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CC2 - Electrolytes August 12, 2014

Electrolytes ions capable of carrying an electric charge Classified as:

Anions - negative charge that move toward the anode

Cations - positive charge and move toward the cathode

Volume and osmotic regulation (Na, Cl, K) Myocardial rhythm and contractility (K, Mg,

Ca) Cofactors in enzyme activation (Mg, Ca, Zn) Regulation of ATPase ion pumps (Mg) Acid-base balance (HCO3, K, Cl) Blood coagulation (Ca, Mg) Neuromuscular excitability (K, Ca, Mg) Production and use of ATP from glucose (Mg,

PO4)

Water 40% - 75% average water content (values

declining with age and with obesity) Solvent for all processes in the human body Transports nutrients into and out of cells Removes waste products by urine Act as body’s coolant by way of sweating Located in the intracellular and extracellular

components Intracellular fluid - fluid INSIDE the

cells and accounts for about 2/3 of total body water

Extracellular fluid - the other 1/3 of total body water and is subdivided into: Intravascular ECF (plasma) Interstitial cell fluid - surrounds the

cells in the tissue Active transport - REQUIRES energy to move

ions across membranes; ATPase-dependent ion

pumps Passive transport - passive movement of

ions across a membrane Diffusion - passive movement of ions

across a membrane and depends on the size and charge of ions being transported

Most biologic proteins are freely permeable to water but NOT TO IONS or PROTEINS

Osmoregulator - concentration of ions and proteins on one side of the membrane, influence the flow of water across a membrane

Osmolality Concentration of solutes per kilogram of

solvent (millimoles/kg) Osmolarity - milliosmoles per liter;

inaccurate in hyperlipidemia or hyperproteinemia, urine specimens, alcohol or mannitol

Regulated by thirst sensation and AVP THIRST SENSATION - response to

consume more fluids and prevents water deficit; diluting elevated Na levels and dec osmolality of plasma

AVP - ADH; posterior pituitary gland;and acts on cells of collecting ducts; Inc reabsorption of water in kidneys; suppressed in excess H2O load; activated in water deficit

Water flow is influenced by: Osmotic effects of Na Proteins Ions Blood pressure

Clinical significance Measure function of pituitary gland Affects concentration of Na Blood volume

Osmolality is regulated by changes in H2O balance Volume is regulated by Na balance Normal osmolality - 275-295mOsm/kg 1-2% inc osmolality - 4x of AVP 1-2% dec osmolality - shuts your AVP Renal water regulation by AVP and thirst -

important roles in regulating plasma osmolality

Water load Excess intake of water - POLYDIPSIA Polydipsia decreases plasma osmolality AVP and thirst are suppressed AVP is absent - water is not reabsorbed Hyposmolality and hyponatremia -occur in

px with impaired renal excretion of water

Water deficit INC plasma osmolality/ Hypernatremia AVP and thirst are activated Signals thirst - major defense against

hyperosmolality and hypernatremia Hypernatremia - evident to infants,

unconscious px, unable to either drink or ask for h2o

Inc cause of dehydration Osmotic stimulation - diminishes < 60 year old Older patient with illness and diminished

mental status, dehydration DIABETES INSIPIDUS - no AVP , may

excrete 10L of urine per day; water intake matches output and plasma Na remains normal

Regulation of blood volume Adequate blood volumes is essential to

maintain blood pressure and good perfusion to all tissue and organs

Regulation of both Na and water is interrelated in controlling blood volume

RAAS responds primarily to decreased blood

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volume Renin is secreted near the renal glomeruli in

response to a decreased renal blood flow (in cases of dec BP and BV; CONVERTS angiotensinogen to angiotensin I - angiotensin II

Angiotensin II - causes vasoconstriction w/c quickly increases blood pressure retention of Na and water

Aldosterone - inc Na retention and H2O reabsorption

Changes in blood volume are detected by STRETCH RECEPTORS located in cardiopulmonary circulation, carotid sinus, aortic arch, glomerular arterioles

Stretch receptors - activates effectors that restore volume by varying resistance, cardiac output, renal Na and water retention; to constrict or restrict vascular activity

Factors affecting blood volume Atrial natriuetic peptide - released from

myocardial atria in response to volume expansion, promotes Na excretion in kidney (B type natriuretic peptide and ANP act together in regulating blood pressure and fluid balance); Inc Na excretion in kidney

Volume receptors independent of osmolality stimulate AVP release w/c conserves water by renal absorption

