CC RA Flashcards
Ions capable of carrying an electric charge (Positive or Negative)
Participate in various metabolic activities so that it can also contribute to normal physiologic actions in the body
It is dissolved in water, thus, it is present where water is located; also contributes to the plasma osmolality
ELECTROLYTES
Ions that carry (-) charge and move toward the anode (+)
ANIONS
Examples of ANIONS
Chloride, Bicarbonate, and Phosphate
Ions that carry (+) charge and move toward the cathode (-)
CATIONS
Examples of CATIONS
Sodium, Potassium, Magnesium, and Calcium
What are the CLASSIFICATIONS According to the charge it carries?
ANIONS and CATIONS
What are the CLASSIFICATIONS According to its location/Distribution?
Intracellular & Extracellular
Intravascular & Extravascular
Present within the cell, specifically in the cytoplasm or cytosol (cytosol is the water component of cytoplasm)
INTRACELLULAR
Examples of INTRACELLULAR
Potassium, Phosphate
Found outside the cell, plasma or interstitial fluid
EXTRACELLULAR
Examples of EXTRACELLULAR
Sodium and Chloride
FACTORS THAT REGULATE ELECTROLYTE CONCENTRATION IN THE BLOOD?
- Diet
- Intestinal absorption of electrolytes
- Renal and skin excretion of electrolytes
- Hormonal activity
Inside the blood vessel → plasma
INTRAVASCULAR
Outside the blood vessel → interstitial fluid/tissue fluid
EXTRAVASCULAR
Any electrolyte that is deficient is reabsorbed while excess electrolytes are excreted through urine/sweat
Renal and skin excretion of electrolytes
Function of Electrolytes: Myocardial rhythm & contractility
Heart activity: K, Mg, Ca
most electrolytes are derived from exogenous source (food or fluid intake)
DIET
T/F. Intestinal absorption of electrolytes are from GIT
TRUE
Function of Electrolytes: Volume and osmotic regulation
Na, Cl, K
Function of Electrolytes: Cofactors in enzyme activation
Non-protein substances that enhance enzymatic reactions
Ex. of Cation Electrolytes
Na+
K+
Ca2+
Mg2+
Function of Electrolytes: Neuromuscular Excitability
Nerve transfusion, regulates synapse (neuromuscular junction): K, Mg, Ca
Function of Electrolytes: Regulation of ATPase ion pumps
Active transport of ion on cell membrane: Mg
Function of Electrolytes: Production & use of ATP from glucose
During glycolysis: Mg, PO4-
Function of Electrolytes: Cofactors in enzyme activation electrolytes that acts as activators
Mg, Ca, Zn
Ex. of Anion Electrolytes
HCO3-
Cl-
HPO2-
SO2-
Anion Intracellular Values
HCO3- (10)
Cl- (1)
HPO2- (50)
SO2- (10)
Cation Extracellular Values
Na+ (136-145)
K+ (3.5-5.1)
Ca2+ (2.15-2.5)
Mg2+ (0.63-1)
Function of Electrolytes: Acid-base balance
Maintains equilibrium in acid-base content of plasma: HCO3-, K, Cl
Cation Intracellular Values
Na+ (15)
K+ (150)
Ca2+ (1)
Mg2+ (13.5)
Anion Extracellular Values
HCO3- (23-29)
Cl- (98-107)
HPO2- (0.78-142)
SO2- (0.5)
NATRIUM
SODIUM
The MOST ABUNDANT CATION in the ECF
Major Extracellular CATION in the plasma
SODIUM
The movement is regulated by active transport through
Na, K - ATPase ion pump
Na+, K+ -ATPase ion pump moves __ Na ions out of the cell in exchange for __ K ions (PISO)
3; 2
balance of charge in and out of the cells
ELECTRONEUTRALITY
T/F. The movement of both K and Na (MAJOR CATIONS) can affect the positive charge distribution in and out of the cell
TRUE
Plasma concentration depends in
RENAL REGULATION
Intake of water in response to
THIRST
T/F. Na+ is one of the MINOR CONTRIBUTORS of plasma osmolality.
