Electrolytes

Introduction to Electrolytes

Electrolytes are essential charged ions that play a pivotal role in numerous physiological processes within the body. They are fundamental for maintaining fluid balance, facilitating the transmission of electrical impulses throughout the nervous system, and enabling the effective contraction of muscles, including those in the heart.

Key Functions of Electrolytes

Electrolytes encompass a variety of ions, each with unique and vital functions in the human body:

Potassium (K+): This major intracellular cation is crucial for maintaining normal heart rhythms and is heavily involved in muscle contractions. It helps regulate cellular functions and is important for normal functioning of nerve cells.
Sodium (Na+): As the primary cation found outside of cells, sodium is key to controlling osmotic pressure and fluid balance. It plays a significant role in the transmission of nerve impulses, making it essential for proper nervous system function.
Calcium (Ca2+): This mineral is indispensable for bone and teeth health, muscle contractions, and the release of neurotransmitters at synapses. Calcium levels must be carefully regulated for functional integrity in these systems.
Chloride (Cl-): Acting in concert with sodium, chloride helps maintain osmotic pressure and contributes to the regulation of the body's acid-base balance, impacting overall metabolic functions.
Magnesium (Mg2+): This mineral is a cofactor in over 300 enzyme reactions, including those involved in muscle contractions and nerve impulse conduction. Magnesium is vital for energy production and helps maintain stable nerve function.

Blood Volume and Plasma Levels

The relationship between blood volume and plasma electrolyte levels is complex and crucial for overall health. Electrolyte imbalances can result in significant changes in blood volume, affecting blood pressure and bodily function. The kidneys serve as essential regulators of this electrolyte balance, filtering blood and reabsorbing necessary ions to maintain homeostasis. Additionally, the endocrine system contributes to this regulation through hormones, such as aldosterone, which enhances sodium reabsorption and modulates potassium excretion, thus influencing blood pressure and electrolyte levels systematically.

Clinical Significance

The monitoring of serum electrolyte levels is vital for effectively assessing an individual’s health status. Abnormal levels of these ions can indicate various underlying medical conditions. For instance, Potassium (K+) is critical for cardiovascular health, and imbalances can lead to dangerous arrhythmias. Similarly, Sodium (Na+) is essential for fluid balance, where both excess and deficiency can manifest in serious symptoms such as confusion or seizures. Electrolytes are also integral in calculating osmolarity and determining the anion gap, both of which are essential for diagnosing acid-base disorders that could threaten homeostasis.

Reference Ranges and Clinical Manifestations

Understanding the reference ranges for serum electrolytes is essential for accurate diagnosis of various health conditions. The typical reference ranges are as follows:

Sodium: 135-145 mmol/L
Potassium: 3.5-5.1 mmol/L
Calcium: 8.8-10.3 mg/dL
Chloride: 90-106 mmol/L
Magnesium: 1.6-2.6 mg/dL
Phosphorus: 2.8-4.5 mg/dL When these electrolytes deviate from their normal ranges, specific clinical manifestations may arise, which can provide critical information about potential health issues that need to be addressed.

For osmolality of the blood. So it when we talk about osmolality, it is the physical property of resolution that is based on the concentration of the solute. So it is usually expressed as millimoles per kilogram of or weight over weight. So parameters to which the hypothalamus response. So depends on the osmolality of our our body.

Homograxyhypothalamus. So it always affects the sodium concentration in the plasma. So the following are the responses to changes in the blood osmolality. So, when it comes to our or when it comes to hyper osmolality, our brain will release some electrical electrical electrical signals.

6:33

Yes. Electrical signals from the hypothalamus releasing ADH. Releasing ADH. Retain or excrete and the potassium will be excreted. So all of that for the maintenance or maintain blood osmolality and also the blood will function will be coming from the brain or specifically our hypothalamus.

7:07

So the balance between the number of cations and anions in both extracellular and intracellular fluid compartments is known as your electro neutrality. So so, again, it will release ADH sodium and so that the potassium will be excreted. And, also, it will be it will be needed or another function that our electrolytes are involved is when it comes to the or the renin neem angiotensin system. Yeah. So renin angiotensin system.

8:00

So the kidney will release the renin that will be needed for the for the conversion or for the activation to angiotensin one. Then your your counts will release the acetylcholine esterase, no, which is the enzyme responsible for for the activation angiotensin one to become angiotensin two blood pressure. Yeah. So blood pressure. Yeah.

8:38

Then, also, another another function will be coming from our heart in which our heart will release your alpha or ALP. The al alpha natriuretic peptide in which our renal sodium and water excretion that will result to vasodilation. Yeah. Vasoconstriction for for for that is involved for renin or the raasnate. And then for the osmolarity it will be coming from your ADH.

