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Diagnostics Exam 3 > Comprehensive Metabolic Panel (CMP) > Flashcards

Comprehensive Metabolic Panel (CMP) Flashcards

1
Q

What is included in a “Comprehensive” Metabolic Panel (BMP)?

A
  • Renal labs
  • Electrolytes
  • Liver
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2
Q

What is included in a “Basic” Metabolic Panel (BMP)?

A

everything except the liver enzymes (AST/ALT)

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3
Q

What are the different proteins in the body?

A
  • Prealbumin
  • Albumin (60%)
  • Globulins: Immunoglobulins IgA, IgE, IgG, IgM (1st responce to infection)
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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
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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
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6
Q

What are the Functions of Albumen?

A
  • Osmotic pressure
  • Transport drugs, hormones, enzymes

Indicator of liver function –> Synthesized in the liver

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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

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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
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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-)

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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%

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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

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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

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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)
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14
Q

Describe what could cause abnormal Sodium ECF?

A

-Due to problems with water control

  • too much water = Hyponatremia
  • too little water = Hypernatremia
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15
Q

Describe Pseudohyponatremia Na+ levels and causes

A
  • Serum Na <135, but normal osmolality

- Due to hypertriglyceridemia or hyperproteinemia (multiple myeloma)

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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)
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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
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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
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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)
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20
Q

How do Potassium Disorders appear on an EKG?

A

Hypokalemia: Uwave
Hyperkalemia: Tall peaked, T wave

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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

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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

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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

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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
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25
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

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26
Q

Describe Hyperkalemia in the presence of Metabolic and respiratory acidosis

A

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

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27
Q

What types of Ca++ do lab values measure?

What does Ca++ an indictor of?

A

-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
Q

In what types of patients would you monitor Ca++ levels?

A
  • Monitor in patients with: renal failure, hyperparathyroidism and malignancies
  • Estimated 10-20% of patient w/ malignancy have elevated Ca++
29
Q

Calcium Pathway review

A
  • Enters body → through GI tract
  • Absorbed from → the intestine under the influence of Vitamin D
  • Stored in → bone
  • Excreted by → the kidney
30
Q

What regulates serum calcium levels?

A

Serum calcium regulated by: PTH, vit D

  • A decrease in serum Ca triggers:
  • PTH secretion = ↑ in serum Ca
31
Q

What are the actions of Parathyroid Hormones

A
  • ↑ vit. D activation (calcitriol)= ↑ Calcium absorption from gut
  • Promotes Ca release from bone
  • Promotes conservation of Ca by kidneys
32
Q

What does Free (ionized) Ca++ do?

A
  • Helps regulate neuromuscular activity (eg. cardiac contractility)
  • Enzymatic reactions
  • Blood clotting
33
Q

What EKG abnormality may be observed in HYPERcalcemia?

A

Short QT

34
Q

Most common causes Hypercalcemia?

A
  • Hyperparathyroidism (#1)

- Malignancy (bone destruction or stimulation of osteoclast activity)

35
Q

What are other 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)
36
Q

Describe Hyperparathyroidism Etiology and symptoms

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

- Typically asymptomatic –> “Bones, stones, abdominal groans, psychic moans with fatigue overtones”

37
Q

How do you diagnose Hypercalcemia

A
  • Hypophosphatemia –> Elevated PTH

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

38
Q

When would you see Hypercalcemia

A

1) Malignancy
2) Solid tumors: Lung, Kidney, Breast
3) Hematologic malignancies: Multiple myeloma, Lymphoma, Leukemia

39
Q

What are the major causes of Hypocalcemia?

A
  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
Q

Describe the effects of Hypocalcemia and Albumin. Equation…

A
  • 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
Q

Hypocalcemia Symptoms

A 
-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
Q

Describe Chvostek’s and Trousseau’s sign

A
  • 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
Q

Hypocalcemia: Treatment

A
  • Asymptomatic: oral calcium chloride or calcium gluconate
  • Tetany: IV calcium gluconate or calcium chloride
  • Chronic: dietary changes; eval Vit D
44
Q

Describe general phosphate stuff

A
  • 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
Q

Describe phosphate absorption and stuff

A
  • 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
Q

Describe the functions of Magnesium

A

SEE PICTURE AND WRITE SHIT DOWN

47
Q

Describe Magnesium location

A

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
Q

Describe Magnesium relationship with other cations

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
49
Q

Describe Magnesium regulation

A

-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
Q

Hypomagnesemia

A

-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
Q

Hypomagnesemia

A

-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
Q

Hypomagnesemia

A

-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
Q

Hypomagnesemia

A

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
Q

Hypermagnesemia

A

↑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
Q

Hypermagnesemia

A

Neuromuscular Effects

  • Hyporeflexia
  • Muscle weakness;

respiratory paralysis

  • Confusion
  • CV Effects
  • Hypotension
  • Cardiac arrhythmias
56
Q

Blood Urea Nitrogen (BUN)

A

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
Q

BUN—Key Info

A

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
Q

Creatinine

A

-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
Q

BUN:Creatinine Ratio

A

Normal Ratio: ~10-20/1

60
Q

Azotemia (↑BUN) disease states

A
  • Prerenal Azotemia: > 20/1 ratio
  • Renal Azotemia: ~10-15/1
  • Postrenal Azotemia: variable ratio
61
Q

PRErenal Azotemia

A
  • 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
Q

Treatment of PRErenal Azotemia

A

-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
Q

RENAL azotemia

A

-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
Q

Treatment of Renal Azotemia

A

-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
Q

POSTrenal Azotemia

A

-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
Q

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), will likely need to consult urologist

Diagnostics Exam 3 (1 decks)

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