FLASE; MAJOR
↑ Na+ intake will ↑ plasma osmolality (solute per kg of solvent ), causing thirst center activation in the _____________ of the brain
HYPOTHALAMUS
Excretion of water as affected by AVP
Arginine Vasopressin; formerly known as ADH
T/F. When there is water loss, there will be INCREASED plasma volume and this could DECREASE the sodium level in the plasma (Increased Plasma Osmolality)
False, decreased plasma volume and this could increase the sodium level in the plasma
T/F. The blood volume status, which affects Na excretion through:
- Since sodium is abundant in the plasma, the plasma volume level will determine how much sodium is removed/ retained/reabsorbed by the kidneys.
TRUE
promotes INCREASED NA+ REABSORPTION in the kidneys
ALDOSTERONE
T/F. In exchange for Na conservation/reabsorption, there must be EXCRETION OF K
TRUE
promotes INCREASED ALDOSTERONE SECRETION by the adrenal glands
Angiotensin II (active angiotensin)
promotes INCREASED EXCRETION OF NA+ in urine; ANTAGONIST OF ALDOSTERONE
ANP (Atrial Natriuretic Peptide)
T/F. The plasma sodium concentration is not depends on HOMEOSTASIS
False, depends greatly on HOMEOSTASIS
T/F. Sodium and potassium are ER REQUEST
TRUE
important for volume regulation &movement of fluid in and out of the vessels
SODIUM
critical for myocardial contractility or movement
POTASSIUM
T/F. High potassium and sodium: severe sequelae
False, Low potassium and sodium
Treatment: Include electrolytes in IV
Purple colored NSS w/ Sodium & Potassium
Reference values of Sodium
135-145 mmol/L
Threshold critical value:
Critical high (HYPERNATREMIA)
160 mmol/L: >160
Threshold critical value:
Critical low for (HYPONATREMIA)
120 mmol/L: <120
CSF Sodium values
136-150 mmol/L
T/F. Sodium is also present in CSF since it can pass through the Blood Brain Barrier
TRUE
CAUSES OF HYPONATREMIA
- Increased Sodium Loss
- Increased Water Retention
- Water Imbalance
Causes of Increased Sodium Loss
- Hypoadrenalism (↓aldosterone)
- Potassium deficiency
- Diuretic use (thiazide)
- Ketonuria (Na loss w/ketones)
- Salt-losing nephropathy
- Prolonged vomiting or diarrhea
Causes of Increased Water Retention
- Renal failure (dilution of Na)
- Nephrotic syn. (↓COP-PV, ↑AVP)
- CHF, Hepatic cirrhosis
Causes of Water Imbalance
- SIADH (↑AVP, ↑water retention)
- Pseudohyponatremia
SIADH means
Syndrome of Inappropriate Anti-Diuretic Hormone
During Potassium deficiency:
Aldosterone will promote Na+ reabsorption, which in return, promote K+ excretion in urine
K+ is increased in plasma
During Potassium deficiency:
K+ must be conserved by the kidneys, in return, Na+ will be excreted in urine
K+ is decreased in plasma
CLASSIFICATION OF HYPONATREMIA BY OSMOLALITY?
- WITH LOW OSMOLALITY
- WITH NORMAL OSMOLALITY
- WITH HIGH OSMOLALITY
↑ Sodium loss
Increased water retention – all solutes including sodium are diluted
WITH LOW OSMOLALITY
Sodium is decreased but the plasma osmolality is not affected.
WITH NORMAL OSMOLALITY
Other solute concentration is too high
Examples: Hyperglycemia, Mannitol Infusion
WITH HIGH OSMOLALITY
CAUSES OF HYPERNATREMIA
- Excess Water Loss
- Decreased Water Intake
- Increased Intake or Retention of Sodium
What are the tube and specimen needed for Specimen Collection of Sodium?
Serum (red)
Plasma (green: Lithium heparin, Ammonium heparin, Lithium oxalate)
T/F. False ↑ with MARKED HEMOLYSIS because sodium is also seen inside the cell
TRUE
What are the interfering agents that might encounter in Sodium?
Hgb
Lipids
Bilirubin
T/F. In Flame Emission Spectroscopy, the color of sodium after excitation is RED
FALSE; YELLOW
NOT COMMONLY USED for sodium
It is used for ions that are not easily excited.
