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 bodys 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; ATPasedependent 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
1

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
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 Bhydroxybutyrate)
Dec freezing point by 1.858C
Inc boiling point by 0.52C
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
Urine 24h
Urine/serum ratio
Random urine
Osmolal gap

275-295mOsm/kg
300-900mOsm/kg
1.0-3.0
50-1200mOsm/kg
5-10mOsm/kg

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
hypernatremia
Hyponatremia
Hypernatremia
Inc Na loss
inc Na intake or
Inc H2O
retention
retention
Excess water
Water imbalance
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
3

 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)
Diabetes insipidus - copious production of
dilute urine 3-20L/d
Hypernatremia - urine osmolality
<300mOsm/k 300>700mOsm/k
g
700mOsm/kg g
Diabetes
Partial defect Loss of thirst;
insipidus
in AVP
Insensible
release or
loss of h2o
response to
(breathing,
AVP;
skin);
Osmotic
GI loss of
diuresis
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; 23mmol/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
hypokalemia
Hypokalemia
Hyperkalemia
GI loss
Decrease renal
Renal loss
excretion
Cellular shift
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, Cushings 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
4

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, Addisons disease, diuretics
Cellular shift - acidosis, muscle/ cellular injury,
chemotherapy, leukemia, hemolysis
Increased intake - oral or IV K replacement
therapy
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 blood
3. Do not transport on ice and should be stored
in room temp

of GI losses,
RTA, metabolic
acidosis

vomiting,
diabetic
ketoacidosis,
aldosterone
deficiency. Saltlosing 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

(see table) Methods, reference range, specimen

Regulation
85% PT
15% DT

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 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

Clinical applications
Hypochloremia
occurs w/
excessive loss of
HCO3 as a result

Methods - Hco3 is used to decarboxylate PEP in the

presence of PEP carboxylase w/c catalyzes the
formation of oxaloacetate

Hyperchloremia
excessive loss of
Cl from
prolonged

(see table) Methods, reference range, specimen

5

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
Henles 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
hypermagnesemia
Hypomagnesemia
Hypermagnesemia
Reduced intake
Decreased
Decreased
excretion
Increased intake
absorption
Increased renal
Miscellaneous
excretion
Increased
excretion endocrine
Increased
excretion - drug
induced
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-ahydroxylase
6

 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)
15% bound to anions (HCO3, citrate, lactate)
Clinical applications - hypercalcemia and
hypocalcemia
Hypocalcemia
Hypercalcemia
Primary
primary
hypoparathyroidi
hyperparathyroidi
sm - glandular
sm - adenoma or
aplasia,
glandular
destruction or
hyperplasia
removal
Hyperparathyroid
Hypomagnesemi
ism
a
Benign family
Hypermagenese
hypocalciuria
mia
Malignancy
Hypoalbunimea
Multiple
(total only,
myeloma
ionized calcium
Increased vitamin
not affected by) D
chronic liver
Thiazide diuretics
disease, nephrotic Prolonged

syndrome,
malnutrition
Acute
pancreatitis
Rhabdomyolysis
Pseudohyypoarat
hyroidism (PTH
target tissue is
dec)

immunization

Severe hypocalcemia - below 1.88mmol/L

Mild 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
7

Clinical applications
Hypophosphatemia
Diabetic
ketoacidosis
Chronic
obstructive
pulmonary
disease
Malignancy
Asthma
Long term
treatment with
total parenteral
nutrition
IBD
Anorexia nervosa
Alcoholism
Increased renal
excretion Hyperparathyroid
ism
Decreased
intestinal
absorption vitamin d
deficiency or
antacid use
Severe hypo <1.0
g/dL or
0.3mmol/L

Hyperphosphatemia
Acute or renal
failure
Neonates - cows
milk or laxatives
Increased
breakdown of
cells
Severe infections
Intensive exercise
Neoplastic
disorders
Intravascular
hemolysis
Hypoparathyroidi
sm
Px with
lymphoblastic
leukemia are
SUSCEPTIBLE
to
hyperphosphatem
ia

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 (600700nm)
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
prognosis
Lactic acidosis
Type A
Type B
Hypoxic conditions
Metabolic conditions
Shock, myocardial
DM, severe infection,
infarction, severe
leukemia, liver or
CHF, pulmonary
renal disease and
edema, severe blood
toxins (ethanol,
loss
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 protein
2. Renal tubules
8

a)
b)
c)
d)

e)
f)

g)

Phosphate reabsorption - inhibited by PTH

and increased by 1,25-|OH|2, D; excretion
of PO4 is stimulated by calcitonin
Ca is reabsorbed by PTH and 1,25-|IH|2D3; calcitonin stimulates excretion of Ca
Mg reabsorption - thick ascending limb of
HENLES LOOP
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
Cl is reabsorbed by passive transport in PT
K is reabsorbed in
i. Active reabsorption in the PT almost
completely conserves K
ii. Exchange with Na is stimulated by
aldosterone
iii. H competes with K for this exchange
Bicarbonate is recovered from the
glomerular filtrate and converted to CO2
i. Henles 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.