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CC and HISTO PLEASE LAST NA > CC RA > Flashcards

CC RA Flashcards

1
Q

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

A

ELECTROLYTES

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2
Q

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

A

ANIONS

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3
Q

Examples of ANIONS

A

Chloride, Bicarbonate, and Phosphate

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4
Q

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

A

CATIONS

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5
Q

Examples of CATIONS

A

Sodium, Potassium, Magnesium, and Calcium

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6
Q

What are the CLASSIFICATIONS According to the charge it carries?

A

ANIONS and CATIONS

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7
Q

What are the CLASSIFICATIONS According to its location/Distribution?

A

Intracellular & Extracellular
Intravascular & Extravascular

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8
Q

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

A

INTRACELLULAR

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8
Q

Examples of INTRACELLULAR

A

Potassium, Phosphate

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9
Q

Found outside the cell, plasma or interstitial fluid

A

EXTRACELLULAR

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10
Q

Examples of EXTRACELLULAR

A

Sodium and Chloride

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11
Q

FACTORS THAT REGULATE ELECTROLYTE CONCENTRATION IN THE BLOOD?

A
  • Diet
  • Intestinal absorption of electrolytes
  • Renal and skin excretion of electrolytes
  • Hormonal activity
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11
Q

Inside the blood vessel → plasma

A

INTRAVASCULAR

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12
Q

Outside the blood vessel → interstitial fluid/tissue fluid

A

EXTRAVASCULAR

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12
Q

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

A

Renal and skin excretion of electrolytes

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13
Q

Function of Electrolytes: Myocardial rhythm & contractility

A

Heart activity: K, Mg, Ca

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13
Q

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

A

DIET

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14
Q

T/F. Intestinal absorption of electrolytes are from GIT

A

TRUE

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14
Q

Function of Electrolytes: Volume and osmotic regulation

A

Na, Cl, K

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15
Q

Function of Electrolytes: Cofactors in enzyme activation

A

Non-protein substances that enhance enzymatic reactions

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15
Q

Ex. of Cation Electrolytes

A

Na+
K+
Ca2+
Mg2+

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15
Q

Function of Electrolytes: Neuromuscular Excitability

A

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

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15
Q

Function of Electrolytes: Regulation of ATPase ion pumps

A

Active transport of ion on cell membrane: Mg

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16
Q

Function of Electrolytes: Production & use of ATP from glucose

A

During glycolysis: Mg, PO4-

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16
Q

Function of Electrolytes: Cofactors in enzyme activation electrolytes that acts as activators

A

Mg, Ca, Zn

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16
Q

Ex. of Anion Electrolytes

A

HCO3-
Cl-
HPO2-
SO2-

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16
Q

Anion Intracellular Values

A

HCO3- (10)
Cl- (1)
HPO2- (50)
SO2- (10)

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17
Q

Cation Extracellular Values

A

Na+ (136-145)
K+ (3.5-5.1)
Ca2+ (2.15-2.5)
Mg2+ (0.63-1)

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17
Q

Function of Electrolytes: Acid-base balance

A

Maintains equilibrium in acid-base content of plasma: HCO3-, K, Cl

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18
Q

Cation Intracellular Values

A

Na+ (15)
K+ (150)
Ca2+ (1)
Mg2+ (13.5)

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18
Q

Anion Extracellular Values

A

HCO3- (23-29)
Cl- (98-107)
HPO2- (0.78-142)
SO2- (0.5)

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18
Q

NATRIUM

A

SODIUM

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19
Q

The MOST ABUNDANT CATION in the ECF
Major Extracellular CATION in the plasma

A

SODIUM

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19
Q

The movement is regulated by active transport through

A

Na, K - ATPase ion pump

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19
Q

Na+, K+ -ATPase ion pump moves __ Na ions out of the cell in exchange for __ K ions (PISO)

A

3; 2

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20
Q

balance of charge in and out of the cells

A

ELECTRONEUTRALITY

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20
Q

T/F. The movement of both K and Na (MAJOR CATIONS) can affect the positive charge distribution in and out of the cell

A

TRUE

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21
Q

Plasma concentration depends in

A

RENAL REGULATION

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22
Q

Intake of water in response to

A

THIRST

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23
Q

T/F. Na+ is one of the MINOR CONTRIBUTORS of plasma osmolality.