Atomic Absorption Spectroscopy
The REFERENCE METHOD as it is rapid (STAT)
ISE
T/F. In Ion Selective Electrode, uses Glass ion-exchange membrane for sodium
TRUE
COLORIMETRIC METHOD for sodium determination
Albanese-Lein
KALIUM
POTASSIUM
Major INTRACELLULAR CATION
Responsible for the regulation of neuromuscular excitability and contraction of heart, Intracellular Fluid volume, and H+ concentration
POTASSIUM
T/F. Potassium can buffer excess H+ ions in the plasma to maintain pH
TRUE
potassium will move out of the cell to allow excess H ions to enter the cell (with sodium) so that pH and concentration of plasma will increase
Increased H+
↑K+ could cause ↑ cell excitability and this could lead to
MUSCLE WEAKNESS
↓K+ could cause ↓ cell excitability and this could lead to
arrhythmia or paralysis
T/F. LOW POTASSIUM LEVEL is maintained as the effect of ↑/↓ levels is severe
False, NORMAL POTASSIUM LEVEL
inversely proportional to cell excitability and K+
Resting Membrane Potential (RMP)
cause ↑K+ excretion for the reabsorption of Na+
ALDOSTERONE
Regulates the Na and K concentration in and out of the cell for ELECTRONEUTRALITY
Na+, K+ - ATPase Pump
Decreased Function, Decreased cellular entry → seen in
hypoxia, digoxin overdose, hypomagnesemia, propranolol (β-blocker)
Increased Function, Increased cellular entry → caused by
insulin, epinephrine
Decreased Cellular entry cause
HYPERKALEMIA
Increased cellular entry will cause
HYPOKALEMIA
T/F. Na+, K+ - ATPase Pump, INCREASED with exercise, hyperosmolality (DM), and cellular breakdown
TRUE
T/F. In Phlebotomy: arm exercise, excessive fist quenching, prolonged tourniquet application may release potassium from muscle, causing false elevation in the plasma.
TRUE
Reference values of Potassium
3.5-5.2 mmol/L
Threshold critical values of Potassium:
critical value for HYPERKALEMIA
≥ 6.5 mmol/L
Threshold critical values of Potassium:
critical value for HYPOKALEMIA
≤ 2.5 mmol/L
CAUSES OF HYPOKALEMIA/HYPOPOTASSEMIA
GI loss
Renal loss
Cellular shift (↑ Potassium uptake)
Decreased Intake
CAUSES OF GI loss
Vomiting, diarrhea
Gastric suction
Intestinal tumor, malabsorption
Cancer therapy, laxatives
CAUSES OF Renal loss
Diuretics, nephritis, CHF
RTA (↓H+, ↑K+ excretion)
Cushing syn. (↑Na, ↓K reabs.)
Hyperaldosteronism
Hypomagnesemia (↑aldosterone)
CAUSES OF Cellular shift (↑ Potassium uptake)
Alkalosis (plasma)
Insulin overdose
CAUSES OF HYPERKALEMIA/HYPERPOTASSEMIA
Decreased renal excretion
Cellular shift
Increased Intake
Artifactual
CAUSES OF Decreased renal excretion
Renal failure
Hypoaldosteronism (↓Na)
Addison’s Disease
(↓Na reabsorption, ↑K reabsorption)
CAUSES OF Cellular shift
Acidosis (plasma will ↓H+, ↑K)
Muscle/cellular injury
Chemotherapy/leukemia
Hemolysis (markedly elevated)
CAUSES OF Increased Intake
Oral/Intravenous
K+ replacement therapy
CAUSES OF Artifactual
Hemolysis, Thrombocytosis
Prolonged tourniquet
↑ H+ in plasma should be decreased. H+ will enter the cell, in return, K+ will go out of the cell (cellular shift)
ACIDOSIS
What are the tube and specimen needed for Specimen Collection of Potassium?
