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Interpreting the Biochemisty Panel

ELECTROLYTE Calcium Absorbed from diet Stored in Bone Excreted in urine Regulated by: PTH Vit D3 Calcitonin 50% bound 50% ionised Increased Values Lipaemia (artefact) Neoplasia CRF HypoA (Addisons) 10 HyperParathyroidism (tumour rare) 20 HyperParathyroidism (low Ca diet or loss of Ca) Hypervitaminosis D (rodenticide, supplements) Hyperalbuminaemia ( total but not ionised Ca) Toxin (Vit D rodenticide) Non-malignant skeletal disorder (rare) High Ca diet (rare) Young growing dog (osteoclastic activity) Absorption o High P diet o Vit D toxicity excretion or bone resorption o Hypoparathyroidism o 1 renal disease o renal 2 hyperPTH o young growing dogs (osteoclastic activity) Water loss electrolyte loss o Dehydration o Hypo or adypsia o DI o Osmotic diuresis (DM, Renal failure, mannitol) Excess retention o 1 Hyperaldosteronism o Iatrogenic (NaCl infusion, salt ingestion) Acidosis Dehydration HypoA ARF Urethral Obstruction Decreased Values Eclampsia Hypoparathyroidism Low Ca diet Lymphangiectasia Malabsorption Pregnancy and lactation CRF (due to low Vit D3 formation) Acute pancreatitis Hypoalbuminaemia (ionised Ca is normal)

Phosphorous Absorbed from diet Stored in Bone Excreted in urine Regulated by: PTH Vit D3 Calcitonin Sodium Travels with ClRegulated by aldosterone (adrenal) o Reab of Na+ o Excretion of K+

absorption o diet (rickets low Vit D3) renal excretion or bone resorption o Hyperparathyroidism o Osteomalacia o Neoplasia (PTH-like substances)

Excess Na loss o End stage renal Disease o GI loss (V+, D+) o Overhydration o CHF Excess Water conservation

Potassium Regulated by aldosterone (adrenal) o Reab of Na+ o Excretion of K+

Bicarbonate

Metabolic alkalosis

Alkalosis HyperA HyperAldosteronism Intestinal obstruction Insulin therapy Polyuria V+, D+ Diuresis Metabolic acidosis

ENZYMES ALP Produced in bone, liver (cells lining bile duct), placenta, gut, kidney Non-specific for liver

ALT Most liver specific enzyme (dogs and cats) AST Present in hepatocytes, muscle and RBCs

Increased Values Cholestatic disease (dog or cat) i.e. biliary obstruction HyperA (dog) i.e. excess glucocorticoids **most common cause in dogs** HyperT (cat) Drugs: Glucocorticoidsm barbiturates, other anti-seizure drugs (dog) Puppies have higher ALP (bone) Liver disease/active hepatocellular damage Mild GI disease if mild liver inflamm or transient bacterial infection Liver disease (hepatocellular) o Esp If ALT > AST Muscle inflammation or necrosis o Mm injection, exercise RBC Haemolysis o Esp if AST > ALT Biliary stasis Steroid hepatopathy Pancreatitis o low sensitivity o low specificity o so do PLi Pancreatitis o low sensitivity

Decreased Values

GGT

Amylase Made in pancreas Excreted in kidney Lipase Made in pancreas Excreted in kidney

ORGANIC COMPOUNDS Albumin made in liver

Increased Values Dehydration/haemoconcentration

Decreased Values production o Liver disease loss o blood loss o GI disease (PLE) o Glomerulonephropathy (PLN) o 3rd space loss

Bilirubin Breakdown product of haeme Carried to liver by albumin for conjugation and excretion in bile BUN Synthesised by liver Excreted in urine (constant fraction)

Cholesterol Produced by the liver Absorbed by the gut into lymphatics

Creatinine Metabolic breakdown product of mm creatinine (constant amount released daily) Excreted in urine Globulin Immune defence proteins Glucose Produced in liver Obtained in diet Uptake affected by insulin Total Protein Albumin + Globulin

Prehepatic = haemolysis Hepatic = intrahepatic cholestasis ( ability to handle and excrete bilirubin) Post-hepatic = bile duct obstruction (accum of bile) o Pancreatitis o Prancreatic or prox GI mass Pre-renal = dehydration, hypovolaemia Renal = renal failure Post-renal = urinary obstruction Extra-renal o Mm catabolism fever, mm trauma, corticosteroid Rx o Recent protein meal o GI bleeding Mobilisation of fat stores in liver o HyperA o DM Liver responding to protein loss by making more of everything it makes o HypoT o Glomerular nephropathy Hyperlipidaemia (Schnauzer) Pre-renal = dehydration Renal disease Post-renal = urinary obstruction

production o end stage liver (hepatic insufficiency) o low protein diet loss o polyuria o diuresis production o liver failure loss o Lymphangiectasia

mm mass/mm wasting (rare)

Chronic immune stimulation (FIP) Dehydration LSA or multiple myeloma HyperA anti-insulin effect DM insulin release, downreg of insulin receptors, blocked receptors uptake of Glu from blood Excitement/stress (cats) Dehydration Chronic immune stimulation

Neonates PLE Blood loss intake fasting, puppies/small breeds insulin release - Insulinoma Insulin overdose production - Liver disease (endstage) insulin use - Sepsis loss o PLE, PLN o Acute or chronic haemorrhage o Lymphangiectasia formation o liver disease o malnutrition o neoplasia o lower in young animals

Electrolyte Physiology
Bicarbonate:
Kidneys and respiratory system help maintain acid-base homeostasis Blood pH below normal kidneys remove H+ from blood and excrete more acidic urine respiratory system compensates by minute ventilation to blow off CO2 Blood pH below normal Kidneys remove HCO3 from blood and excrete more alkaline urine Minute ventilation may

Calcium & Phosphorus


Absorbed from diet, stored in bone, excreted in urine 50% bound to albumin, 50% active ionised o if Ca levels measure ionised Ca

Ca vital for nervous, skeletal and cardiac muscle function tightly regulated by three hormones: o PTH o Calcitonin o Vit D3 Plasma Ca PTH release Ca and P resorption from bone & Ca resoption but P excretion from kidney Net effect = serum Ca levels but NOT P Vit D3 formation in kidney Ca and P uptake from diet Ca and P resorption from bone and kidney Plasma Ca Calcitonin Ca and P resorption from bone and kidney lowered levels of Ca and P

Sodium and Potassium


regulated by Aldosterone (mineralocorticoid) primarily in distal tubules and collecting ducts Aldosterone reabsorption of Na and excretion of K Hypoadrenocorticism aldosterone levels Hyponatremia & hyperkalaemia ( Na/K ratio) The body regulates water by regulating [Na] tightly regulated by RAAS RAAS is triggered by hypovolaemia & sympathetic tone pH affects K levels o K+ moves in opposite direction to H+ o Acidotic patient (H+ in plasma moves out) = hyperkalemic patient (K moves into plasma) Diuretics and high water intake increased K excretion (due to increased gradient for K secretion)

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