A

FLASE; MAJOR

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24
Q

↑ Na+ intake will ↑ plasma osmolality (solute per kg of solvent ), causing thirst center activation in the _____________ of the brain

A

HYPOTHALAMUS

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25
Q

Excretion of water as affected by AVP

A

Arginine Vasopressin; formerly known as ADH

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26
Q

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)

A

False, decreased plasma volume and this could increase the sodium level in the plasma

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27
Q

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.

A

TRUE

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28
Q

promotes INCREASED NA+ REABSORPTION in the kidneys

A

ALDOSTERONE

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29
Q

T/F. In exchange for Na conservation/reabsorption, there must be EXCRETION OF K

A

TRUE

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30
Q

promotes INCREASED ALDOSTERONE SECRETION by the adrenal glands

A

Angiotensin II (active angiotensin)

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31
Q

promotes INCREASED EXCRETION OF NA+ in urine; ANTAGONIST OF ALDOSTERONE

A

ANP (Atrial Natriuretic Peptide)

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32
Q

T/F. The plasma sodium concentration is not depends on HOMEOSTASIS

A

False, depends greatly on HOMEOSTASIS

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33
Q

T/F. Sodium and potassium are ER REQUEST

A

TRUE

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34
Q

important for volume regulation &movement of fluid in and out of the vessels

A

SODIUM

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35
Q

critical for myocardial contractility or movement

A

POTASSIUM

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36
Q

T/F. High potassium and sodium: severe sequelae

A

False, Low potassium and sodium

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37
Q

Treatment: Include electrolytes in IV

A

Purple colored NSS w/ Sodium & Potassium

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38
Q

Reference values of Sodium

A

135-145 mmol/L

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39
Q

Threshold critical value:
Critical high (HYPERNATREMIA)

A

160 mmol/L: >160

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40
Q

Threshold critical value:
Critical low for (HYPONATREMIA)

A

120 mmol/L: <120

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41
Q

CSF Sodium values

A

136-150 mmol/L

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42
Q

T/F. Sodium is also present in CSF since it can pass through the Blood Brain Barrier

A

TRUE

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43
Q

CAUSES OF HYPONATREMIA

A
  1. Increased Sodium Loss
  2. Increased Water Retention
  3. Water Imbalance
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44
Q

Causes of Increased Sodium Loss

A
  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
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45
Q

Causes of Increased Water Retention

A
  1. Renal failure (dilution of Na)
  2. Nephrotic syn. (↓COP-PV, ↑AVP)
  3. CHF, Hepatic cirrhosis
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46
Q

Causes of Water Imbalance

A
  1. SIADH (↑AVP, ↑water retention)
  2. Pseudohyponatremia
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47
Q

SIADH means

A

Syndrome of Inappropriate Anti-Diuretic Hormone

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48
Q

During Potassium deficiency:
Aldosterone will promote Na+ reabsorption, which in return, promote K+ excretion in urine

A

K+ is increased in plasma

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49
Q

During Potassium deficiency:
K+ must be conserved by the kidneys, in return, Na+ will be excreted in urine

A

K+ is decreased in plasma

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50
Q

CLASSIFICATION OF HYPONATREMIA BY OSMOLALITY?

A
  1. WITH LOW OSMOLALITY
  2. WITH NORMAL OSMOLALITY
  3. WITH HIGH OSMOLALITY
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51
Q

↑ Sodium loss
Increased water retention – all solutes including sodium are diluted

A

WITH LOW OSMOLALITY

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52
Q

Sodium is decreased but the plasma osmolality is not affected.