9:27

So it's created by your hypothalamus. Yeah. So for for osmolarity, so we have two sodium plus glucose and m cheaper d l divided by 20 plus b u n mg per d l divided by three. And 1.86 sodium plus glucose divided by 18 plus b u n divided by 2.8 plus. So references reference range for us.

10:04

We have $4.00 275 to 495 per kilogram. For urine, we have 300 to 300 per kilogram. For urine, serum ratio, one point zero to three point zero. For random urine, 50 to 1,200 per kilogram. For osmol, we have five to ten milliosmol per kilogram.

10:36

The physiologic response when it comes to the increased ACF, Latin, or extracellular fluid that affects our, PLASMOS modality. So first, we have the antidiuretic hormone or reciprocillin released by hypothalamic chemoreceptors. Yeah. So hypothalamus ADH or antidiuretic hormone, it will result to sodium retention in potassium excretion. So so when it comes to our blood osmolality.

11:17

Then stimulation of the hypothalamic thirst center with the function Alright. Yes. Yes. So Then redistribution of water from the intracellular fluid compartment. So we go with the distribute water from the intracellular fluid compartment.

11:39

So for the regulation ECM volume, so regulation of sodium or glomerular filtration rate. So 70% of sodium is reabsorbed by the earlier parts of the renals we use. And as for our aldosterone, the of the kidneys will release the renin that will convert angiotensinogen to angiotensin one. Then to to convert our angiotensin one to angiotensin two, the will release the acetyl co acetyl co ACEN enzyme activate angiotensin one to angiotensin two that will stimulate adrenal cortex to produce aldosterone and promote retention of sodium and excretion of your potassium. So regulation for the extracellular fluid.

12:44

For the disorders of water balance, first, we have the hydration. So the hydration will be coming from two sources. So maybe pure water loss or deficit. So it leads to increased extracellular fluid osmolality solutes water. So it compensates by recruiting water from the ICF.

13:11

So water from the intracellular fluid with lalapas into the extracellular fluid, and it will lower total body water, but total body sodium remains normal. So as for the water and sodium loss, so it will result to hypovolemia that is readily so melting water and sodium plus it will result to hypovolemia. Then, also, we have I overhydration. And so water so it will result to excessive reabsorption of your water. Yeah.

13:54

So let's proceed with the electrolytes. So what are electrolytes? Electrolytes are ions that carry an electrical charge. So they may be an ion or cation depending on the charge electrolytes. So, again, now when it comes to electron neutrality, it will talk about the balance between the number of cations and alions in both intracellular and extracellular fluid compartment.

14:23

So, again, balance intracellular and extracellular, both cation and anion, and that is electro neutrality. So the dissociation of solutes into charged particles depends on the chemical composition of the compound and on the concentration of the of other charged particles in the region. So for the regulation electrolyte, so we have active transport and diffusion. So for active transport mechanism that requires energy to move ions across cellular membranes. For diffusion is a passive way of movement of ions across a membrane.

15:10

So active in diffusion. So functions, we have volume and osmotic fibrillation, myocardial rhythm and contractility, cofactors and enzyme regulation enzymes, the regulation of adenosine triphosphate or ATP's iron pump, the acid base balance, blood coagulation, neuromuscular excitability, and production and use of ATP from glucose. An iron gap. For the an iron gap, it refers to the difference between the sounds of the concentration of the principal cation, which is sodium and potassium, and of the principal anion, which is chloride and bicarbonate. So for the formula for for computation and ion drops, so we have mojo minus your chloride plus your bicarbonate.

16:20

And a normal value is 10 to 14 millimoles per liter. Yeah. Another formula for the computational is we have sodium plus potassium minus chlor chlorine plus bicarbonate. So normal value is 10 to 18 millimoles per liter. Yeah.

16:53

So what are the different clinical conditions that is aligned when it comes to increase iron gas. So first, we have uremia. No? So uremia. Next, we have ketoacidosis, starvation, or diabetes.

17:13

Methanol, aspirin, or ethylene glycol poiseling, severe hydration, and also lactic acidosis. For decrease on ion Kaplan, we have multiple myeloma, protein, and instrument error. So let's discuss further the different electrolytes that we that we usually test under the laboratory. So first, we have the sodium. So sodium is the major cation in the extracellular fluid, and it plays so, again, sodium is a cation.

So major major cation in the ECF. So outside cell. So it plays a central role in maintaining the normal distribution of water and osmotic pressure in the ECF compartments. And so ACF push, and it plays the role of maintaining the normal distribution of water and osmotic pressure. And, also, for the renal regulation for our blood pressure.