Serum, Plasma (Heparin), 24-hour urine
T/F. False ↑ with hemolysis
TRUE
T/F. In FES, the color of potassium after excitation is purple/violet
TRUE
Not commonly performed in potassium
AAS
REFERENCE METHOD for potassium
ISE
T/F. In ISE, Uses for Valinomycin membrane for potassium because this antibiotic has a low affinity to the potassium ions (↑specificity)
False, high affinity to the potassium ions
COLORIMETRIC METHOD for the determination of potassium
Chemical Method (Lockhead and Purcell)
MAJOR EXTRACELLULAR ANION
CHLORIDE
T/F. In the plasma, Cl Level is same with Na (DIRECTLY PROPORTIONAL)
TRUE
Involve in maintaining osmolality, blood volume and electric neutrality (chloride shift)
CHLORIDE
involved in maintaining the NEGATIVE CHARGE balance in and out of the cell (ELECTRONEUTRALITY) thru chloride shift
Cl- and HCO3-
T/F. Rate limiting component in Sodium reabsorption: Na+ and Cl- may exist as salt since opposite charge attract each other
TRUE
Cl is passively reabsorbed as well
When Na+ is reabsorbed
Cl is passively excreted as well
When Na+ is excreted
Cl- can also be excreted in skin through perspiration
With Na+
Formation of carbonic acid produces bicarbonate and hydrogen ions
CHLORIDE SHIFT
T/F. In, CHLORIDE SHIFT.
When bicarbonate is generated inside the cell, most of them would diffuse and stay the cell, thus decreasing the negative charge of the cell
False, diffuse and leave the cell
T/F. In CHLORIDE SHIFT, Chloride present in the plasma would then enter the cell to compensate for lost bicarbonate negative charge
TRUE
T/F. In CHLORIDE SHIFT, The produced hydrogen ions is buffered/will bind with the deoxyhemoglobin of red cell
TRUE
Reference values of Chloride
98-107 mmol/L
CAUSE OF HYPERCHLOREMIA
Excess loss of HCO3
CAUSE OF Excess loss of HCO3
GI losses
Renal Tubular Acidosis
Metabolic Acidosis
CAUSES OF HYPOCHLOREMIA
Excess loss of Cl
CAUSES OF Excess loss of Cl
Prolonged vomiting
Diabetic ketoacidosis
Aldosterone deficiency
Salt-losing pyelonephritis
What are the tube and specimen needed for Specimen Collection of Chloride?
Serum, Plasma (Lithium heparin), 24-hour urine
T/F. False ↓ with marked hemolysis due to dilution
TRUE
In ISE, Membrane used for chloride should contain
Tri-n-octylpropyl ammonium chloride decanol
REFERENCE METHOD for chloride
ISE
- Used for the measurement of chloride level in sweat.
- This is useful for the diagnosis of CYSTIC FIBROSIS (MUCOVISCIDOSIS)
- REACTION: Ag2+ + 2Cl- → AgCl2
AMPEROMETRIC-COULOMETRIC: (COTLOVE CHLORIDOMETER)
(sweat inducing drug) is given to patient to collect sufficient sweat specimen
PILOCARPINE
- COLORIMETRIC METHOD for determination of chloride (now an obsolete test)
- REACTION: Cl- + Hg(NO3)2 –S-diphenylcarbazone → Hg-S- diphenylcarbazone (violet)
SCHALES AND SCHALES
Principle of SCHALES AND SCHALES
Titration with mercuric nitrate
Indicator of SCHALES AND SCHALES
S-diphenylcarbazone
Cl + Mercuric thiocyanate (SCN)2 → HgCl2 + free thiocyanate ions
Thiocyanate ions + FeCl3 → ferric thiocyanate (reddish color)
COLORIMETRIC
T/F. Absorbance is directly proportional to the Cl concentration
TRUE
2ND MOST ABUNDANT ANION IN THE ECF
Accounts for more than 80% of total CO2 with HCO3-
An alkaline agent (↑plasma pH ↑ HCO3-)
BICARBONATE
T/F. Chloride Shift: Gets out of the cell once it is produced in exchange for chloride
TRUE
T/F. Major component of BICARBONATE- CARBONIC ACID BUFFER SYSTEM of the blood
TRUE
Major buffer system in maintaining the normal plasma pH
BICARBONATE- CARBONIC ACID BUFFER SYSTEM
can buffer excess H+ by combining w excess acid to produce H2CO3
HCO3-
T/F. HCO3- is reabsorbed abnormally in the kidneys
False, reabsorbed normally
Percentage of Bicarbonate that reabsorbed in the PROXIMAL CONVOLUTED TUBULE
85%
Percentage of Bicarbonate that reabsorbed in DISTAL CONVOLUTED TUBULE
15%
CAUSE of Increased BICARBONATE
Metabolic Alkalosis
CAUSES of Metabolic Alkalosis
Severe vomiting, Hypokalemia
Hypoventilation
Excessive alkali intake
CAUSE of Decreased BICARBONATE
Metabolic Acidosis
CAUSE of Metabolic Acidosis
Hyperventilation
What are the tube and specimen needed for Specimen Collection of Bicarbonate?