A

WITH NORMAL OSMOLALITY

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53
Q

Other solute concentration is too high
Examples: Hyperglycemia, Mannitol Infusion

A

WITH HIGH OSMOLALITY

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54
Q

CAUSES OF HYPERNATREMIA

A
  1. Excess Water Loss
  2. Decreased Water Intake
  3. Increased Intake or Retention of Sodium
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55
Q

What are the tube and specimen needed for Specimen Collection of Sodium?

A

Serum (red)
Plasma (green: Lithium heparin, Ammonium heparin, Lithium oxalate)

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56
Q

T/F. False ↑ with MARKED HEMOLYSIS because sodium is also seen inside the cell

A

TRUE

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57
Q

What are the interfering agents that might encounter in Sodium?

A

Hgb
Lipids
Bilirubin

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58
Q

T/F. In Flame Emission Spectroscopy, the color of sodium after excitation is RED

A

FALSE; YELLOW

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59
Q

NOT COMMONLY USED for sodium
It is used for ions that are not easily excited.

A

Atomic Absorption Spectroscopy

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60
Q

The REFERENCE METHOD as it is rapid (STAT)

A

ISE

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61
Q

T/F. In Ion Selective Electrode, uses Glass ion-exchange membrane for sodium

A

TRUE

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62
Q

COLORIMETRIC METHOD for sodium determination

A

Albanese-Lein

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63
Q

KALIUM

A

POTASSIUM

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64
Q

Major INTRACELLULAR CATION
Responsible for the regulation of neuromuscular excitability and contraction of heart, Intracellular Fluid volume, and H+ concentration

A

POTASSIUM

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65
Q

T/F. Potassium can buffer excess H+ ions in the plasma to maintain pH

A

TRUE

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66
Q

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

A

Increased H+

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67
Q

↑K+ could cause ↑ cell excitability and this could lead to

A

MUSCLE WEAKNESS

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68
Q

↓K+ could cause ↓ cell excitability and this could lead to

A

arrhythmia or paralysis

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69
Q

T/F. LOW POTASSIUM LEVEL is maintained as the effect of ↑/↓ levels is severe

A

False, NORMAL POTASSIUM LEVEL

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70
Q

inversely proportional to cell excitability and K+

A

Resting Membrane Potential (RMP)

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71
Q

cause ↑K+ excretion for the reabsorption of Na+

A

ALDOSTERONE

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72
Q

Regulates the Na and K concentration in and out of the cell for ELECTRONEUTRALITY

A

Na+, K+ - ATPase Pump

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73
Q

Decreased Function, Decreased cellular entry → seen in

A

hypoxia, digoxin overdose, hypomagnesemia, propranolol (β-blocker)

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74
Q

Increased Function, Increased cellular entry → caused by

A

insulin, epinephrine

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75
Q

Decreased Cellular entry cause

A

HYPERKALEMIA

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76
Q

Increased cellular entry will cause

A

HYPOKALEMIA

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77
Q

T/F. Na+, K+ - ATPase Pump, INCREASED with exercise, hyperosmolality (DM), and cellular breakdown

A

TRUE

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78
Q

T/F. In Phlebotomy: arm exercise, excessive fist quenching, prolonged tourniquet application may release potassium from muscle, causing false elevation in the plasma.

A

TRUE

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79
Q

Reference values of Potassium

A

3.5-5.2 mmol/L

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80
Q

Threshold critical values of Potassium:
critical value for HYPERKALEMIA

A

≥ 6.5 mmol/L

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81
Q

Threshold critical values of Potassium:
critical value for HYPOKALEMIA

A

≤ 2.5 mmol/L

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82
Q

CAUSES OF HYPOKALEMIA/HYPOPOTASSEMIA

A

GI loss
Renal loss
Cellular shift (↑ Potassium uptake)
Decreased Intake

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83
Q

CAUSES OF GI loss

A

Vomiting, diarrhea
Gastric suction
Intestinal tumor, malabsorption
Cancer therapy, laxatives

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84
Q

CAUSES OF Renal loss

A

Diuretics, nephritis, CHF
RTA (↓H+, ↑K+ excretion)
Cushing syn. (↑Na, ↓K reabs.)
Hyperaldosteronism
Hypomagnesemia (↑aldosterone)

