CC RA Flashcards by Armani Yulong

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

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Ions that carry (-) charge and move toward the anode (+)

ANIONS

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Examples of ANIONS

Chloride, Bicarbonate, and Phosphate

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Ions that carry (+) charge and move toward the cathode (-)

CATIONS

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Examples of CATIONS

Sodium, Potassium, Magnesium, and Calcium

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What are the CLASSIFICATIONS According to the charge it carries?

ANIONS and CATIONS

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What are the CLASSIFICATIONS According to its location/Distribution?

Intracellular & Extracellular
Intravascular & Extravascular

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Present within the cell, specifically in the cytoplasm or cytosol (cytosol is the water component of cytoplasm)

INTRACELLULAR

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Examples of INTRACELLULAR

Potassium, Phosphate

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Found outside the cell, plasma or interstitial fluid

EXTRACELLULAR

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Examples of EXTRACELLULAR

Sodium and Chloride

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FACTORS THAT REGULATE ELECTROLYTE CONCENTRATION IN THE BLOOD?

Diet
Intestinal absorption of electrolytes
Renal and skin excretion of electrolytes
Hormonal activity

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Inside the blood vessel → plasma

INTRAVASCULAR

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Outside the blood vessel → interstitial fluid/tissue fluid

EXTRAVASCULAR

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Any electrolyte that is deficient is reabsorbed while excess electrolytes are excreted through urine/sweat

Renal and skin excretion of electrolytes

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Function of Electrolytes: Myocardial rhythm & contractility

Heart activity: K, Mg, Ca

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most electrolytes are derived from exogenous source (food or fluid intake)

DIET

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T/F. Intestinal absorption of electrolytes are from GIT

TRUE

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Function of Electrolytes: Volume and osmotic regulation

Na, Cl, K

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Function of Electrolytes: Cofactors in enzyme activation

Non-protein substances that enhance enzymatic reactions

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Ex. of Cation Electrolytes

Na+
K+
Ca2+
Mg2+

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Function of Electrolytes: Neuromuscular Excitability

Nerve transfusion, regulates synapse (neuromuscular junction): K, Mg, Ca

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Function of Electrolytes: Regulation of ATPase ion pumps

Active transport of ion on cell membrane: Mg

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Function of Electrolytes: Production & use of ATP from glucose

During glycolysis: Mg, PO4-

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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

1. Increased Sodium Loss 2. Increased Water Retention 3. Water Imbalance

Causes of Increased Sodium Loss

1. Hypoadrenalism (↓aldosterone) 2. Potassium deficiency 3. Diuretic use (thiazide) 4. Ketonuria (Na loss w/ketones) 5. Salt-losing nephropathy 6. Prolonged vomiting or diarrhea

Causes of Increased Water Retention

1. Renal failure (dilution of Na) 2. Nephrotic syn. (↓COP-PV, ↑AVP) 3. CHF, Hepatic cirrhosis

Causes of Water Imbalance

1. SIADH (↑AVP, ↑water retention) 2. 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?

1. WITH LOW OSMOLALITY 2. WITH NORMAL OSMOLALITY 3. 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

1. Excess Water Loss 2. Decreased Water Intake 3. 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:

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

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)

CC RA Flashcards

(257 cards)