18:30

So for the vasoconstriction and vasodilation, they will be needing the or it it will play a bigger part, you know, when it comes to vasoconstriction and vasodilation. Principal osmotic particle outside the cell and for every 100 milligrams per d l increase in blood glucose, serum sodium decreases by 1.6 millivolts per liter. Yeah. So the more increase blood glucose, so 100 milligrams per decrease by 1.6 millimoles per liter. So for the regulation blood blood sodium levels, so first, it will be regulated by our diet.

19:31

Yes. So diet So, also, it is regulated by your kidney via the system or the or which is the renal threshold for our in which 110 to 130 millimoles per liter the the. So 70 to 80% is reabsorbed at the proximal convoluted tubule. Yeah. So, again, via the system or the really angiotensin system that release aldosterone.

20:06

So to release aldosterone. Now, also, we have the atrial natriuretic factor. Again, so a and f natin. It is an endogenous antihypertensive agent natin secreted from the cardiac atria. So it is produced by the atrial myocardium that promotes natriuresis and relaxation of the vascular smooth muscle.

20:33

And I I forgot to mention that your is what also called as your natrium. So rium Natrium. No? So it will promote for our a and f. So for the relaxation of to promote that pleurosis and relaxation of the vascular smooth muscle.

21:03

So for a and f passive. So passive in a way block aldosterone and saline secretion to inhibit the action of angiotensin two and vasopressin. So release BP or blood pressure So our heart will release your atrial natriuretic factor blood pressure. So blood pressure. Yeah.

21:41

So it will promote experiences and relaxation of vascular smooth muscle. Yeah. So as for the, it will increase or it will result to increased BP or blood pressure. ANF so passive or diffusion. So k?

22:11

So okay. So conditions that is related to the concentration of our sodium levels. So first, we have the hyponatremia. So hyponatremia is an electrolyte disturbance in which the sodium concentration in the serum is lower than the normal. Now from the limb itself, no hypo then So low levels So low sodium levels So hyponatremia is defined as a serum level of less than 135 milliequivalents per liter and is considered severe when the serum level is below 135 milliequivalents per liter.

22:58

Yeah. So yeah. So yeah. So memorize reference ranges for our for our for our flights hyper. So so so hypo. Yeah.

Yeah. So below, less than 135 milliequivalents per liter, and it is considered as hyponatremia. So causes of hyponatremia includes the following. So the main causes so first, we have increased sodium loss, increased water retention, and nighttime water imbalance. So for increased water retention, it's usually seen when it comes to renal failure, nephrotic syndrome, aldosterone, hypoadrenalism.

24:07

So hypoadrenalism for it aldosterone, potassium deficiency, diuretic use, ketonuria, soft dosing nephropathy, prolonged vomiting or diarrhea, and severe burns. For increased water retention, we have renal failure, nephrotic syndrome, hepatic cirrhosis, and congestive heart failure. Yeah. We also have myasthenia, drug intake, the Rocky Mountain spotted fever, and let's check the rock. Sorry.

24:50

Good result too. Hyponatremia. Also, we have water imbalance such as excess water intake in s I a v h and pseudohypohyponatremia. So causes of hyponatremia. So first, the use of your diuretics and also the syndrome of inappropriate ADH secretion or s I a d h.

25:27

So secrete ADH. So secrete ADH, it will result to sodium retention sodium retention. So inappropriate secretion. So current loss of, sodium because of increased, increased secretion ADH. Then aldosterone deficiency secondary to Addison's disease.

26:01

Yeah? So when it comes to aldosterone, it will be a evaluate or factor k? So so Borger syndrome is a rare condition wherein sodium chloride grid gradients cannot form in the loop of Henle because of the retention of chloride ion that is not available or the contract to your. Then diabetic hyperosmolar stigmatine, it causes reflux of cellular water with con consequent osmotic dilution of serum sodium. Other causes of hyponatremia includes congestive heart failure, azathemia, burns, and vomiting.

26:50

Causes hyponatremia. Then symptoms of hyponatremia, so one hundred twenty five to one hundred thirty millimoles per liter, north meat, gastrointestinal part, yeah, Or down the GI tract. So below 125. Cost is neuropsychiatry. So it will result to nausea and vomiting, muscular sickness, headache, lethargy, and ataxia.

27:31

Severe symptoms, comma, and respiratory depression. And below one twenty millimoles per liter for forty eight hours or less, no, it will result to acute hyponatremia that is considered as a medical emergency. Next, we have pseudohyponatremia. So for pseudohyponatremia, it is the reduction in serum sodium, cause of fusion caused by systematic error in measurements. So most common cause is in vitro hemolysis.

28:10

In vitro hemolysis. So when the RBCs since positive NA positive. Yeah. So So RBC, yeah, it will be diluted. Yeah.