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85
Q

CAUSES OF Cellular shift (↑ Potassium uptake)

A

Alkalosis (plasma)
Insulin overdose

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86
Q

CAUSES OF HYPERKALEMIA/HYPERPOTASSEMIA

A

Decreased renal excretion
Cellular shift
Increased Intake
Artifactual

87
Q

CAUSES OF Decreased renal excretion

A

Renal failure
Hypoaldosteronism (↓Na)
Addison’s Disease
(↓Na reabsorption, ↑K reabsorption)

88
Q

CAUSES OF Cellular shift

A

Acidosis (plasma will ↓H+, ↑K)
Muscle/cellular injury
Chemotherapy/leukemia
Hemolysis (markedly elevated)

89
Q

CAUSES OF Increased Intake

A

Oral/Intravenous
K+ replacement therapy

90
Q

CAUSES OF Artifactual

A

Hemolysis, Thrombocytosis
Prolonged tourniquet

91
Q

↑ H+ in plasma should be decreased. H+ will enter the cell, in return, K+ will go out of the cell (cellular shift)

A

ACIDOSIS

92
Q

What are the tube and specimen needed for Specimen Collection of Potassium?

A

Serum, Plasma (Heparin), 24-hour urine

93
Q

T/F. False ↑ with hemolysis

A

TRUE

94
Q

T/F. In FES, the color of potassium after excitation is purple/violet

A

TRUE

95
Q

Not commonly performed in potassium

A

AAS

96
Q

REFERENCE METHOD for potassium

A

ISE

97
Q

T/F. In ISE, Uses for Valinomycin membrane for potassium because this antibiotic has a low affinity to the potassium ions (↑specificity)

A

False, high affinity to the potassium ions

98
Q

COLORIMETRIC METHOD for the determination of potassium

A

Chemical Method (Lockhead and Purcell)

99
Q

MAJOR EXTRACELLULAR ANION

A

CHLORIDE

100
Q

T/F. In the plasma, Cl Level is same with Na (DIRECTLY PROPORTIONAL)

A

TRUE

101
Q

Involve in maintaining osmolality, blood volume and electric neutrality (chloride shift)

A

CHLORIDE

102
Q

involved in maintaining the NEGATIVE CHARGE balance in and out of the cell (ELECTRONEUTRALITY) thru chloride shift

A

Cl- and HCO3-

103
Q

T/F. Rate limiting component in Sodium reabsorption: Na+ and Cl- may exist as salt since opposite charge attract each other

A

TRUE

104
Q

Cl is passively reabsorbed as well

A

When Na+ is reabsorbed

105
Q

Cl is passively excreted as well

A

When Na+ is excreted

106
Q

Cl- can also be excreted in skin through perspiration

A

With Na+

107
Q

Formation of carbonic acid produces bicarbonate and hydrogen ions

A

CHLORIDE SHIFT

108
Q

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

A

False, diffuse and leave the cell

109
Q

T/F. In CHLORIDE SHIFT, Chloride present in the plasma would then enter the cell to compensate for lost bicarbonate negative charge

A

TRUE

110
Q

T/F. In CHLORIDE SHIFT, The produced hydrogen ions is buffered/will bind with the deoxyhemoglobin of red cell

A

TRUE

111
Q

Reference values of Chloride

A

98-107 mmol/L

112
Q

CAUSE OF HYPERCHLOREMIA

A

Excess loss of HCO3

113
Q

CAUSE OF Excess loss of HCO3

A

GI losses
Renal Tubular Acidosis
Metabolic Acidosis

114
Q

CAUSES OF HYPOCHLOREMIA

A

Excess loss of Cl

115
Q

CAUSES OF Excess loss of Cl

A

Prolonged vomiting
Diabetic ketoacidosis
Aldosterone deficiency
Salt-losing pyelonephritis

116
Q

What are the tube and specimen needed for Specimen Collection of Chloride?