Serum, Plasma (heparin)
T/F. False ↓ if left uncapped
TRUE
False ↓ if left uncapped because CO2 can be released into atmospheric air and this could
decrease 6 mmol/L of bicarbonate per hour
Uses pCO2 electrode for bicarbonate
ISE
Reaction:
Phosphoenolpyruvate + HCO3 – PEP carboxylase → Oxaloacetate + H2PO4–
Oxaloacetate + NADH + H+ –MDH → Malate + NAD+
ENZYME METHOD
T/F. INCREASED ABSORBANCE of the oxidized NAD+ at 340nm is measured
FALSE; DECREASED
DIVALENT CATION (Mg2+)
2ND MAJOR INTRACELLULAR CATION
MAGNESIUM
Involved in neuromuscular conduction, enzyme phosphorylation, and protein anabolism
MAINLY DERIVED FROM DIET (Exogenous source)
MAGNESIUM
Distribution of Magnesium
Bone:
53%
Distribution of Magnesium
o Muscle and other organs and soft tissues:
46%
Distribution of Magnesium
Serum and RBC:
<1%
Forms of Magnesium in serum
Protein Bound:
33%
Forms of Magnesium in serum
Free or ionized:
61% (physiologically ACTIVE FORM)
Forms of Magnesium in serum
Complexed with PO4- and citrate:
6%
PTH means
parathyroid hormone
Produced by parathyroid gland
PTH
Responsible for the increase renal reabsorption of magnesium
PTH
T/F. PTH, Increases the intestinal absorption of Mg2+ because it can also be derived from the diet
TRUE
T/F. PTH activity is INVERSELY PROPORTIONAL to the calcium & magnesium level in the blood
False, DIRECTLY PROPORTIONAL
T4 means
Aldosterone and thyroxine
T/F. Aldosterone and thyroxine (T4), promotes ↑ RENAL EXCRETION of magnesium and calcium
TRUE
T/F. Aldosterone and thyroxine (T4), promotes sodium absorption
TRUE
Normal range of Magnesium
0.63-1.0 mmol/L or 1.26-2.10 mEq/L
T/F. Normal level of Mg is HIGHER compared with Na+ & Cl-
False, Normal level is LOWER
CAUSES OF HYPOMAGNESEMIA
Reduced Intake
Decreased Absorption
Causes of Reduced Intake
Poor diet/starvation
Prolonged Mg+ - deficient IV
Chronic Alcoholism
Causes of Decreased Absorption
Malabsorption Syndrome
Pancreatitis, Diarrhea
Vomiting, Laxative use, etc.
Neonatal – due to surgery
Primary – selective malabsorption
Congenital – transport defect in SI
Other Causes of HYPOMAGNESEMIA
Excess Lactation
Pregnancy (developing fetus)
CAUSES OF HYPOMAGNESEMIA (DUE TO INCREASED EXCRETION)
Renal
Endocrine
Drug Induced
Causes of Renal
Tubular disorder, Pyelonephritis
Glomerulonephritis
Causes of Endocrine
Hyperparathyroidism - ↑Ca ↓Mg
Hyperaldosteronism - ↑Na ↓Mg
Hyperthyroidism - ↑Mg excretion
Hypercalcemia - ↑Ca ↓Mg
Diabetic Ketoacidosis – glycosuria
Causes of Drug Induced
Diuretics (Furosemide, Thiazide)
Antibiotics (Gentamicin)
Cyclosporin (Immunosuppressant)
Digitalis and Digoxin (Glycosides)
What are the tube and specimen needed for Specimen Collection of Magnesium?
