Osmolality
A
- Solute or particle concentration of a fluid
- The concentration of a solution expressed as the total number of solute particles per kilogram.
-Main solutes: sodium, glucose, and urea
12
Q
How do you Calculated Osmolality
A
Calculated Osmolality = 2 x Sodium(mEq/L) + Glucose (mg)/18 + BUN(mg)/2.8
Normal osmolarity range: 280 - 295 mOsm/kg
13
Q
Describe what could cause abnormal ECFV (Extracellular Fluid Volume)?
A
-Due to sodium control mechanisms (Sodium determine the volume)
- too little sodium = Fluid Volume Deficit (FVD)
- too much sodium = Fluid Volume Excess (FVE)
14
Q
Describe what could cause abnormal Sodium ECF?
A
-Due to problems with water control
- too much water = Hyponatremia
- too little water = Hypernatremia
15
Q
Describe Pseudohyponatremia Na+ levels and causes
A
- Serum Na <135, but normal osmolality
- Due to hypertriglyceridemia or hyperproteinemia (multiple myeloma)
16
Q
Describe Hyponatremia Na+ levels and causes
A
-Due to hyperosmolar state
- Increased glucose in ECF causes shift of water from ICF to ECF, thus lowering serum Na
- Na drops 1.6 mEq/L for every 100mg/dl rise of plasma glucose (2.4 mEq/L > 400mg/dl)
17
Q
What are some conditions associated with Hyponatremia (low Na) with Hypervolemia (High H20 in plasma)
A
Fluid overload conditions:
- Congestive heart failure
- Renal failure
- Nephrotic syndrome
- Hepatic cirrhosis
Observe clinical findings such as:
- Pedal edema, pulmonary crackles, JVD.
- Anemia, may be dilutional
- Other signs of heart, liver, or renal disease
18
Q
What are some conditions associated with Hyponatremia (low Na+) with Hypovolemia (decrease blood volume)
A
Due to renal or non-renal causes
- Renal: Diuretics – thiazides
- Nonrenal: GI = Vomiting, fistula (un natural opening)
Clinical characteristics of dehydration.
- Reduced skin turgor; dry mucus membranes
- Orthostatic BP and Pulse changes
19
Q
What are some diagnosis associated with Hyponatremia (low Na+) with Euvolemia (fluid balance)
A
No evidence of fluid overload, volume depletion or dehydration
Differential diagnosis includes:
- Hypothyroidism (check thyroid function)
- SIADH (syndrome of inappropriate ADH secretion)
- The most common cause of euvolemic low Na.
- Due to impaired renal free water excretion
- Diuretic use (without volume depletion)
- Adrenal Insufficiency
- Primary (diabetes insipidus –> high thirst) or psychogenic polydipsia
- Tea and toast diet
- (low solute or excessive beer drinking)
20
Q
How do Potassium Disorders appear on an EKG?
A
Hypokalemia: Uwave
Hyperkalemia: Tall peaked, T wave
21
Q
What is the major route of potassium elimination?
A
-Renal excretion is the major route of elimination
• Glomerular Filtration Rate < 20% = hyperkalemia
• Aldosterone increases Na reabsorption/K secretion
22
Q
What are some Potassium sources?
A
-Dietary intake
-Breakdown of tissue (rhabdomyolysis, hemolysis, after
chemo for leukemia or lymphoma)
-Blood transfusion
-GI hemorrhage
-IV potassium and parenteral nutrition
-Potassium in medications
23
Q
What are some Clinical manifestations of Hypokalemia
A
-Neuro: weakness, fatigue, paralysis, rhabdomyolysis
-GI: constipation, ileus
-Nephrogenic Diabetes Insipidus
-ECG changes (prominent U waves, flattened T waves,
ST segment changes)
-Cardiac arrhythmias
24
Q
Describe Hypokalemia in the presence of alkalosis
A
- In the presence of alkalosis, a low K+ concentration needs to be corrected
- If the pH > 7.45 there will be a 0.3mEq/L K decrease for each 0.1 increase in pH
25
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
26
Describe Hyperkalemia in the presence of Metabolic and respiratory acidosis
Elevated potassium correction in acidosis:
-Metabolic acidosis
• 0.7 mEq/L increase for every 0.1 decrease in pH
-Respiratory acidosis
• 0.3 mEq/L increase for every 0.1 decrease in pH
27
What types of Ca++ do lab values measure?
| What does Ca++ an indictor of?
-Lab value is a measure of BOTH free and protein
bound Ca++ (to albumin)
-About 40% of Ca++ in the ECF is bound to
albumin; about 50% is free
- Used as a measure of parathyroid function
- Inverse relationship with Phosphorus
- Direct relationship with Magnesium
28
In what types of patients would you monitor Ca++ levels?