28:50

So pseudo hyponatremia. How far in vitro hemolysis? Mark hemolysis may cause decrease sodium levels due to dilutional effect. Then hemoglobin released from the RBCs caused additional reduction in serum sodium similar to hyperprotelemia. So, also, artifact hyponatremia is also associated with hyperlipidemia and hyper protein and lipids causing it or causing our sodium to be falsely decreased.

29:32

And, also yeah. So, usually, it occurs active measurement is or measurement method for our sodium levels is indirect ion selective electrodes. Yeah. So indirect ion selective and. We have hypernatremia.

For hypernatremia, it is characterized by increased plasma sodium. So wherein hypernatremia more than 145, minimums per liter concentration of our sodium. So it is caused by loss of water, gain of sodium, or both. No? So it's either water intake or loss of water or increase sodium intake So it is a serum sodium concentration above the upper limit of the reference.

30:38

So symptom setting of hyperlatremia when it comes to your CNS, so there will be altered mental status, letter g, irritability, restlessness, seizures, muscle itching, hyper reflexes, fever, nausea, vomiting, difficult respiration, and increased thirst. One hundred sixty millimoles per liter sodium levels. It will be associated with mortality rate of sixty to seventy five percent. So so hypernuclear is usually caused by, again, loss of water, clean of sodium, or wood. So usually occur unless thirst mechanism is impaired.

31:33

So perspiration and breathing will result in one liter water loss or per day in adults. Yeah. So or water loss per day. One liter water loss per day in adults. Okay.

31:59

So causes of hypernuclein includes excess water loss, decreased water intake, and increased intake or retention. So excess water loss, we have diabetes and sipidus. Renal tubular disorder, prolonged diarrhea, pupus, profuse sweating, severe burns. Decreased water intake, in older persons, infant's mental impairment for increase intake or retention, hyperaldosteronism, sodium bicarbonate excess, and dialysis fluid excess. So for the causes of hypernatremia, we have, again, diabetes insipidus and hyperaldosteronism and hyperadrenocorticos or adrenocorticism.

32:54

Yeah. Adrenocorticism. So for the methods of determination for sludge and methods, we have ion select ion specific electrodes, atomic absorption spectrophotometry, flame emission spectrophotometry, emission flame photometry, and colorimetric method is Albany's name. Combine sodium with zinc uranyl acetate, sodium uranyl acetate precipitate, then we're going to add water, produce a yellow solution. Then so as for our ISEs, so this is the diagram for sodium ISA with glass capillary membrane.

33:44

So So for our sodium electrode, internal reference electrode, which is usually a glass. Yeah. It has a plastic body, an internal feeding solution, plastic clip, and a video wire to connect for. So, yeah, so for the schematic diagram of the ISE system for the potentiometric slide on the Vitros. Mhmm.

34:21

So upper slide mouse. So it will be spreading layer when it comes to our dry slide in which it will be basis is remove contaminants that there such as your proteins. Yeah. Also, contain your paper bridge, your iron selective membrane that contain methyl monos monosine, your reference layer that contains your sodium chloride and buffer at pH 5.6. Then next layer, we have the silver and silver chloride layer, support layer, and the lower slide mouth.

35:16

Reference interval. Have again one thirty five to one forty five millimoles per liter for. Forty to two hundred twenty millimoles per liter for urine, and 130 to 150 millimoles per liter for your CSF. So, again, so less than one thirty five. So less than one thirty five.

35:47

Hyponatremia. Hyponatremia more than one forty five demands. One more than one forty five. That is hypernatremia. Hyper natally.

36:07

So levels in the body into our body system. Next, we have potassium. For potassium for your potassium, it is otherwise known as your calcium. So calcium. Calcium.

36:40

Calcium potassium. Its function includes regulation of your neuromuscular excitability, contraction of the heart, intracellular fluid volume, and hydrogen ion selection. Yeah. So major intracellular cation. Mhmm.

36:59

So cation. Oh, yeah. Major intracellular cadion. Yes. The option cells.

37:24

And that your sodium also, potassium is cation. Yeah. So positively charged that is found on the intracellular fluid. So, also, it is the single most important analyte in terms of an abnormality being life threatening. So it will result to life in that situation.

37:56

Yeah. So around fifty fifty patient quoting or quitting potassium. So for the regulation of potassium, so we have the sodium potassium ATPase pump that is fueled by oxidative energy that transports potassium to the cell against concentration gradient. For the diffusion of our potassium, so potassium out of the cell into the ACF and plasma to that will further result to the decreased pump activity. So there will be depletion of metabolic substrate.