A

Serum, Plasma (Lithium heparin), 24-hour urine

117
Q

T/F. False ↓ with marked hemolysis due to dilution

A

TRUE

118
Q

In ISE, Membrane used for chloride should contain

A

Tri-n-octylpropyl ammonium chloride decanol

119
Q

REFERENCE METHOD for chloride

A

ISE

120
Q
  • Used for the measurement of chloride level in sweat.
  • This is useful for the diagnosis of CYSTIC FIBROSIS (MUCOVISCIDOSIS)
  • REACTION: Ag2+ + 2Cl- → AgCl2
A

AMPEROMETRIC-COULOMETRIC: (COTLOVE CHLORIDOMETER)

121
Q

(sweat inducing drug) is given to patient to collect sufficient sweat specimen

A

PILOCARPINE

122
Q
  • COLORIMETRIC METHOD for determination of chloride (now an obsolete test)
  • REACTION: Cl- + Hg(NO3)2 –S-diphenylcarbazone → Hg-S- diphenylcarbazone (violet)
A

SCHALES AND SCHALES

123
Q

Principle of SCHALES AND SCHALES

A

Titration with mercuric nitrate

124
Q

Indicator of SCHALES AND SCHALES

A

S-diphenylcarbazone

125
Q

Cl + Mercuric thiocyanate (SCN)2 → HgCl2 + free thiocyanate ions
Thiocyanate ions + FeCl3 → ferric thiocyanate (reddish color)

A

COLORIMETRIC

126
Q

T/F. Absorbance is directly proportional to the Cl concentration

A

TRUE

127
Q

2ND MOST ABUNDANT ANION IN THE ECF
Accounts for more than 80% of total CO2 with HCO3-
An alkaline agent (↑plasma pH ↑ HCO3-)

A

BICARBONATE

128
Q

T/F. Chloride Shift: Gets out of the cell once it is produced in exchange for chloride

A

TRUE

129
Q

T/F. Major component of BICARBONATE- CARBONIC ACID BUFFER SYSTEM of the blood

A

TRUE

130
Q

Major buffer system in maintaining the normal plasma pH

A

BICARBONATE- CARBONIC ACID BUFFER SYSTEM

131
Q

can buffer excess H+ by combining w excess acid to produce H2CO3

A

HCO3-

132
Q

T/F. HCO3- is reabsorbed abnormally in the kidneys

A

False, reabsorbed normally

133
Q

Percentage of Bicarbonate that reabsorbed in the PROXIMAL CONVOLUTED TUBULE

A

85%

134
Q

Percentage of Bicarbonate that reabsorbed in DISTAL CONVOLUTED TUBULE

A

15%

135
Q

CAUSE of Increased BICARBONATE

A

Metabolic Alkalosis

136
Q

CAUSES of Metabolic Alkalosis

A

Severe vomiting, Hypokalemia
Hypoventilation
Excessive alkali intake

137
Q

CAUSE of Decreased BICARBONATE

A

Metabolic Acidosis

138
Q

CAUSE of Metabolic Acidosis

A

Hyperventilation

139
Q

What are the tube and specimen needed for Specimen Collection of Bicarbonate?

A

Serum, Plasma (heparin)

140
Q

T/F. False ↓ if left uncapped

A

TRUE

141
Q

False ↓ if left uncapped because CO2 can be released into atmospheric air and this could

A

decrease 6 mmol/L of bicarbonate per hour

142
Q

Uses pCO2 electrode for bicarbonate

A

ISE

143
Q

Reaction:
Phosphoenolpyruvate + HCO3 – PEP carboxylase → Oxaloacetate + H2PO4–
Oxaloacetate + NADH + H+ –MDH → Malate + NAD+

A

ENZYME METHOD

144
Q

T/F. INCREASED ABSORBANCE of the oxidized NAD+ at 340nm is measured

A

FALSE; DECREASED

145
Q

DIVALENT CATION (Mg2+)
2ND MAJOR INTRACELLULAR CATION

A

MAGNESIUM

146
Q

Involved in neuromuscular conduction, enzyme phosphorylation, and protein anabolism
MAINLY DERIVED FROM DIET (Exogenous source)