- Monitor in patients with: renal failure, hyperparathyroidism and ***malignancies***
- Estimated 10-20% of patient w/ malignancy have elevated Ca++
29
Calcium Pathway review
- Enters body → through GI tract
- Absorbed from → the intestine under the influence of Vitamin D
- Stored in → bone
- Excreted by → the kidney
30
What regulates serum calcium levels?
Serum calcium regulated by: PTH, vit D
- A decrease in serum Ca triggers:
- PTH secretion = ↑ in serum Ca
31
What are the actions of Parathyroid Hormones
- ↑ vit. D activation (calcitriol)= ↑ Calcium absorption from gut
- Promotes Ca release from bone
- Promotes conservation of Ca by kidneys
32
What does Free (ionized) Ca++ do?
- Helps regulate neuromuscular activity (eg. cardiac contractility)
- Enzymatic reactions
- Blood clotting
33
What EKG abnormality may be observed in HYPERcalcemia?
Short QT
34
Most common causes Hypercalcemia?
- Hyperparathyroidism (#1)
| - Malignancy (bone destruction or stimulation of osteoclast activity)
35
What are other 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)
36
Describe Hyperparathyroidism Etiology and symptoms
- Etiology: usually parathyroid adenoma F>M; > 60 yo
| - Typically asymptomatic --> “Bones, stones, abdominal groans, psychic moans with fatigue overtones"
37
How do you diagnose Hypercalcemia
- Hypophosphatemia --> Elevated PTH
| - Parathyroid scan (nuclear medicine test); parathyroid bx & surgical removal
38
When would you see Hypercalcemia
1) Malignancy
2) Solid tumors: Lung, Kidney, Breast
3) Hematologic malignancies: Multiple myeloma, Lymphoma, Leukemia
39
What are the major causes of Hypocalcemia?
1. Decreased ability to mobilize bone stores
- ↓ PTH (eg. hypoparathyroidism)
- Mg deficiency (causes inhibition of PTH)
2. Excess loss of Ca from kidneys
- Renal failure causes phosphate retention, & reciprocal loss of Ca
3. Increased protein binding
- Less free Ca (eg: alkalosis )
40
Describe the effects of Hypocalcemia and Albumin. Equation...
- Hypoalbuminemia = most common cause of reported hypocalcemia (not true hypocalcemia)
- If serum albumin is low, Ca measurement must be corrected:
- Adjusted Ca = Serum Ca – Ser. Alb + 4.0
41
Hypocalcemia Symptoms
```
-Neuromuscular (↑excitability)
◦ Paresthesia's; muscle cramps
◦ Hyperactive reflexes; carpopedal spasms
◦ Positive Chvostek and Trousseau signs
◦ Tetany- sustained mm spasm
```
CV Effects
-Hypotension; EKG changes (prolonged QT interval); arrhythmias
42
Describe Chvostek’s and Trousseau's sign
- Chvostek’s sign: tapping facial nerve against the bone just anterior to the ear results in contraction of facial muscles
- Trousseau’s sign: occluding brachial artery for 3 minutes with BP cuff induces carpal spasms
43
Hypocalcemia: Treatment
- Asymptomatic: oral calcium chloride or calcium gluconate
- Tetany: IV calcium gluconate or calcium chloride
- Chronic: dietary changes; eval Vit D
44
Describe general phosphate stuff
- Used to investigate parathyroid and calcium abnormalities
- ***Inverse relationship w Ca++***
-“Phosphate” used interchangeably with “phosphorous”
-The majority of phosphorous is found in
bone (~85%).
45
Describe phosphate absorption and stuff
- Dietary phosphate absorbed in small intestine
- Decreased with antacids (opposite of Ca)
- Inverse relationship between calcium and phosphate (when one goes up, other down…usually)
- PTH decreases phosphate reabsorption by the kidneys
- Incr. urinary PO4 excretion; Incr. Ca absorption
46
Describe the functions of Magnesium
SEE PICTURE AND WRITE SHIT DOWN
47
Describe Magnesium location
The second most common intracellular cation
- 50-60% in bone; 40-50% in body cells
- 1% is in the ECF
- ~1/3 is protein-bound (mainly to albumin)
48
Describe Magnesium relationship with other cations
- 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
49
Describe Magnesium regulation
-Eliminated primarily through the kidney
-Mg level regulated by the kidneys:
-Increased serum Mg? --> Kidney excretes Mg
(urine)
-Increased serum Ca? --> Kidney excretes Mg
(urine)
-Mg excretion INCREASED by loop diuretics (eg. furosemide)
-Magnesium is present in: green veggies, grains, nuts, meats, & seafood
50
Hypomagnesemia
-Often seen in sick (ICU ) patients & ED
-Common in pt’s w CHF due to diuretic use
-Usually caused by conditions that:
◦ Limit GI intake of Mg (feeding problems, EtOH abuse)
◦ Increase GI or Renal losses of Mg (diarrhea, DKA)
51
Hypomagnesemia
-Clinically, more common/ more significant than hypermagnesemia
Neuromuscular Effects, similar to low Ca
- Hyperactive reflexes, paresthesias, muscle weakness & tremors
- Tetany with +Chvostek & +Trousseau signs
CV Effects
- Hypertension
- Tachycardia & arrhythmias
52
Hypomagnesemia
-Magnesium deficiency can cause: hypocalcemia
& hypokalemia.