Glomerular filtration rate - inc w/ volume expansion and dec w/ volume depletion

Inc plasma Na = inc urinary Na excretion; N 98-99 of the filtered (conserved 150L of glomerular filtrate)

Urine osmolality - dec in D.I. (inadequate AVP) and polydipsia; inc in SIADH secretion and hypovalemia

Determination of osmolality Serum or urine Na, Cl, HCO3 - largest contribution to the

osmolality value of serum NOT Plasma - osmotically active subs may

be introduced from the anticoagulant

Discussion Inc osmolality - dec freezing point and

vapor pressure Freezing point depression and vapor

pressure decrease - two most frequently used methods of analysis

Specimens w/c are turbid should be centrifuged before analysis

Estimate the time osmolality by determining osmolal gap

Osmometers - operate by freezing point depression are standardized using NaCl reference solutions

Osmolal gap - difference between the measured osmolality and the calculated osmolality; indirectly indicates the presence of osmotically active substances (Na, urea, glucose, ethanol, methanol, ethylene, glycol, lactate, or B-hydroxybutyrate)

Dec freezing point by 1.858’C Inc boiling point by 0.52’C Dec vapor pressure (dew point) by

0.3mmHg Inc osmotic pressure by 17,000mmHg Main contributors are Na, Cl, urea, glucose

Formula:

Reference range: Serum 275-295mOsm/kgUrine 24h 300-900mOsm/kgUrine/serum ratio 1.0-3.0Random urine 50-1200mOsm/kgOsmolal gap 5-10mOsm/kg

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Sodium Determines the osmolality of the plasma To prevent equilibrium - active transport

systems like ATPase ion pumps are present in all cells

Na, K, ATPase ion pump moves 3 Na ions OUT in exchange for 2 K ions moving INTO the cell

Regulation Depends on intake and excretion of water Important 3 processes

Intake of water - stimulated or suppressed plasma osmolality

Excretion of water - affected by AVP release

Blood volume status - affects Na excretion through aldosterone, angiotensin II, ANP

60-75% - filtered Na is reabsorbed in PT ELECTRONEUTRALITY - maintained by

Cl reabsorption or H secretion Some is reabsorbed in the loop and DT

Clinical applications - hyponatremia and hypernatremiaHyponatremia Hypernatremia Inc Na loss Inc H2O

retention Water imbalance

inc Na intake or retention

Excess water loss

Decreased water intake

1. Hyponatremia - less than 135mmol/L Increase Na loss - can occur with:

hypoadrenalism, diuretic use (thiazide), ketonuria (na lost with ketones), salt losing nephropathy, prolonged vomiting or diarrhea

Increased h2o retention - causes dilution of serum/ plasma Na as with acute or chronic

renal failure, nephrotic syndrome and hepatic cirrhosis (plasma proteins are DECREASED = dec colloid osmotic pressure and edema results), CHF (inc venous pressure), Pag ang urine Na is >20mmol/d iyon

ay baka acute or chronic failure Pero pag ang urine <20mmol/d -

water retention maybe a result of nephrotic syndrome, hepatitis cirrhosis or CHF

Water imbalance - can occur with: polydipsia (excess H2o intake at kailangan daw muna maging chronic bago maging water imbalance and may cause mild to severe hyponatremia); SIADH - cause an increase in water retention b/c of INCREASE AVP production (defect in AVP production ay nalilink sa pulmonary disease, malignancies, CNS d/o, infections na gaya ng Pneumocystis carinii pneumonia) Pseudohyponatremia can occur if Na

is measured using indirect ISE in a px who is hyperlipidemic or hyperproteinemic; can be seen in in vitro hemolysis (common cause of false dec)

Ung indirect ISE kasi dilutes the sample prior to analysis and as a result of plasma/serum water displacement; ung ion levels daw ay nagdedecrease

Hyponatremia - can be classified according to plasma/serum osmolality (low osmolality, normal osmolality, high osmolality) Low osmolality - inc Na loss and

water retention Normal osmolality - result of high inc

in nonsodium cations High osmolality - associated w/

hyperglycemia

Symptoms 125 - 130mmol/L - GI Below 125mmol/L - neuropsychiatric (nausea,

vomiting, muscle weakness, headache, lethargy and ataxia)

Below 120mmol/L - Medical emergency

Treatment Fluid restriction and providing hypertonic

saline and other pharmacological agents Too rapid correction causes CEREBRAL

MYELINOLYSIS Too slow correction causes CEREBRAL

EDEMA Conivaptan - blocks the action of AVP in the

CD of nephrons thus decreasing h2o reabsorption; NOT FOR hypovolemic hyponatremia