A

MAGNESIUM

147
Q

Distribution of Magnesium
Bone:

A

53%

148
Q

Distribution of Magnesium
o Muscle and other organs and soft tissues:

A

46%

149
Q

Distribution of Magnesium
Serum and RBC:

A

<1%

150
Q

Forms of Magnesium in serum
Protein Bound:

A

33%

151
Q

Forms of Magnesium in serum
Free or ionized:

A

61% (physiologically ACTIVE FORM)

152
Q

Forms of Magnesium in serum
Complexed with PO4- and citrate:

A

6%

153
Q

PTH means

A

parathyroid hormone

154
Q

Produced by parathyroid gland

A

PTH

155
Q

Responsible for the increase renal reabsorption of magnesium

A

PTH

156
Q

T/F. PTH, Increases the intestinal absorption of Mg2+ because it can also be derived from the diet

A

TRUE

157
Q

T/F. PTH activity is INVERSELY PROPORTIONAL to the calcium & magnesium level in the blood

A

False, DIRECTLY PROPORTIONAL

158
Q

T4 means

A

Aldosterone and thyroxine

159
Q

T/F. Aldosterone and thyroxine (T4), promotes ↑ RENAL EXCRETION of magnesium and calcium

A

TRUE

160
Q

T/F. Aldosterone and thyroxine (T4), promotes sodium absorption

A

TRUE

161
Q

Normal range of Magnesium

A

0.63-1.0 mmol/L or 1.26-2.10 mEq/L

162
Q

T/F. Normal level of Mg is HIGHER compared with Na+ & Cl-

A

False, Normal level is LOWER

163
Q

CAUSES OF HYPOMAGNESEMIA

A

Reduced Intake
Decreased Absorption

164
Q

Causes of Reduced Intake

A

Poor diet/starvation
Prolonged Mg+ - deficient IV
Chronic Alcoholism

165
Q

Causes of Decreased Absorption

A

Malabsorption Syndrome
Pancreatitis, Diarrhea
Vomiting, Laxative use, etc.
Neonatal – due to surgery
Primary – selective malabsorption
Congenital – transport defect in SI

166
Q

Other Causes of HYPOMAGNESEMIA

A

Excess Lactation
Pregnancy (developing fetus)

167
Q

CAUSES OF HYPOMAGNESEMIA (DUE TO INCREASED EXCRETION)

A

Renal
Endocrine
Drug Induced

168
Q

Causes of Renal

A

Tubular disorder, Pyelonephritis
Glomerulonephritis

169
Q

Causes of Endocrine

A

Hyperparathyroidism - ↑Ca ↓Mg
Hyperaldosteronism - ↑Na ↓Mg
Hyperthyroidism - ↑Mg excretion
Hypercalcemia - ↑Ca ↓Mg
Diabetic Ketoacidosis – glycosuria

170
Q

Causes of Drug Induced

A

Diuretics (Furosemide, Thiazide)
Antibiotics (Gentamicin)
Cyclosporin (Immunosuppressant)
Digitalis and Digoxin (Glycosides)

171
Q

What are the tube and specimen needed for Specimen Collection of Magnesium?

A

Serum, Plasma (Lithium heparin), 24-hour urine

172
Q

T/F. Hemolysis causes false ↑ as it is also found in the RBC

A

TRUE

173
Q

REFERENCE METHOD for Mg

A

AAS

174
Q

Magnesium concentration is DIRECTLY PROPORTIONAL to the absorbance

A

COLORIMETRIC METHOD

175
Q

Reaction: Mg2+ + Calmagite → Reddish-violet (532 nm)
The level of Magnesium is DIRECTLY PROPORTIONAL with the reddish-violet product

A

CALGAMITE METHOD

176
Q

Reaction: Mg2+ + Dye → colored complex (660 nm)

A

FORMAZEN DYE METHOD

177
Q

Reaction: Mg2+ + Chromogen → colored complex

A

METHYL THYMOL BLUE METHOD

178
Q

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

A

TITAN YELLOW

179
Q

Reaction: Mg2+ + 8-hydroxyl-5-quinoline sulfonic acid → fluorescence
(Wavelength: 380-410nm)

