ANIONS KEYTERMS

 Major extracellular anion ; eliminated through sweating

Chloride
 2nd to Na and HCO3 movement
ECF  2nd most abundant anion in ECF
Bicarbonate
 Major component of buffering system of the blood
Lactate  Byproduct of glycolysis (anaerobic metabolism)
 Predominant ICF in anion; omnipresent
 Circadian rhythm - highest in late morning, lowest in evening
ICF Phosphorus/ Phosphate
 In genetic materials (DNA&RNA are phosphodiesters), coenzymes ( phosphoric/pyrophosphoric
acid) , reservoir of biochemical energy, affects 2-3 bishphosphoglycerate
CATIONS
 Most abundant cation in ECF
Sodium
 Hormones: Aldosterone, Atrial natriuretic peptide, Angiontensin
ECF
Calcium  5th most common element
Zinc
 Major intracellular cation; 1st most abundant in ICF
Potassium
 Inverse relationship with Sodium
ICF  4th most abundant cation in the body; 2nd in ICF
Magnesium
 Cofactor (300) for enzyme activity
Zinc

VOLUME AND OSMOTIC REGULATION MYOCARDIAL RHYTHM AND CONTRACTILITY

1. Sodium 1. Potassium
2. Chloride 2. Magnessium
3. Potassium 3. Calcium
COFACTORS IN ENZYME REGULATION REGULATION OF ATPASE ION PUMP
1. Magnesium 1. Magnesium
2. Calcium
3. Zinc
ACID-BASE BALANCE BLOOD COAGULATION
1. Bicarbonate 1. Calcium
2. Potassium 2. Magnesium
3. Chloride
NEUROMASCULAR EXCITABILITY PRODUCTION AND USE OF ATP FROM THE GLUCOSE
1. Potassium 1. Magnesium
2. Calcium 2. Phosphorus/Phosphate
3. Magnesium

SODIUM
Hyponatremia (Decreased)
Hypernatremia (Increased) 125-130 mmol/L – GI
<125 mmol/L - neuropsychiatric symptoms
<120 mmol/L – medical emergency
 Diabetes insipius  Hypoadrenalism
 Renal tubular disorder  K deficiency ( inverse relationship)
Excess water  Prolonged diarrhea/Profuse sweating/Vomiting/Severe Increased Na  Diuretic use that targets Na
loss burns loss  Ketonuria
 Salt losing nephropathy
 Vomiting/ Diarrhea/ Severse burns
 Older persons  Renal failure
 Infants  Nephrotic syndrome/ hepatic
 Mental impairment Increased cirrhosis (edema)
Decreased
water  Aldosterone deficiency
water intake
retention  Cancer
 Severe of inappropriate ADH
secretion
 Hyperoaldosteronism  Excess water intake (polydipsia,
Increased  Sodium bicarbonate infusion Water polyphaga, polyuria
intake/retention  Hyperadrenocorticism imbalances  SIADH
 Pseudohyponatremia
URINE OSMOLALITY
Increased Decreased
Low Diabetes Insipidius Increased sodium loss and water retention
a. Partial defect in AVP release a. Inc. non sodium ions
Normal
b. Osmotic diuresis b. Lithium excess
 c. Inc. gamma globulins
d. Severe hyperkalemia/hyercalcemia/ proteinemia
e. Pseudohyponatremia
a. Loss of thirst a. Hyperglycemia
High b. Insensible loss b. Mannitol infusion
c. GI loss of hypotonic fluid
Treatment ( hyponatremia) Methods
1. Sodium replacement 1. Ion selective electrode – routine
2. Fluid restriction 2. Atomic absorption spectrophotometry
3. Giving hypertonic saline 3. Flame emission spectrophotometry
4. Colorimetry
5. Chemical method (outdated)

CHLORIDE
Hyperchloremia Hypochloremia
 GI losses  Vomiting
 Hyperchloremic acidosis (RTA)  Diabetic ketoacidosis
Loss of Cl
 Metabolic acidosis  Alosterone deficiency
Excess loss of
HCO3  Salt losing nephritis (Pyelonephritis)
Low  High serum HCO3 (Compensated respiratory
serum acidosis/ metabolic alkalosis)
level of Cl
Determination Method
 Serum, Plasma, 24h urine 1.Ion selective electrode
Sample  Sweat(thick&sticky) – for cystic fibrosis, 2.Coulorimetric-amperometric titration (silver bind to Cl)
chromosal 7 disorder 3.Mercuric titration (schales-schales) chloridometer
Anticoagulant Lithium Heparin (green) 4. Digital chloridometer