Serum, Plasma (Lithium heparin), 24-hour urine
T/F. Hemolysis causes false ↑ as it is also found in the RBC
TRUE
REFERENCE METHOD for Mg
AAS
Magnesium concentration is DIRECTLY PROPORTIONAL to the absorbance
COLORIMETRIC METHOD
Reaction: Mg2+ + Calmagite → Reddish-violet (532 nm)
The level of Magnesium is DIRECTLY PROPORTIONAL with the reddish-violet product
CALGAMITE METHOD
Reaction: Mg2+ + Dye → colored complex (660 nm)
FORMAZEN DYE METHOD
Reaction: Mg2+ + Chromogen → colored complex
METHYL THYMOL BLUE METHOD
Serum will undergo deproteinization process using TCA to precipitate and remove proteins → TCA filtrate of the serum
Reaction: Serum TCA filtrate + Titan Yellow → Red compound
TITAN YELLOW
Reaction: Mg2+ + 8-hydroxyl-5-quinoline sulfonic acid → fluorescence
(Wavelength: 380-410nm)
FLUOROMETRIC METHOD
- DIVALENT CATION; 5TH MOST COMMON ELEMENT in the body
- For muscle contraction
- For blood coagulation
CALCIUM
Ca is evaluated with phosphorus for
BONE METABOLISM
T/F. Ca is MAJOR INORGANIC COMPONENT of the osseous tissues (bone)
TRUE
T/F. Presence of calcium cannot activate enzymes in coagulation cascade
False, can activate enzymes in coagulation cascade
Absorbed in the upper Small Intestine in the presence of
Vitamin D (Active Form)
Percentage of Ca that found in bones and teeth
99%
Percentage of Ca that found in blood and ECF
1%
Ca DISTRIBUTION IN BLOOD through:
IONIZED
PROTEIN BOUND
COMPLEX
Physiological ACTIVE form of calcium (UNBOUND/FREE FORM)
45% of total Calcium in the plasma
IONIZED
Attached to a protein (Albumin – protein transporter)
40% of Total Calcium
PROTEIN BOUND
Bound to ANIONS (opposite charge)
Ex: Bicarbonate, Phosphate, & Lactate
15% of Total Calcium
COMPLEX
What are the FACTORS AFFECTING CALCIUM LEVEL IN THE BLOOD?
BONE RESORPTION
BONE DEPOSITION
INTESTINAL ABSORPTION
Bone matrix destruction by the Osteoclast → calcium release in blood
Promoted by PTH, which mobilizes calcium from the bone to the blood
BONE RESORPTION
Also known as Bone Mineralization (Bone formation)
Cause ↓ blood calcium level
Promoted by calcitonin (inhibits PTH and vitamin D activity)
BONE DEPOSITION
Promoted by Vitamin D in the active form
Can INCREASE BONE RESORPTION
INTESTINAL ABSORPTION
will result to the inhibition of PTH release
Presence of HYPERCALCEMIA
will induce PTH secretion by the parathyroid gland to act on the bone & kidney, stimulating bone resorption and calcium absorption in the kidneys
Presence of HYPOCALCEMIA
promotes:
PTH stimulates osteoclastic activity which releases Ca++ and HPO4-
In BONE
promotes:
Absorption of Ca2+
Excretion of HPO4-
Activation of renal 1-a-hydroxylas
In KIDNEY, PTH
coverts 25-OH Vitamin D to 1,25 (OH)2 Vit D (active form)
1-α-hydroxylase
T/F. 1,25 (OH)2 Vit D, promotes Intestinal Absorption and Renal Reabsorption of Ca2+ and HPO4-
TRUE
T/F. The UV rays from the early morning sunlight (best time) accelerates and hastens the activation of Vitamin D in the blood or biologic system. However, prolonged exposure to UV rays is damaging. Melanin cannot PROTECT us from it.