38:40

Example, if there will be production of glucose or consumption of glucose for ATP production and competition for ATP between the pump and other energy consuming activities. So slowing of cellular metabolism, passive diffusion when it comes to making the making potassium out of the excess intracellular or extracellular fluid. Yeah. Conditions conditions that medical conditions for potassium, we have first hyperkalemia. So it is a zero potassium concentration above the upper limit to the reference interval.

39:34

So more than five more than 5.1 millimoles per liter. No? More than about more than 5.1 millimoles per liter, that is considered as hyperkalemia. So hyperkalemia is seen in the following condition. So first, we have hydration, diabetes insipidus, hypoadrenalism, acidosis, and hemolysis.

40:10

For symptoms of hyperkalemia, so we have muscle weakness, tingling numbness, or mental confusion by altering neuromuscular conduction. And hyperkalemia disturbs cardiac conduction that will affect your cardiac arrhythmias and possible cardiac arrest. So for electrocardiogram, man, it will or six to seven millimoles per liter may may alter the electrocardiogram. And, also, more than ten millimole per liter may cause fatal cardiac arrest. So or potassium levels it will cause, fatal cardiac arrest.

41:08

So causes of hyperkalemia, decreased renal excretion, acute or chronic renal failure, hypoaldosteronism, Addison's disease, diuretics. For cellular shift, it includes acidosis, muscle or cellular injury, chemotherapy, leukemia, hemolysis, increased intake of oral or IV potassium replacement therapy, artifactual. We have sample hemolysis, thrombocytosis, and prolonged coronary use or excessive fins fist clenching. For hypokalemia potassium. So, usually, it starts with less than three point five millimoles per liter or for critical levels is two point five millimoles per liter.

42:03

So it is a serum potassium concentration below the lower limit of the reference interval. It is seen in the following conditions. So infusion of insulin to diabetics, alkalosis, vomiting, overhydration, new cell flow, diuretics, syndrome of inappropriate ADH secretion. So because of ADH secretion. Parker's syndrome, it is condition whose primary cause is the excess excretion of potassium.

42:47

In terms of hypokalemia, again, less than three millimoles or 3.1 or 3.5 per liter, no adding potassium levels will result to weakness, fatigue, constipation. It can also lead to muscle weakness or paralysis. Sudden death would be caused by arrhythmia. Causes of hypokalemia, we have GI loss, vomiting, diarrhea, gastric suction, intestinal tumor, malabsorption, cancer therapy, chemotherapy, radiation therapy, large doses of laxatives. For renal losses, we have diuretics, thiazides, mineralocorticoids, nephritis, renal tubular acidosis, hyperaldosteronism, Cushing's syndrome, hypomagnesemia, acute leukemia, or cellular shift, you have alkalosis, insulin overdose, and also decreased intake of your potassium.

43:52

For hypokalemia, acute myelogenous leukemia, acute myelomonocytic leukemia, and acute lymphocytic leukemia. Analytical methods, we have ISEs is the method of choice method, and atomic absorption spectrophotometry and flame emission spectrophotometry. Since this type of analyte is easily excited. So it it is actually excited flame emission spectrophotometry here. For our ISP membrane, polynomial gel, which is a routine method for termination of actin potassium.

44:44

As for our colorimetry, we can use lockhead and Purcell, reagent added sodium, cobalt cobalt t nitride, which yield to blue color blue coloration. Reference interval is 3.5 to 5.1 millimoles per liter for plus 3.5 to 4.5 per liter. For female, three point four to four point four millimoles per liter. For yearly, '24 using twenty four hour yearly, there will be twenty five to one hundred twenty five millimoles per day that that is normally present in a twenty four hour yearly. Next, we have chloride.

45:38

For chloride, dyspezure, extracellular, iron together with sodium. And they present the majority of this osmotically active constituent of P plus one. So ACF anion. So your chloride is negatively charged. Yeah.

46:02

So negatively charged chloride. And it maintains electrical neutrality, further regulation of fluid content of the body and its influence in the kidney. Again, it will be the chief counterion sodium in the extracellular fluid. So your fluoride is also found in the extracellular fluid together with your sodium. So it promotes maintenance of water balance and smoothed pressure in conjunction with sodium and which is an enzyme activator and maintains electrolyte.

46:47

So it is the only an ionatin that serve as an enzyme activator. So, usually, your chloride is being excreted in the urine and sweat, and these orders of chloride are the same as sodium since they both they are both extracellular cations. So for the concentration, it is influenced by your aldosterone. Conditions affecting chloride level chloride concentration in the body. So first, we have your hyperchloremia.