A

FLUOROMETRIC METHOD

180
Q
  • DIVALENT CATION; 5TH MOST COMMON ELEMENT in the body
  • For muscle contraction
  • For blood coagulation
A

CALCIUM

181
Q

Ca is evaluated with phosphorus for

A

BONE METABOLISM

182
Q

T/F. Ca is MAJOR INORGANIC COMPONENT of the osseous tissues (bone)

A

TRUE

183
Q

T/F. Presence of calcium cannot activate enzymes in coagulation cascade

A

False, can activate enzymes in coagulation cascade

184
Q

Absorbed in the upper Small Intestine in the presence of

A

Vitamin D (Active Form)

185
Q

Percentage of Ca that found in bones and teeth

A

99%

186
Q

Percentage of Ca that found in blood and ECF

A

1%

187
Q

Ca DISTRIBUTION IN BLOOD through:

A

IONIZED
PROTEIN BOUND
COMPLEX

188
Q

Physiological ACTIVE form of calcium (UNBOUND/FREE FORM)
45% of total Calcium in the plasma

A

IONIZED

189
Q

Attached to a protein (Albumin – protein transporter)
40% of Total Calcium

A

PROTEIN BOUND

190
Q

Bound to ANIONS (opposite charge)
Ex: Bicarbonate, Phosphate, & Lactate
15% of Total Calcium

A

COMPLEX

191
Q

What are the FACTORS AFFECTING CALCIUM LEVEL IN THE BLOOD?

A

BONE RESORPTION
BONE DEPOSITION
INTESTINAL ABSORPTION

192
Q

Bone matrix destruction by the Osteoclast → calcium release in blood
Promoted by PTH, which mobilizes calcium from the bone to the blood

A

BONE RESORPTION

193
Q

Also known as Bone Mineralization (Bone formation)
Cause ↓ blood calcium level
Promoted by calcitonin (inhibits PTH and vitamin D activity)

A

BONE DEPOSITION

194
Q

Promoted by Vitamin D in the active form
Can INCREASE BONE RESORPTION

A

INTESTINAL ABSORPTION

195
Q

will result to the inhibition of PTH release

A

Presence of HYPERCALCEMIA

196
Q

will induce PTH secretion by the parathyroid gland to act on the bone & kidney, stimulating bone resorption and calcium absorption in the kidneys

A

Presence of HYPOCALCEMIA

197
Q

promotes:
PTH stimulates osteoclastic activity which releases Ca++ and HPO4-

A

In BONE

198
Q

promotes:
Absorption of Ca2+
Excretion of HPO4-
Activation of renal 1-a-hydroxylas

A

In KIDNEY, PTH

199
Q

coverts 25-OH Vitamin D to 1,25 (OH)2 Vit D (active form)

A

1-α-hydroxylase

200
Q

T/F. 1,25 (OH)2 Vit D, promotes Intestinal Absorption and Renal Reabsorption of Ca2+ and HPO4-

A

TRUE

201
Q

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.

A

First sentence is correct, Second sentence is incorrect
*Melanin can PROTECT us from it

202
Q

protection is low and is prone to skin disorders

A

Too low melanin

203
Q

excess melanin can block UV rays which leads to poor activation of available Vitamin D → prone to bone disorders

A

Too high melanin

204
Q

Reference range of Calcium

A

8.6-10 mg/dL

205
Q

CAUSES OF HYPOCALCEMIA

A

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

206
Q

CAUSES OF HYPERCALCEMIA

A

Primary hyperparathyroidism
Malignancy
Multiple Myeloma
↑ Vitamin D
Thiazide diuretics (↑ Ca reabsorption)
Prolonged immobilization (↑ resorption)

207
Q

What are the tube and specimen needed for Specimen Collection of Calcium?