PHOSPHATE
Hyperphosphatemia Hypophosphatemia
 Increased intake  Inc. renal excretion
 Increased release of cellular phosphate  Hyperparathyroidism
 Neonates  Dec. intestinal absorption
 Inc. in intestine – from food  Vit. D deficiency
 Inc. in bone - storage  Antacid use ( med for heart burn)
 Vitamin D - promote absorbtion&reabsorption  Dec. in kidney – excreted and absorbed
 Growth hormone -decrease renal excretion  Parathyroid hormone ( PTH) – renal excretion

Determination Types of phosphates

1. Total PO4 – 12mg/dl
Sample Serum & 24H urine 2. Organic – 8-9mg/dl
3. Inorganic PO4 – 3-4mg/dl
Anticoagulant Lithium Heparin Method Fiske-Subbarow – shows blue colored product

LACTATE
Regulation Types of Lactic Acidosis
Major organ that removes lactate (gluconeogenesis;  Hypoxic conditions
lactate->pyruvate->acetyl coenzyme)  Shock, severe blood loss
Liver  Aerobic – produce 38 mol ATP Type A  Congestive heart failure
 Anaerobic – produce 2 mol ATP  Pulmonary edema

Determination  Diabetes mellitus

1. Lithium heparin – placed in ice  Severe infection, toxicity
Type B
Anticoagulant 2. Iodoacetate & fluoride – inhibit glycolysis without  Leukemia
affecting coag.  Liver and renal disease
Enzymatic method
Method  Lactate oxidase – to form pyruvate
 Peroxidase – produce colored product

POTASSIUM
Hyperkalemia Hypokalemia (<3mmol/L)
  Acute/chronic renal failure  Vomiting, Diarhhea
 Hypoaldosteronism  Gastric suction
 Addison’s disease Gastrointestinal  Intestinal tumor
Decreased renal excretion
 Diuretics loss  Malabsorption
 Cancer therapy
 Laxative
 Acidosis  Diuretics(inhibit water excretion) –
 Muscle/cellular injury thiazides
 Chemotherapy  Nephritis
Cellular shift  Leukemia Renal loss  Renal tubular acidosis
 Hemolysis  Hyperaldosteronism
 Cushing syndrome & mineralocorticoids
 Hypomagnesemia
Increased Intake  Oral/Iv K+ replacement Cellular shift  Alkalosis and insulin overdose
 Hemolysis
Artifactual  Thrombocytosis Decreased Intake
 Fist clenching/tourniquet
1. Captopril – inhibits ACE Treatment for hypokalemia
2. NSAIDS – inhibit aldosterone 1. KCL replacement
3. Spironolactone - potassium 2. IV replacement
sparring diuretic
Drugs 4. Digoxin – inhibit Na-K pumps
5. Cyclosporine – Inhibit renal
response to aldosterone
6. Heparin – inhibit aldosterone
secretion
Determination Method
Sample Serum(0.1-0.7) , Plasma, 24 hour urine 1. Ion selective electrode with valincomycin gel
 Coagulation – release of K from platelets
Anticoagulant Lithium heparin

BICARBONATE
Enzyme Carbonic Anhydrase
Regulation Clinical Applications
Reabsorption of HCO3 as CO2 – semipermeable with Changes in HCO3 and Co2 levels
HCO3
 Proximal Convulating tubule – 85-90% of Acid-Base
Kidney
C02 reabsorbed imbalance
 Distal Convulating tubule – 15% of Co2
reabsorbed
Metabolic  Decrease of HCO3; lungs eliminate Co2
Methods
Acidosis  Kidney problem
1. Ion selective electrode - measure total C02, uses acid reagent  Increase HCO3 (retained) w/ pCO2; lungs retain
- Convert CO2 to CO2 gas Co2
Metabolic
2. Enzymatic Method – Convert all forms of O2 to HCO3  Hypoventilation, vomiting, hypokalemia, excessive
Alkalosis
(carboxylate phosphoenolpyruvate using PEP carboxylase) alkali intake
- Consumes NADH
Determination
Serum, Plasma Lithium Heparin
 Arterial can be used, collected anaerobically
Sample Anticoagulant
 Uncapped sample – HCO3 is converted to CO2
(deceased)