47:28

So hyperchloremia can be seen the following conditions. First, we have the atrial, renal tubular acidosis, acute renal failure, and metabolic acidosis associated with prolonged diarrhea. For hypochlorine minimal is seen in prolonged vomiting, prefeed sweating, increased gastric juice secretion, soft dosing, nephritis, and Addison's disease. For analytical methods, Nathan, you have your ISEs or ion selective electrode, mercury metric titration, skills skills method, colorimetric method that uses mercury thiocyanate and ferric nitrate to form a reddish convert complex with a peak at 480 nanometers, collometric, amperometric titration on the cutoff, chloridometer. Methods for the termination chloride.

48:26

Yeah. For the specimen causing the ratio so, of course, in any electrolyte determination, of course, more hemolysis, it may cause decreased levels of chloride due to dilutional effect since ECF chloride. For for potential for in cases of marked hemolysis, there will be an increase. No? Increase in or false increase, no, in the concentration of our potassium.

49:00

So slightly lower values are observed in postprandial specimen nantin, and low serum values are expected with high bicarbonate levels. Reference interval is in normal serum concentration is 90 to 106 millimoles per liter, and linear output is 110 to 250 millimoles per liter. For calcium level, next, we have calcium. So calcium level is the fifth most common element and most prevalent cation in the human body. And so, like, for your sodium and potassium, it's also positively charged.

49:42

And fifth most common element and most prevalent in the human body. So it is present almost exclusively in the plasma, and it is involved in blood coagulation, enzyme activity, excitability of skeletal and cardiac muscle, and maintenance of your blood pressure. It is maximally absorbed in the duodenum, and absorption is favored at an acidic pH. So increase intestinal pH or alkaline pH pH when it comes to our blood, it will reduce calcium absorption. So 99% of our calcium is part of the bones, and 1% is in the extracellular fluid and soft tissues.

50:30

And so most of our calcium bone bone 1% extracellular fluid and soft tissues. So symptoms of severe hypocastin in which our total calcium will result to less than seven point five milligrams per ml. So, again, for for the function, now adding calcium, it is important for skeletal mineralization since most of our calcium will be found or 99% of our calcium will be found on your bone. So it plays a vital role in blood coagulation, neural transmission, enzyme activity, maintenance of normal tone, excitability of skeletal and cardiac muscle. So it is involved in glandular cell disease and regulation of exocrine and endocrine glands, and it preserves the cell membrane's integrity and permeability, particularly in terms of sodium and potassium exchange.

51:35

As for the regulation, calcium levels, so we have the following hormones that affect plasma calcium levels. So first, we have the one twenty five. We have one twenty five dihydroxy cholecalciferol. Calciferol that increases intestinal absorption of our so that increases the intestinal absorption of our calcium. So increase absorption of of our calcium in the intestine.

52:17

And, also, it it increases reabsorption of our calcium in the kidneys. So for the intestine so calcium will be absorbed, then reabsorbed when it comes to our kidneys. So increases mobilization of calcium from our bones. So next hormone that we have, the parathyroid hormones or the PTH. So PTH will conserve calcium by increasing the absorption in the kidneys.

52:56

Yeah. Sorry. Absorption of our conserved calcium by increasing the absorption in the kidneys. Yeah? So absorption of our calcium, excretion of our phosphate, and activation of our renal one alpha hydroxyls.

53:22

Then, also, it activates the process of bone resorption suppresses urinary loss of calcium. Calcium the thyroid gland increase. No? In cases of PTH Then convertion of inactive vitamin d to active vitamin d in the kidneys. As for the calcitoline, yeah, so calcitoline, the mannatum is secreted by the parafollicular c cells of the thyroid gland.

54:11

Mhmm. So that is found at the anterior part of the or thyroid gland thyroid gland. That secretes calcitonin. So calcitonin is a hypocalcinic factor or hormone. No?

54:33

In in cases of acid. Wrapped. Sorry. So one twenty five o h hydroxychloroquine. Hang on.

54:53

One twenty five o. Two would be three or the vitamin It will promote positive absorption or increase increase calcium. One twenty five n PTH. Calcitonin is a diffusion. No?

55:15

So in cases of increase calcium increase calcium thyroid gland calcitonin. Calcitonin. From the thyroid gland calcitonin from the thyroid gland inhibit function the vitamin d on one twenty five o h two. Release enough So for the calcitonin, it will inhibit the PTH and vitamin three d three and inhibits bone resorption and promotes urinary excretion of. For the regulation, first, we have the PTH or parathyroid hormone.

56:24

The secretion in blood is stimulated by decrease in ionized calcium. And, conversely, PTH secretion is stopped by increase in the ionized calcium. So calcium ionized calcium secrete parathyroid gland parathyroid hormone ionized calcium. Then ironized calcium PTH hormone, which is the function of your calcitonin. So in the code, PTH activates classes known as your bone resorption in which activated o ostrac class break down bone and subsequent calcium into the ECM.