A

Serum, Plasma (lithium heparin), 24-hour urine

208
Q

T/F. Hemolysis cause False ↑

A

TRUE

209
Q

REFERENCE METHOD for Calcium and Magnesium

A

AAS

210
Q

uses liquid membrane electrode

A

ISE

211
Q

used for the colorimetric measurement of serum calcium

A

Ortho-cresolphthalein complexone (CPC)

212
Q

Colorimetric Method for Ca

A

Arsenzo III dye

213
Q

chelating agent for calcium

A

EDTA Titration method

214
Q

Ex. of chelating agent for calcium

A

BACARA, Gower, Sobel

215
Q

(Redox Titration method)
- Precipitation of Calcium as Calcium Oxalate(CaC2O4)
- CaC2O4 + H2SO4 → oxalic acid (H2C2O4)
- H2C2O titrated with KMNO4 → PINK COLOR

A

Clark and Collip

216
Q

(Precipitation with Chloranilic acid)
- Ca2+ + Sodium chloranilate → Ca Chloranilate
- Ca Chloranilate + EDTA → Chloranilic acid

A

Ferro and Ham

217
Q

MAJOR INTRACELLULAR ANION
Component of phospholipids, nucleic acids, creatine phosphate and ATP

A

PHOSPHATE

218
Q

Phosphate in diet is MAXIMALLY absorbed in the jejunum

A

SMALL INTESTINE

219
Q

Percentage of Phosphate in bones

A

85%

220
Q

Percentage of Phosphate in extracellular environment

A

15%

221
Q

found in many parts of tissues/cells

A

OMNIPRESENT

222
Q

T/F. Growth Hormone increases renal excretion of phosphate

A

False, decreases renal excretion

223
Q

T/F. The level of phosphate is INVERSELY RELATED TO CALCIUM

A

TRUE

224
Q

T/F. In the kidneys through the action of the PTH, calcium is absorbed while phosphate is excreted.

A

TRUE

225
Q

FORMS OF PHOSPHATE IN CELLS

A

ORGANIC
INORGANIC

226
Q

Inside the cell; the principal anion in the cell

A

ORGANIC

227
Q

Outside the cell; blood buffer present in the plasma or serum
The one measured in tests

A

INORGANIC

228
Q

CAUSE OF HYPOPHOSPHATEMIA

A

Hyperparathyroidism (↑ renal excretion)
Vitamin D Deficiency or antacid use (↓intestinal absorption)

229
Q

CAUSE OF HYPERPHOSPHATEMIA

A

Hypoparathyroidism
Lymphoblastic leukemia, intensive exercise, neoplastic disorders
Hypervitaminosis

230
Q

What are the tube and specimen needed for Specimen Collection of Phosphate?

A

Serum, Plasma (lithium heparin), 24-hour urine

231
Q

T/F. Hemolysis cause False ↑

A

TRUE

232
Q

Absorbance of (340 nm)

A

Ammonium phosphomolybdate complex

233
Q

Fiske-Subbarow Method
Reducing agent:

A

Pictol (Amino Naphthol Sulfonic acid)

234
Q

Fiske-Subbarow Method
Other reducing agents:

A
  • Elon or Methyl Amino Phenol
  • Ascorbic acid
  • Senidine or N-Phenyl-PhenyleneDiamineHyrochloride
235
Q

Anion that is an INDICATOR of severity of oxygen deprivation (hypoxia)
BYPRODUCT of anaerobic metabolism and mechanism in the body

A

LACTATE

236
Q

Marker for low/deficient oxygen in tissues:

A

INCREASED LACTATE

237
Q

INSIGNIFICANT because it shows normal O2 levels

A

DECREASED LACTATE

238
Q

What are the 2 types of LACTATE ACIDOSIS?

A

Hypoxic Conditions (Type A)
Metabolic Origin (Type B)

239
Q

Causes of Hypoxic Conditions (Type A)

A

Lactate Acidosis
Shock, MI, Severe CHF
Pulmonary edema, severe blood loss

240
Q

Causes of Metabolic Origin (Type B)

A

DM, severe infection, leukemia, liver, or renal disease
Toxins (ethanol, methanol or salicylate poisoning)

CC and HISTO PLEASE LAST NA (4 decks)

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