Electrolytes Part 3 PDF

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Summary

Bone and Minerals- Bones function to support the body and maintain homeostasis. - Osteoblasts, synthesize bones and are high in ALP. - Osteocytes, synthesize a small amount of matrix for bone integrity. - Osteoclasts, reabsorb bone and break down bone tissue to release bone minerals. - Bone Remodell...

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MLSC-3111, Clinical Biochemistry II Bone and Minerals -

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Bones function to support the body and maintain homeostasis. Osteoblasts, synthesize bones and are high in ALP. Osteocytes, synthesize a small amount of matrix for bone integrity. Osteoclasts, reabsorb bone and break down bone tissue to release bone minerals. Bone Remodelling, the process of bone reabsorption coupled with bone creation and destruction. Parathyroid Hormone, produced in the parathyroid. Activates osteoclasts in the bone to release calcium. Stimulates renal calcium reabsorption back into the blood in exchange for phosphorus. Stimulates the gut to reabsorb calcium. Released in low calcium and inhibited in high calcium. PTH increases calcium, decreases phosphorus and activated vitamin D. Calcitriol, active hormone from vitamin D. Increases calcium and phosphorus reabsorption in the intestines and kidneys. In the bone, it enhances the effects of PTH. Calcitonin, activates osteoblasts to retain calcium and deposit it into new bone tissue. Inhibits PTH and VITD to decrease calcium levels.

Parathyroid Disorders -

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Hyperparathyroidism, excess release of PTH by one or more parathyroid glands. Complications include osteoporosis and kidney stones. o Primary Hyperparathyroidism, increased PTH caused by parathyroid glands  Adenoma, benign tumour on one or more parathyroid glands.  Hyperplasia, enlargement of one or more parathyroid glands.  Parathyroid Malignancy, malignant tumour of the parathyroid glands. o Secondary Hyperparathyroidism, increased PTH due to insufficient plasma calcium which stimulates the excessive PTH.  Severe Calcium Deficiency, insufficient calcium intake.  Renal Failure, decreased calcium from loss in urine with increased phosphorus from lack of excretion.  Vitamin D Deficiency, causes calcium to not be fully absorbed. Deficiency due to lack of sunlight.  Calcium Malabsorption, GI disorders. Lab results include high serum and urine calcium with low serum and high urine phosphorus. Hypoparathyroidism, deficiency of PTH. Much less frequent than hyperthyroidism. Complications include tetany and paresthesia. Causes include: o Removal of parathyroid glands, during thyroid surgery. o Extensive Radiation Treatment, to the face and neck. o Autoimmune Disorders, damages all parathyroid glands.

MLSC-3111, Clinical Biochemistry II

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o Hungry Bone Syndrome, PTH decreases suddenly after treatment of hyperparathyroidism. The body has gotten used to the high calcium and upon successful treatment, the bones start to pull in calcium very quickly. Results in low calcium. o In Newborns, from hypoparathyroidism mothers. o Low Blood Magnesium, normal MG levels required for optimal PTH secretion. Lab results include low serum and urine calcium with high serum phosphorus and low urine phosphorus (remains in the serum since there is no calcium to excrete in urine).

Calcium -

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Most common mineral in the human body. Used as a cofactor, bone and teeth constituents and used in vasoconstriction and in muscle contraction. The reference interval for calcium is 2.20 – 2.80 mmol/L. The amount of calcium in the ECF is very small compared to how much is found in the bone. Calcium is a critical care test and can be ordered STAT. Bound Calcium, calcium that is bound to either albumin or complexed with anions Unbound Calcium, free calcium that is also known as ionized calcium. Calcium implies the measurement of both bound and ionized calcium. Ionized calcium is a measurement of only the ionized calcium. Free ionized calcium (ICAL) is the physiologically active form of calcium. PTH only regulates ionized calcium. It doesn’t matter how much bound calcium there is, the body will only respond to ionized calcium. Most labs only measure TCAL and not ICAL. Hypercalcemia, occurs at calcium levels > 2.80 mmol/L. Greater than 3.00 mmol/L are critical. Seen in primary hyperthyroidism and: o Malignancy, may cause patients to release PTH-related protein, which the body thinks its PTH and it will react accordingly. o Excessive Na+ Reabsorption, seen in Conn’s disease. Kidneys reabsorb Na+ over CAL and causes an increase loss of CAL in the urine. o Overconsumption of Calcium o Renal Failure o Paget’s Disease, seen as a high ALP level. o Milk-Alkali Syndrome, ingestion of large amounts of calcium together with absorbable bicarbonate. o Hypothyroidism Hypocalcemia, calcium levels < 2.20 mmol/L. Levels < 1.75 mmol/L are critical. Seen in: o Primary Hypoparathyroidism o Chronic Renal Failure o Vitamin D Deficiency o Magnesium Deficiency, very low magnesium levels decrease the osteoclast’s responsiveness to PTH. Causes low calcium. o Insufficient Dietary Intake

MLSC-3111, Clinical Biochemistry II

Methods of Analysis -

Total Calcium, colorimetric measurement of calcium adapted to many automated analyzers. O-Cresolphthalein complexone with calcium makes a red complex proportional to the TCAL concentration. Ionized Calcium, use an ISE electrode which is costly and hard to use. Not available in all labs.