57:17

So in the kidneys, PTH content conserves calcium by increasing tubular absorption of calcium ions, and it also stimulates renal production of your active vitamin D. Yeah. So produce calcium. For the vitamin D or the cholecalciferol, it is obtained from the diet or exposure of skin to sunlight. So vitamin three, b three, or biologically active form is one twenty five dihydroxycholicalciferol.

57:58

So it, the active form of your vitamin D increases calcium absorption in the intestine and enhances the effect of your PTH on bone resorption. And so, again, vitamin D and your and your PTH will be your primary hormone for primary hormone to increase calcium reabsorption Then for the calcitoline will be our passive hormone in which the function acetylcytine is to inhibit the function of your PTH and vitamin D. So release PTH and active form vitamin D produce further calcium. So, again, is secreted by your parafenicular cells, c cells, though found in your thyroid gland or thyroid gland that is secreted when the concentration of your calcium in the blood increases. Calcium secretes thyroid gland calcitonin to to lower the concentration of your calcium.

59:24

So calcitonin exerts its calcium lowering effect by inhibiting the actions of both your PTH and vitamin D. So that's secreted during normal regulation of the ionized calcium concentration in blood, and it is secreted in response to a hypercalcemic stimulus. For distribution, we have 50% in the form of your free or ionized form, but the plasma protein, we have 40%, and complex form of calcium is 10%. Medical significance, increased calcium levels are seen in periods of rapid growth in children, pregnancy, and lactation. Decreased calcium level is seen in old age.

60:09

Factors in calcium levels, increased calcium absorption, and decreased calcium absorption. For increased calcium absorption, vitamin d, which is the major stimulus of calcium absorption. Also, include hormone and increased dietary protein. For decreased calcium absorption, formation of insoluble salts with phosphorus, phytic acid, dietary oxidate, fatty acids, and cortisol. Another factor that will influence calcium levels, will be increased urinary calcium excretion such as your hypercalcemia, phosphate deprivation, acidosis, and glucocorticoid.

61:01

For the diminished urinary calcium excretion, have PTH and certain diuretics and vitamin D. Hypercalcemia is a condition characterized by increased syndrome calcium level. It is associated with anorexia, nausea, vomiting, constipation, hypnotosia, depression, and comma, so causes hypo hypercalcemia is have primary hyperthyroidism, multiple endocrine neoplasia, familial hypercalcemia, vitamin D intoxication, thyrotoxicosis, hypoadrenalism, multiple myeloma. Hypocalcemia, in a man, is a condition represents by a low serum calcium level. Severe hypoglycemia will eventually lead to tetanus.

62:02

So causes of hypocalcemia includes the following. So have hypoparathyroidism, pseudohypoparathyroidism, deficiency in vitamin D or its metabolite, chronic renal failure, have hypomagnesemia, and acute pancreatitis. For the analytical methods for determination of total calcium, have spectrophotometric analysis with the metallochromic indicators that we usually or we both by the use indicators that are on for tocrysotelin complex zone and arseno arsenazo three. Then titration of fluorescent calcium complex with ethylene diamine tetraacetic acid or ethylene glycol tetraacetic acid. Atomic absorption spectrophotometry, Clarke and Collip method, induction infusion method.

63:04

And for ionized calcium, have ISVs or ion selective for calcium. Reference interval, plus point zero, half 8.8 to ten point three milligrams per d l for total calcium in adults, four point six to five point three milligrams per d l, and is calcium in adults. For urine, three hundred milligrams per day is normal seen in adults. Is a essential electrolyte for the function of cellular enzymes and energy metabolism. So it has an important role in membrane stabilizing short, nerve conduction, and iron transport, and calcium channel activity.

63:54

It also plays an important role in maintenance of intracellular intracellular potassium concentration. So as per the regulation of our, the Hindus loop of hemi loop of Henle is a major renal regulatory site for our magnesium in which 50 to 60% of filtered magnesium is reabsorbed in the descending limb of Henle. So renal threshold for magnesium is approximately 0.6 to 0.85 millimoles per liter. For the parathyroid hormone that then increases the renal reabsorption of magnesium and enhances the absorption of magnesium in the intestine. As for our loserone and tyrosine, it has an opposite effect on the PTH or viral hormone hormone in the kidney, therefore, increasing the renal excretion of magnesium.

64:58

Hypermagnesemia is a cognition with high level of serum magnesium in which increased magnesium level in the blood is very neutrophilic. So elderly and patients with bowel disorder and renal insufficiency are the most addressed. So clinical manifestations include hypotension, bradycardia, respiratory depression, depressed mental status, and electrocardiographic abnormalities. For causes of hypermagnesemia, decreased excretion, acute or chronic renal failure, hypothyroidism, hypoaldosteronism, hypopitrism, or decreased food hormone, increased intake, antacids, enemas, cathartics, therapeutic, or when it comes to eclampsia, cardiac arrhythmia, miscellaneous dehydration, bone carcinoma, and bone metastasis. For symptoms of hypermagnesemia, cardiovascular, neurovascular.