Euvolemic hypernatremia is assoc with SIADH, hypothyroidism, adrenal insufficiency

Hypervolemic hyponatremia is assoc with liver cirrhosis with ascites, CHF, overhydrated postoperative px

2. Hypernatremia - inc Na conc; occurs in px who are unable to ask or obtain h2o like adults w/ altered mental status and infants Loss of hypotonic fluid - may occur either by

the kidney or through profuse sweating, diarrhea, severe burns

Loss of water - Diabetes insipidus, (Ung DI na hindi nagrerespond sa AVP, nephrogenic d.i. yun. Yun namang DI na impaired ung AVP secretion central DI); Renal tubular disease (acute tubular necrosis - unable to fully concentrate the urine)

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Diabetes insipidus - copious production of dilute urine 3-20L/d

Hypernatremia - urine osmolality<300mOsm/kg

300-700mOsm/kg

>700mOsm/kg

Diabetes insipidus

Partial defect in AVP release or response to AVP;Osmotic diuresis

Loss of thirst;Insensible loss of h2o (breathing, skin);GI loss of hypotonic fluid;Excess intake of Na

Chronic hypernatremia - indicative of hypothalamic disease

Reset osmostat - may occur on primary hyperaldosteronisml excess aldosterone induces mild hypercolemia that retards AVP release

Hypernatremia can also be from excess ingestion of salt or administration of hypertonic solutions (sodium bicarbonate or hypertonic dialysis)

Symptoms CNS - altered mental status, lethargy,

irritability, restlessness, seizures muscle twitching, hyperrefelexes, fever nausea, vomiting, difficult respiration and increased thirst

Treatment Correction of underlying condition Too rapid correction cause cerebral edema and

death

Potassium

Elevated K decreases RMP severe hyperkalemia - cause a lack of

muscle excitability leading to paralysis or fatal cardiac arrhythmia

Hypokalemia - increases EMP resulting to excitability or paralysis

Regulation Distal nephron - principal determinant of

urinary K excretion 3 factors that influence the distribution of

K K loss frequently occurs whenever

Na, K -ATPase pump is inhibited by hypoxia, hypomagnesemia, digoxin overdose

Insulin promotes acute entry of K into skeletal muscle and liver by inc Na K -ATPase activity

Catecholamines like epinephrine (B2 stimulator), promote cellular entry; propanolol (B blocker), impairs cellular entry

Exercise - inc plasma by 0.3 to 1.2mmol/L with mild to moderate exercise; 2-3mmol/L w/ exhaustive exercise; forearm exercise before veni

Hyperosmolality - in DM causes water to diffuse from the cells, carrying K w/ h2o leading to gradual depletion

Cellular breakdown - releases K into the ECF; severe trauma, tumor lysis syndrome, massive blood transfusions

Clinical applications - hyperkalemia and hypokalemiaHypokalemia Hyperkalemia GI loss Renal loss Cellular shift

Decrease renal excretion

Cellular shift

Decreased intake Increased intake, Artifactual

1. Hypokalemia - K concentration below ref range; can occur with GI loss (vomiting, diarrhea, gastric suction,

intestinal tumor, malabsorption, cancer therapy) Renal loss (diuretics, nephritis,

hyperaldosteronism, RTA, Cushing’s syndrome. Hypomagnesemia, acute leukemia)

Cellular shift (alkalosis) Decreased intake Inc cellular uptake of K - encountered in

alkalemia and w/ elevated levels of insulin via therapeutic treatment of diabetes

Alkalemia and insulin - inc K cellular uptake

Symptoms Weakness, fatigue, constipation - plasma K dec

below 3mmol/L Can lead to muscle weakness and paralysis Mild hypokalemia (3.0-3.4mmol/l) is

asymptomatic

Treatment Oral KCl replacement of K IV Chronic mild hypokalemia - corrected by

including food with high K content (dried fruits, nuts, bran cereals, bananas, orange juice)

2. Hyperkalemia - caused by dec renal excretion, cellular shift, increased intake, artifactual Dec renal excretion - acute or chronic failure,

hypoaldosteronism, Addison’s disease, diuretics Cellular shift - acidosis, muscle/ cellular injury,

chemotherapy, leukemia, hemolysis Increased intake - oral or IV K replacement

therapy

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Artifactual - hemolysis, thrombocytosis, prolonged tourniquet use or excessive fist clenching