MAGNESIUM
Hypermagnesemia Hypomagnesemia
 Acute/chronic renal failure  Poor Diet/starvation
 Increased Intake  Prolonged magnesium
Decreased excretion  Antacids Reduced Intake  Deficient IV therapy
 Enemas  Chronic Alcoholism
 Cathartics
 Eclampsia  Malabsorption syndrome
Decreased
Therapeutics  Cardiac arrhythmia  Surgical resection of S.I
absoprtion
 Nasogenic suction
  Pancreatitis – LPS binds Mg
 Vomiting/Diarhhea/Laxative abuse
 Neonatal & Congenital– malabsoprtion
 Dehydration  Tubular disorder
Increased
Miscellaneous  Carcinoma  Glomerulonephritis
excretion-renal
 Bone metastasis  Pyelonephritis
Decrease renal function and high intake Increased  Hyperparathyroidism & hypercalcemia
Most severe
excretion-  Hyperaldosteronism
elavations
endocrine
Parathyroid hormone and Thyroxine  Diuretics
Increased
 Antibiotics
Hormone excretion-drug
 Cyclosporine
induced
 Digitalis
Symptoms Miscellaneous Excess lactation & pregnancy
Hypotension, bradycardia, heart block 1. Gentamicin, Diuretics, Cisplatin – inhibit
ability of renal to conseve Mg
2. Furosemide – Increase renal loss of Mg
3. Thiazide – Cause hypomagnesemia
Cardiovascular Drugs
4. Cisplatin – Inhibits ability of renal tubule to
conserve Mg
5. Cardiac glycosides – interfere with Mg
reabsorption
Dermatologic Flushing, warm skin Hormones Aldosterone
Neurologic Lethargy, coma Symptoms
Dec. reflexes, dysarthria, respiration
neuromascular Cardiovascular Arrhythmia, hyperternsion
depression, paralysis
hypocalcemia Weakness, cramps, ataxia, tremor, seizure, tetany,
Metabolic Neuromuscular
paralysis, coma
Hemostatic Dec. thrombin generation and platelet
Psychiatric Depression, agitation, psychosis
abnormalities adhesion
Treatment Supportive therapy Methods
1. Calmagite method – binds with reddish violet complex
2. Formazen dye – binds with Mg
3. Methyl thymol blue method – binds with chromogen first then
Mg
4. Atomic absorption spectrophotometry

CALCIUM
Hypercalcemia Hypocalcemia
 Primary hyperparathyroidism  Primary hypoparathyroidism
 Hyperthyroidism  Hypomagnesemia
 Benign familial hypocalciuria  Hypermagnesemia
 Malignancy  Acute pancreatitis
 Multiple myeloma  Vitamin D deficiency
 Inc. Vitamin D  Renal disease
 Thiazide diuretics  Rhabdomyolysis
 Prolonged immobilization  Pseudohypoparathyroidism
1. Parathyroid hormone Calcitonin
Hormone 2. Vitamin D2 ( cholecalciferol) Hormone

Symptoms Neuromascular excitability

Symptoms
Cardiac abnormalities
mild asymptomatic Treatment Oral calcium therapy with Vit. D
Mild drowsiness, weakness, depressions, lethargy,
Neurologic Determination
coma
Constipation, N/V, anoxia, peptic ulcer  Total calcium – serum in lithium heparin
GI Sample  Ionized Calcium – heparinized whole blood
 24h urine
Renal Nephrolithiasis, nephrocalcinosis
Methods
symptoms
1. Estrogen replacement with Ca+ - for menoposal 1. Total Ca+ analysis
women 2. Ortho-cresolphthalein complexone (CPC)/ Arsenzo III dye –
Treatment 2. Bisphosphonate – to lower Ca levels uses 8-hydroxyquinolone to prevent Mg interference
3. Atomic absorption spectrophotometry
3. Ion selective electrophoresis