Comprehensive Metabolic Panel Flashcards

(109 cards)

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
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
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What causes Hyponatremia with HYPOvolemia?
◦Renal causes--\> Diuretics- thiazides ◦Non-renal--\> GI: vomiting and diarrhea
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Hyponatremia with HYPOvolemia--\> What are clinical characteristics of dehydration?
◦Reduced skin turgor; dry mucus membranes ◦Orthostatic BP and pulse changes (neck veins are flat)
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Hyponatremia with Euvolemia
No evidence of fluid overload, volume depletion or dehydration
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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)
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Overview of Hyponatremia--\> differential diagnosis for hyponatremia
31
Serum potassium
Normal= 3.5-5.0 ## Footnote * 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
32
What are potential sources of excess potassium?
* Dietary intake * Breakdown of tissue (rhabdomyolysis, hemolysis) * Potassium supplements (Rx vs. OTC) * Potassium-sparing medications
33
What are the serum K levels in hypokalemia?
Serum K+ \< 3.5 mEq/L Potassium \<3.0 is potentially dangerous
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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)
35
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
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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
37
Serum potassium levels in Hyperkalemia
Serum potassium \> 5.0 K+ \> 6.5 may cause serious problems
38
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)
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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
40
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
41
When to monitor calcium levels
-Monitor in patients with: renal failure, hyperparathyroidism & malignancies (~ 10-20% of pt w malignancy have elevated Ca++)
42
Calcium physiology
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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Regulation of blood calcium level
Serum calcium regulated by: PTH, vit D --\>A decrease in serum Ca triggers: PTH secretion = ↑ in serum Ca
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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
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Role of Free (ionized) Ca++
- Helps regulate neuromuscular activity (eg. cardiac contractility) - Enzymatic reactions - Blood clotting
46
What EKG abnormality may be observed in HYPERcalcemia?
Short QT
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What are the most common causes of hypercalcemia
Hypercalcermia= \>10.5 ## Footnote Hyperparathyroidism (#1) Malignancy (bone destruction or stimulation of osteoclast activity)
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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
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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)”
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How to diagnose hyperparathyroidism?
Hypercalcemia Hypophosphatemia Elevated PTH Parathyroid scan (nuclear medicine test); parathyroid bx & surgical removal
51
What is the second leading cause of hypercalcemia?
\*\*Malignancy Solid tumors: Lung, Kidney, Breast Hematologic malignancies: Multiple myeloma, Lymphoma, Leukemia
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Main causes of HYPOcalcemia
hypocalcemia= \<9 1. Decreased ability to mobilize bone stores 2. Excess loss of Ca from kidneys 3. Increased protein binding
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Cause of hypocalcemia- Decreased ability to mobilize bone stores
Hypoparathyroidism Mg deficiency (causes inhibition of PTH)
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Cause of hypocalcemia- Excess loss of Ca from kidneys
Renal failure causes phosphate retention, & reciprocal loss of Ca
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Cause of hypocalcemia- increased protein binding
Less free Ca (eg: alkalosis )
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What are less common causes of hypocalcemia
Hypoparathyroidism Vit D deficiency Renal failure Hypomagnesemia
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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
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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
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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
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Hypocalcemia- testing for carpopedal spasms: Trousseau's sign
occluding brachial artery for 3 minutes with BP cuff induces carpal spasms
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Relationship b/w calcium and phosphorus
as calcium increases, phosphorus decreases As calcium decreases, phosphorus increases
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Use of phosphate labs
Used to investigate parathyroid and calcium abnormalities \*\*Inverse relationship w Ca++
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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
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Conditions associated with increased phosphate
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Magnesium
Normal= 1.5-2.3 ## Footnote 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
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
68
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)
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How can Mg excretion be increased?
Mg excretion INCREASED by loop diuretics (eg. furosemide)
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What types of food is Magnesium present in?
green veggies, grains, nuts, meats, & seafood
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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
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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)
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Hypomagnesemia- neuromuscular effects
similar to low Ca ## Footnote Hyperactive reflexes, paresthesias, muscle weakness & tremors Tetany with +Chvostek & +Trousseau signs
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Hypomagnesemia- CV effects
HTN Tachycardia and arrhythmias
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What can hypomagnesemia cause
hypocalcemia & hypokalemia. - impairs ability of the kidney to conserve K+--\> Need to correct Mg deficit to fix K level
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Severe hypomagnesemia
severe hypomagnesemia--\>hypocalcemia Probably related to low PTH levels Need to correct Mg deficit to fix Ca level
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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
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Neuromuscular effects of hypermagnesemia
Hyporeflexia Muscle weakness; respiratory paralysis Confusion
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CV effects of hypermagnesemia
Hypotension Cardiac arrhythmias
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BUN
BUN= Blood Urea Nitrogen RR( adult)= 10-20 -Rough measurement of renal function and glomerular filtration
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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”
83
What are the bodily functions of Magnesium?
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)
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What is something that almost all renal diseases cause?
Inadequate excretion of urea--\> causes BUN to rise
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What is urea?
Substance formed in liver when body breaks down protein Liver disease= decreased BUN
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What happens to BUN with liver disease?
BUN decreases
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What happens to BUN when someone eats a low protein diet?
Low protein diets reduce BUN
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What happens to BUN when someone eats a high protein diet?
High protein diets increase BUN
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How does hydration status affect BUN?
Overhydration dilutes BUN, causing it to decrease Dehydration concentrates BUN--\> BUN incerases
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What is creatinine used to assess?
In conjunction with BUN, it is useed to assess renal function \*\*\*Creatinine is the best assessment of GFR
92
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
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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
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What is the normal BUN:Creatinine ratio?
~10-20/1 Typical: BUN 10-20; Creat 0.5-1.2
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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
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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)
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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)
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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
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Renal Azotemia
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)
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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
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POSTrenal azotemis
Physiologic effects AFTER kidney ## Footnote 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
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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
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What are normal values of magnesium?
RR 1.5-2.3
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What are the normal values for phosphate?
RR 3.0-4.5
105
What is the normal range for calcium?
RR 9.0-10.5
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What part of the CMP are the renal labs?
BUN Creatinine Calculated BUN/creat
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Which part of the CMP are the electrolytes?
Sodium Potassium Chloride Carbon Dioxide
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Which part of the CMP has to do with the liver?
Alkaline phophatase AST ALT
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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