Underlying d/o - DM, metabolic acidosis, renal insufficiency contributing to hyperkalemia

Impairment of urinary K excretion is usually associated with chronic hyperkalemia

Healthy persons: acute oral load of K will inc plasma K

Shift of K from cells into plasma occurs TOO RAPIDLY - acute hyperkalemia

DM - insulin deficiency and hypoerglycemia promotes cellular loss of K

Metabolic acidosis - excess H moves intracellulary, K leaves the cell for electroneutrality; plasma inc by 0.2- 1.7 mmol/L, treatment with insulin and bicarbonate causes severe hyperkalemia

Inc cellular breakdown dahil sa trauma, administration of cytotoxic agents, massive hemolysis, tumor lysis syndrome, blood transfusions

Symptoms Muscle weakness - does not develop until

plasma K reaches 8mmol/L Tingling Numbness Mental confusion Cardiac arrhythmias and possible cardiac arrest

Treatment Should be initiated when K is 6.0 - 6.5 mmol/L

or greater or if there are ECG changes Ca2+ provides immediate but short-lived

protection to the myocardium against theeffects of hyperkalemia

Sodium bicarbonate, glucose or insulin Renal function is adequate = sodium

polystyrene sulfonate

hemodialysis

Collection of samples 1. Thrombocytosis -use heparinized tube 2. Tourniquet - proper care in drawing blood3. Do not transport on ice and should be stored in room temp (see table) Methods, reference range, specimen

Chloride Chloride shift - CO2 generated by cellular

metabolism within the tissue diffuses out into both H2CO3 which splits into H and HCO3

Deoxyhgb - buffers H, whereas HCO3 diffuses out into the plasma and Cl diffuses into the red cell to maintain electric balance

Clinical applicationsHypochloremia Hyperchloremia occurs w/

excessive loss of HCO3 as a result of GI losses, RTA, metabolic acidosis

excessive loss of Cl from prolonged vomiting, diabetic ketoacidosis, aldosterone deficiency. Salt-losing dse (Pyelonephritis)

(See table) Methods, reference range, specimen

Bicarbonate Total CO2 - HCO3, H2CO3, dissolved

co2, with hco3

Total co2 measurement is indicative of HCO3 measurement

Carbonic anhydrase in RBC converts CO2 and H2O to H2CO3

Regulation 85% PT 15% DT

Clinical applications Metabolic acidosis - decreased HCO3 METABOLIC ACIDOSIS - compensation by

hyperventilation lowering pco2 Elevated total CO2 concentrations - metabolic

alkalosis METABOLIC ALKALOSIS - HCO3 retained

with increased pco2 as a result of compensation by hypoventilation

Methods - Hco3 is used to decarboxylate PEP in the presence of PEP carboxylase w/c catalyzes the formation of oxaloacetate

(see table) Methods, reference range, specimen

Magnesium Average human body contains 1 mol or 24g of

Mg 53% - bone 46% - muscle, organs and other soft tissue <1% - serum and rbcs Mg present in serum 1/3 is bound to albumin;

2/3 (61%) is free or ionized; 5% is complexed with other ions (PO4 and citrate)

Free ion ang active sa katawan

Regulation Small intestine -20%-65% of dietary mg Controlled by kidney 25-30% - PCT

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Henle’s loop is the main regulatory site PTH - increases renal reabsorption and

enhances mg in intestine Aldosterone and thyroxine - increasing renal

excretion of mg

Clinical applications- hypomagnesemia and hypermagnesemiaHypomagnesemia Hypermagnesemia Reduced intake Decreased

absorption Increased renal

excretion Increased

excretion - endocrine

Increased excretion - drug induced

Miscellaneous

Decreased excretion

Increased intake Miscellaneous

1. Hypomagnesemia Reduced intake - poor diet, starvation,

prolonged mg-deficient IV therapy, chronic alcoholism

Decreased absorption - malabsorption syndrome, laxative abuse, neonatal

Increased excretion-renal -- tubular d/o, glomerulonephritis, pyelonephritis

Increased excretion - endocrine -- hyperparathyroidism, hyperaldosteronism, hypercalcemia, diaetic ketoacidosis

Increased excretion-drug induced -- diuretics, antibiotics, cyclosporin, digitalis