Sample Collection -

Total Calcium, serum or heparinized plasma may be used. Does not matter what kind of heparin tube. Must be separated from RBCs promptly to avoid uptake of calcium. Avoid hemoconcentration during collection. Blue top tubes chelate calcium to stop coagulation. They cannot be used since they remove all the calcium from the sample. Ionized Calcium, heparinized whole blood is used because it is required for chemical electrode analysis.

pH and Calcium -

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Sample must be protected from pH changes and collected anaerobically. Must transport on ice slurry and analyzed promptly. Tourniquet must be released within one minute. Leads to acid buildup and lowered pH. pH alters the binding of ionized calcium. They are inversely related. Low pH increases the amount of H+ in the tube. H+ displaces calcium that was bound to albumin, resulting in less bound and more ionized calcium (falsely elevated). An increase in pH causes the reverse effect on ionized calcium as the low pH scenario (falsely lowered). Many labs report the ICAL plus pH corrected ICAL. Using algorithms, the original ICAL can be calculated prior to the improper collection. Works well except in patients with acidbase balance issues. pH does not affect TCAL. Only the ratio of bound vs unbound is affected but there is still the same amount of total calcium present in the sample.

Albumin and Calcium -

High albumin results in more albumin available to bind with ionized calcium. Results in less free calcium to excrete through urine and an increased TCAL.

MLSC-3111, Clinical Biochemistry II -

Low albumin results in less albumin available to bind with calcium. Results in more free calcium to excrete through urine and a decrease in TCAL. In both cases, the ICAL stays the same. The body only regulates ICAL and when it is low or high it will react accordingly. If ICAL goes up, the body will excrete the excess through the urine. If albumin goes up, PTH will be released to release calcium from the bone to replenish the ICAL. Albumin has a direct relationship with TCAL, not ICAL. TCAL can be corrected for ALB levels. Corrected calcium = TCAL + [0.02 (47 – ALB in g/L)] The equation is recommended in the presence of abnormally low albumin levels. Also not used with high albumin. Calcium will be up if albumin is because usually its only caused by dehydration.

Phosphorus -

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Combines with other substances to form organic and inorganic phosphate compounds. The reference range for phosphorus is 0.80 – 1.40 mmol/L. Phosphorus exists as monohydrogen phosphate HPO42- and dihydrogen phosphate H2PO4- in the ECF. 1% of it is found in the blood. Inorganic phosphate is measured in the phosphorus lab assay. Organic phosphates inside cells are released and converted to inorganic phosphates via action of phosphatases. Hyperphosphatemia, levels > 1.45 mmol/L. Caused by: o Primary Hypoparathyroidism, low PTH. o Renal Failure, most common cause. Hypophosphatemia, levels < 0.85 mmol/L. Caused by: o Primary Hyperparathyroidism o DKA Treatment, insulin causes shift of phosphorus into cells.

Methods of Analysis -

Molybate Colorimetric Reaction, interfered by hemolysis because RBCS have high phosphorus (falsely elevated). Assay produces a blue colour proportional to phosphorus concentration and is read at 600 – 700 nm.

Magnesium -

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More critical than phosphorus and the second most abundant intracellular ion after K+. Functions as a cofactor in over 300 enzyme reactions and high magnesium depresses neuromuscular function. The human body contains 25g of Mg, with only 1% in the ECF and even less in the plasma. Concentration is 10x greater in RBCs than the plasma, so hemolyzed samples are rejected (falsely elevated). EDTA and Na Citrate chelate all metals including Calcium and Magnesium (falsely lowered). Hypermegnesemia, > 1.00 mmol/L. Less frequent than hypomagnesemia.

MLSC-3111, Clinical Biochemistry II -

Becomes critical at > 4.00 mmol/L. High magnesium causes diarrhea, and as a result it is the active ingredient in laxative. Hypomagnesemia, magnesium is controlled by PTH to enhance renal and intestinal absorption of Mg when it is low. Chronic loss of Mg overtime results in parathyroid failure because it is needed for parathyroid function. Results in hypoparathyroidism and hypocalcemia. Seen in diabetes mellitus with glycosuria since Mg is excreted into the urine with glucose.

Methods of Analysis -

Total Magnesium, various colorimetric assays. Ionized Magnesium, ion selective electrodes.

Magnesium Clinical Application -

Magnesium sulfate is often administered during pregnancy to reduce pre-term contractions. Pre-eclampsia, presence of blood pressure, protein in the urine and severe edema during pregnancy due to low magnesium. Eclampsia, pre-eclampsia with the addition of seizures and convulsions. Magnesium sulfate is the treatment of choice in pre-eclampsia to prevent eclampsia. However, to much magnesium can also cause cardiac arrest. Results in many STAT magnesium orders from the maternity ward.

Acid Base Balance -

Arterial Blood Gas Testing, used to determine the amount of gas exchange levels in the blood related to lung function. This test only uses blood from the arteries and not the veins. However, if O2 status is not an issue, venous whole blood may also be used. Blood gas samples are STAT, critical and not easy to recollect. Patient status also changes overtime so they must be assayed quickly. Used most to determine pH, pCO2, pO2, and bicarbonate in the blood. Blood gas testing helps to evaluate: o Acid Base Status o Alveolar Ventilation o Oxygenation Status o O2 Transport o Presence of Abnormal Hemoglobins...