66:06

For cardiovascular, we have hypertension, bodycardia, heart block, dermatologic, flushing, warm skin, GI, nausea, vomiting, neurologic, vomiting, comma, for neuromuscular crease reflexes dysarthria, respiratory depression, paralysis, metabolic hypocalcemia, hemostatic, decreased thrombin, generating heart, and decreased platelet adhesion. For hypophobalgysmia, it's a condition with a low serum level. So the most common cause of hypomagnetic polycythemia are loss of magnesium in the GI tract as in chronic diarrhea and malabsorption steatorrhea, diabetes mellitus, secondary to glycosuria, and osmotic laryngitis, alcohol, and stress. So for the causes of hypomagnesemia, will be due to the reduce intake of your magnesium, decrease absorption, increase excretion in the renal or in the kidney, increase excretion in when it comes to endocrine, increase excretion, drug induced and miscellaneous, such as your excess lactation and pregnancy. As for the symptoms of hypomagnesemia, we have the following cardiovascular and psychiatric symptoms.

For analytic methods, we have total magnesium is being analyzed using atomic absorption spectrophotometry, which is the reference method, but is not particularly done in the clinical laboratory. Photometric methods on automated analyzers, these methods employ or employ metallochromic indicators for dye, such as Galmagide, Pharmazan dye, Pagon, and Titan yellow dye. For ionized or free magnesium, we have ion selective electrode formulation. Basically, testing your intracellular magnesium, fluorescence measurement using Furapta magnesium binder, and the PR magnetic resonance spectrophotoscopy and your ion selective microelectrode and your electro probe microanalysis. Yeah.

68:35

For the reference interval, 1.6 to 2.6 milligrams per l and 0.66 to 1.07 milligrams per liter. Phosphorus is an important constituent in anapnic acid. Phospholipid, and phosphoproteins. It forms high energy compounds such as a p and cofactor, NADP, and is involved in intermediary metabolism and various enzyme systems. So it is essential for muscle contractility, neurological or neurologic function, electrolyte transport, and oxygen carrying by hemoglobin.

69:44

Hyperphosphatemia is a condition characterized by serum phosphorus level or concentration above the upper limit of the reference interval. So usual causes are decreased renal excretion, acute and chronic renal failure, increased intake of with excessive oral and rectal intravenous administration, increased extracellular load due to transcellular shift in acidosis, secondary to over medication with vitamin D and production of vitamin bigranulomatous tissue. For hypophosphatemia, it is condition characterized by serum phosphorus concentration below the lower limit of the reference interval. So it can be seen in alcohol abuse, intestinal loss due to vomiting, diarrhea, and use of phosphate binding antacids induced by shift of phosphorus from central cellular fluid into cells, increased urinary excretion, secondary to hyperparathyroidism, renal tubular defects, and diuretic therapy. Decreased intestinal absorption is observed in malabsorption and vitamin D deficiency in steatorrhea.

71:04

For the analytical methods, we have this to borrow the reaction of phosphate with ammonium molybdenum, reduction of phospho molybdenum two, which can be measured at 600 to 700 nanometers spectrophotometrically. And, also, we have enzymatic methods that will be used for the termination of our date phosphorus. Reference interval in adult, you have two point eight to four point five milligrams per TL. In children, four point zero to seven point zero milligrams per TL. For the electrolyte and renal function, so for the renal tubules, Latin phosphate absorptions inhibited by your PTH and increased by one twenty five dihydroxy polycalciferol or the active form vitamin D.

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So for the excretion of your phosphate, this is stimulated by calcitriol. So the same with the same goes with your or calcium. So calcium is reabsorbed under the influence of PTH and one twenty five dihydroxycal hydroxycholicalciferol as for our calcitonin, stimulates excretion of your calcium. Then magnesium reabsorb or reabsorption occurs largely in the thick ascending lip of Henle. Then for chloride limines absorb in part by passive transport in the proximal tubule along with the concentration gradient and created by your.

72:01

for the excretion of your phosphate, this is stimulated by calcitriol. So the same with the same goes with your or calcium. So calcium is reabsorbed under the influence of PTH and one twenty five dihydroxycal hydroxycholicalciferol as for our calcitonin, stimulates excretion of your calcium. Then magnesium reabsorb or reabsorption occurs largely in the thick ascending lip of Henle. Then for chloride limines absorb in part by passive transport in the proximal tubule along with the concentration gradient and created by your.