Other - pregnancy, excess lactation

Symptoms Cardiovascular - arrhythmia, hypertension,

digitalis toxicity Neuromuscular - weakness, cramps, atazia,

tetany, paralysis, coma Psychiatric - depression, agitation,

psychosis Metabolic - hypokalemia, hypocalcemia,

hypophosphatemia, hyponatremia

Treatment Oral intake of mg lactate, mg oxide, mg cl

or an antacid with Mg, Mgso4 - taken parenterally,

2. Hypermagnesemia Decreased excretion - acute or renal failure

(GFR <30mL/min), hypothyrodism, hypoaldosteronism, hypopituitarism (dec GH)

Increased intake - antacids, enemas, cathartics, therapeutic - eclampsia, cardiac arrhythmia

Miscellaneous - dehydration, bone carcinoma, bone metastases

Symptoms Cardiovascular - hypotension, bradycardia,

heart block Dermatologic - flushing, warm skin GI - nausea, vomiting Neurologic - lethargy, coma Neuromuscular - decreased reflexes,

dysthartia, respiratory depression, paralysis

Metabolic -hypocalcemia Hemostatic - decreased thrombin

generation, decreased platelet adhesion

Treatment Discontinue the source of Mg Supportive therapy Hemodialysis

Specimen Nonhemolyzed serum Plasma -lithium heparin Oxalate, citrate, EDTA - NOT ACCEPTABLE 24hr urine - must be acidified with HCl

(See table) Methods, reference range, specimen

Calcium Decrease ionized Ca ca cause neuromuscular

excitability = irregular muscle spasms called tetany

Regulation PTH

in bone: BONE RESORPTION stimulates osteoclastic activity w/c releases Ca and HPO4

in kidney: promotes absorption of Ca, excretion of HPO4, activation of renal 1-a-hydroxylase

decrease in ionized ca stopped by increased ca

Calcitonin - originates in the medullary cells and is secreted when Ca conc increases; inhibits action of PTH and Vitamin D; in response to hypercalcemic stimulus

VITAMIN D3- cholecalciferol; obtained from the diet or exposure of skin of sunlight; converted to 25-OH-D3 -- 1.25-|OH2|D3 (in intestine: promotes intestinal absorption of ca and HPO4 and enhances PTH on bone resorption

Distribution 99% - bone 1% - blood and other ECF 45% circulates as free Ca ions 40% bound to protein (albumin)

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15% bound to anions (HCO3, citrate, lactate)

Clinical applications - hypercalcemia and hypocalcemiaHypocalcemia Hypercalcemia Primary

hypoparathyroidism - glandular aplasia, destruction or removal

Hypomagnesemi a

Hypermagenese mia

Hypoalbunimea (total only, ionized calcium not affected by) - chronic liver disease, nephrotic syndrome, malnutrition

Acute pancreatitis

Rhabdomyolysis Pseudohyypoarat

hyroidism (PTH target tissue is dec)

primary hyperparathyroidism - adenoma or glandular hyperplasia

Hyperparathyroidism

Benign family hypocalciuria

Malignancy Multiple

myeloma Increased vitamin

D Thiazide diuretics Prolonged

immunization

Severe hypocalcemia - below 1.88mmol/LMild hypercalcemia - 2.62 to 3.00 mmol/L is often asymptomatic Moderate to severe Ca elevations Bisphophonate - lower Ca levels

Treatment of hypocalcemia Oral or parenteral therapy of Ca Vitamin D

Treatment of hypercalcemia Primary hyperparathyroidism -

asymptomatic estrogen replacement - lowers Ca

Parathyroidectomy Reduce ca levels Aalt and water intake to inc Ca excretion

and avoid dehydration Thiazide diuretics Bisphosphonates - main drug to lower Ca

levels

Specimen Serum Lithium heparin plasma collected without

venous stasis EDTA, oxalate NO Anaerobic sample Urine acidified with 6mol/L HCL Dry heparin

Methods Orthocresolphthalein complexone - uses 8

hydroxy quinoline to prevent Mg interference

Arsenazo dye III ISEs for ionized Ca AAS

Phosphate Found everywhere in living cells DNA and RNA are complex

phosphodiesters ATP, creatine phosphate, PEP Phosphate deficiency leads to ATP

depletion Inorganic phosphate is regulated by the

kidney

Regulation Absorbed in the intestine Released from cells into blood Lost from bone Vitamin d, calcitonin, GH, acid-base status can

affect renal regulation of phosphate Renal excretion or reabsorption of phosphate PTH - lowers blood concentrations by

increasing renal excretion Vitamin d - increase phosphate in the blood Growth hormone - regulate skeletal growth