Severe hypomagnesemia --> hypocalcemia
- Probably related to low PTH levels
- Need to correct Mg deficit to fix Ca level
Hypomagnesemia impairs ability of the kidney to conserve K+
-Need to correct Mg deficit to fix K level
53
Hypomagnesemia
Oral replacement:
◦ Magnesium chloride (Slo-mag)
◦ Use caution in patients with renal disease
IV replacement:
◦ Magnesium sulfate infusion
◦ Use caution in patients with renal disease
54
Hypermagnesemia
↑Mg is rare
- Kidney is usually able to excrete excess Mg
- Renal insufficiency is most likely cause of ↑Mg
-Beware using Mgcontaining medications such as Milk of Magnesia, Maalox, Mylanta, etc. → can lead to ↑Mg
55
Hypermagnesemia
Neuromuscular Effects
- Hyporeflexia
- Muscle weakness;
respiratory paralysis
- Confusion
- CV Effects
- Hypotension
- Cardiac arrhythmias
56
Blood Urea Nitrogen (BUN)
Rough measurement of renal function and glomerular filtration
- Urea is a by-product of protein metabolism
- If urea poorly excreted by kidneys = ↑BUN …..which is “AZOTEMIA”
57
BUN—Key Info
Almost all renal diseases cause inadequate excretion of urea, which causes BUN to rise.
-Urea = substance formed in liver when body breaks down protein. Therefore, severe liver disease = ↓BUN.
Changes in protein intake affect BUN:
- Low protein diets reduce BUN
- High protein diets increase BUN
Hydration status affects BUN:
- Overhydration dilutes BUN, causes it to decrease.
- Dehydration concentrates BUN, causes increase.
58
Creatinine
-Used in conjunction with BUN to assess renal function.
-The best assessment of GFR.
-Elderly and children typically have lower levels due to
decreased muscle mass.
- Creatinine is a byproduct of creatine phosphate which is used in skeletal muscle contraction.
- Critical value >4 mg/dl= kidney failure (recall RIFLE criteria)
59
BUN:Creatinine Ratio
Normal Ratio: ~10-20/1
60
Azotemia (↑BUN) disease states
- Prerenal Azotemia: > 20/1 ratio
- Renal Azotemia: ~10-15/1
- Postrenal Azotemia: variable ratio
61
PRErenal Azotemia
- Elevated BUN/Cr ratio > 20/1
- No inherent kidney disease
Hypovolemia (intravascular vol. depletion)
- Trauma (hemorrhage, burns), shock
- Dehydration
- GI losses or decreased intake
- Diuretic therapy
- Infection (sepsis)
- Low cardiac output (eg. CHF)
62
Treatment of PRErenal Azotemia
-Prerenal azotemia is sign of intravascular volume depletion or hypotension (reduced renal perfusion pressure)
Treatment:
- Restore intravascular volumeà GIVE FLUIDS (oral or IV)
- Reduce or D/C diuretics
- Follow clinical fluid status, watch BUN/Cr closely when changes in meds are made (eg. after increasing a patient’s diuretic dose)
63
RENAL azotemia
-BUN/Cr ratio: ~ 10-15/1
The Problem is the Kidney Itself!
-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
64
Treatment of Renal Azotemia
-When BUN and Cr both increase, suspect intrinsic renal disease
◦ Medical management helpful, but dialysis may be necessary
-Optimize fluid management
◦ Follow intake, output closely – minimizes likelihood of
fluid overload
65
POSTrenal Azotemia
-BUN/Cr ratio is variable and non-diagnostic
Obstruction to urine flow is the cause:
- Ureter and renal pelvis
- Blood clot, stones, sickle cell disease
Bladder
- Prostatic hypertrophy or malignancy
- Neuropathic bladder with urinary retention
- Blood clot
Urethral stricture * Note – patient will have symptoms!*
66
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), will likely need to consult urologist