First sentence is correct, Second sentence is incorrect
*Melanin can PROTECT us from it
protection is low and is prone to skin disorders
Too low melanin
excess melanin can block UV rays which leads to poor activation of available Vitamin D → prone to bone disorders
Too high melanin
Reference range of Calcium
8.6-10 mg/dL
CAUSES OF HYPOCALCEMIA
Primary hypoparathyroidism: (PTH ↑ excretion of Ca2+)
Hypo/hypermagnesemia: ↓ PTH quantity and activity; Vit. D. resistance
Hypoalbuminemia: Chronic liver disease, Nephrotic syndrome, Malnutrition
Acute Pancreatitis: (↑ lipase)
Vitamin D deficiency: (↓ absorption)
Renal Disease
Rhabdomyolysis: ↑ PO4 release from cells which binds calcium
CAUSES OF HYPERCALCEMIA
Primary hyperparathyroidism
Malignancy
Multiple Myeloma
↑ Vitamin D
Thiazide diuretics (↑ Ca reabsorption)
Prolonged immobilization (↑ resorption)
What are the tube and specimen needed for Specimen Collection of Calcium?
Serum, Plasma (lithium heparin), 24-hour urine
T/F. Hemolysis cause False ↑
TRUE
REFERENCE METHOD for Calcium and Magnesium
AAS
uses liquid membrane electrode
ISE
used for the colorimetric measurement of serum calcium
Ortho-cresolphthalein complexone (CPC)
Colorimetric Method for Ca
Arsenzo III dye
chelating agent for calcium
EDTA Titration method
Ex. of chelating agent for calcium
BACARA, Gower, Sobel
(Redox Titration method)
- Precipitation of Calcium as Calcium Oxalate(CaC2O4)
- CaC2O4 + H2SO4 → oxalic acid (H2C2O4)
- H2C2O titrated with KMNO4 → PINK COLOR
Clark and Collip
(Precipitation with Chloranilic acid)
- Ca2+ + Sodium chloranilate → Ca Chloranilate
- Ca Chloranilate + EDTA → Chloranilic acid
Ferro and Ham
MAJOR INTRACELLULAR ANION
Component of phospholipids, nucleic acids, creatine phosphate and ATP
PHOSPHATE
Phosphate in diet is MAXIMALLY absorbed in the jejunum
SMALL INTESTINE
Percentage of Phosphate in bones
85%
Percentage of Phosphate in extracellular environment
15%
found in many parts of tissues/cells
OMNIPRESENT
T/F. Growth Hormone increases renal excretion of phosphate
False, decreases renal excretion
T/F. The level of phosphate is INVERSELY RELATED TO CALCIUM
TRUE
T/F. In the kidneys through the action of the PTH, calcium is absorbed while phosphate is excreted.
TRUE
FORMS OF PHOSPHATE IN CELLS
ORGANIC
INORGANIC
Inside the cell; the principal anion in the cell
ORGANIC
Outside the cell; blood buffer present in the plasma or serum
The one measured in tests
INORGANIC
CAUSE OF HYPOPHOSPHATEMIA
Hyperparathyroidism (↑ renal excretion)
Vitamin D Deficiency or antacid use (↓intestinal absorption)
CAUSE OF HYPERPHOSPHATEMIA
Hypoparathyroidism
Lymphoblastic leukemia, intensive exercise, neoplastic disorders
Hypervitaminosis
What are the tube and specimen needed for Specimen Collection of Phosphate?
Serum, Plasma (lithium heparin), 24-hour urine
T/F. Hemolysis cause False ↑
TRUE
Absorbance of (340 nm)
Ammonium phosphomolybdate complex
Fiske-Subbarow Method
Reducing agent:
Pictol (Amino Naphthol Sulfonic acid)
Fiske-Subbarow Method
Other reducing agents:
- Elon or Methyl Amino Phenol
- Ascorbic acid
- Senidine or N-Phenyl-PhenyleneDiamineHyrochloride
Anion that is an INDICATOR of severity of oxygen deprivation (hypoxia)
BYPRODUCT of anaerobic metabolism and mechanism in the body
LACTATE
Marker for low/deficient oxygen in tissues:
INCREASED LACTATE
INSIGNIFICANT because it shows normal O2 levels
DECREASED LACTATE
What are the 2 types of LACTATE ACIDOSIS?
Hypoxic Conditions (Type A)
Metabolic Origin (Type B)
Causes of Hypoxic Conditions (Type A)
Lactate Acidosis
Shock, MI, Severe CHF
Pulmonary edema, severe blood loss
Causes of Metabolic Origin (Type B)
DM, severe infection, leukemia, liver, or renal disease
Toxins (ethanol, methanol or salicylate poisoning)