Distribution 12 mg/dL Most is organic 3-4mg/dL is inorganic phosphate Phosphate is predominant in the intracellular

anion 80% bone 20% soft tissues <1% plasma/serum

Clinical applicationsHypophosphatemia Hyperphosphatemia Diabetic

ketoacidosis Chronic

obstructive pulmonary disease

Malignancy Asthma Long term

treatment with total parenteral nutrition

IBD Anorexia nervosa Alcoholism Increased renal

Acute or renal failure

Neonates - cow’s milk or laxatives

Increased breakdown of cells

Severe infections Intensive exercise Neoplastic

disorders Intravascular

hemolysis Hypoparathyroidi

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excretion - Hyperparathyroidism

Decreased intestinal absorption - vitamin d deficiency or antacid use

Severe hypo <1.0 g/dL or 0.3mmol/L

Px with lymphoblastic leukemia are SUSCEPTIBLE to hyperphosphatemia

Specimen Serum Lithium heparin plasma Oxalate, citrate, EDTA NO Avoid hemolysis 24hr urine samples

Methods Formation of ammonium phosphate

molybdate complex 340nm Reduced to form molybdenum blue (600-

700nm)

Lactate By productt of an emergency mechanism that

produces a small amount of ATP Pyruvate is the normal end product of glucose

met

Regulation Oxygen delivery decreases, blood lactate rises

rapidly and indicate tissue hypoxia Liver is the major organ for removing lactate

by converting lactate back to glucose - gluconeogenesis

Clinical applications Useful for metabolic monitoring of ill px Useful for indicating severity of illness Useful for objectively determining px

prognosisLactic acidosis

Type A Type B Hypoxic conditions Metabolic conditionsShock, myocardial infarction, severe CHF, pulmonary edema, severe blood loss

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

(See table) Methods, reference range, specimen

Methods Enzymatic methods

Lactate + O2 ===> pyruvate + H2O2

H2O2 + H donor ===> colored dye + 2H2O

Anion gap Routine measurement of electrolytes

usually involves Na, K, Cl, HCO3 Difference b/w unmeasured anions and

unmeasured cations Calculated by the concentration difference

b/w measured anions Useful in indicating an increase in one or

more of the unmeasured anions in the serum and also as a form of quality control

Calculating AG:Ag2+ = Na - (Cl + HCO3)

Equivalent to unmeasured anions minus the unmeasured cations in this way:

(PO4 + 2SO4) -( K +2Ca + Mg) reference range for this is 7-16mmol/L

Ag = (Na + K) - (Cl + HCO3) Reference range is 10-20mmol/L ELEVATED AG - uremia/ renal failure leading

to PO4 and SO4 retention; ketoacidosis (seen in starvation/ diabetes); methanol, ethanol, glycol, salicylate poisoning; lactic acidosis hypernatremia and instrument error

LOW AG - reare, hypoalbuminemia (decreased in unmeasured anions), severe hypercalcemia (increased unmeasured cations)

Electrolytes and renal function Kidney is the central regulation and

conservation of electrolytes in the body 1. Glomerulus - portion of nephron, FILTER; retain large proteins and protein bound constituents; should be equal to the ECF without protein2. Renal tubules

a) Phosphate reabsorption - inhibited by PTH and increased by 1,25-|OH|2, D; excretion of PO4 is stimulated by calcitonin

b) Ca is reabsorbed by PTH and 1,25-|IH|2-D3; calcitonin stimulates excretion of Ca

c) Mg reabsorption - thick ascending limb of HENLE’S LOOP

d) Sodium reabsorption i. 70% Na in the filtrate is reabosrbed in

PT by iso-osmotic reabsorption ii. Na is reabsorbed in exchange for H

and is linked with HCO3 and depends on carbonic anhydrase

iii. Stimulated by aldosterone, Na is reabsorbed in exchange for K in the DT

e) Cl is reabsorbed by passive transport in PT f) K is reabsorbed in

i. Active reabsorption in the PT almost

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completely conserves K ii. Exchange with Na is stimulated by

aldosteroneiii. H competes with K for this exchange

g) Bicarbonate is recovered from the glomerular filtrate and converted to CO2 i. Henle’s loop: with n AVP function,

creates an osmotic gradent that enables water reabsorption to be inc or dec in response to body changes in osmolality

ii. Collecting ducts: also under AVP influence, this is where final adjustment of water excretion is made.