isotonic dehydration=water lost contains solutes at a concentration that is isotonic to body fluids

Na serum concentrations normal

PCV and TP are increased

hypertonic dehydration=fluid loss is hypotonic to plasma (e.g. free water loss); Na and Cl are increased

diabetes insipidus (central or nephrogenic)

water loss from panting (or cow sweat)

hypotonic dehydration=hypertonic fluid has been lost; plasma Na is decreased

secretory diarrhea (e.g. calf scours)

vomiting

third-spacing (fluid is actually displaced, not lost)

sweating (horses)

Dilution of sodium

excess ADH

hyperglycemia

mannitol administration

Sodium loss

secretory diarrhea

hypertonic sweating (horses)

renal tubular disease (loss through urine)

third-spacing

potential space fills with fluid

sodium follows fluid into that space

animal experiences perceived hypovolemia

if animal continues to drink, sodium is diluted even more

salt toxicity (excess salt ingestion with restricted water intake)

diabetes insipidus

free water loss from panting, sweating (cows)

high gastric vomiting (loss of HCl)

loop/thiazide diuretics (loss from kidneys)

chronic respiratory acidosis (loss through kidneys with H+)

secretory diarrhea (more Na lost that Cl)

renal tubular acidosis (rare, abnormal retention of chloride)

chronic respiratory alkalosis

redistributional (from ECF-->ICF)

alkalosis (metabolic or respiratory)

insulin

excitement (rare)

absolute

decreased intake

anorexia

diarrhea (Na in lumen absorbed, K+ excreted)

vomiting

renal loss (K+ is excreted with excess anions or excess sodium)

cardiac arrhythmias

generalized muscle weakness

redistributional

metabolic acidosis (protons enter cells, K+ leaves)

DM (insulin deficiency)

absolute

metabolic acidosis (redistribution, then decreased secretion)

renal failure (terminal chronic or severe acute)

uroabdomen

hypoadrenocorticism (aldosterone normally responsible for excretion of K+)

hyperkalemia coming from reasons other than true electrolyte imbalance (usually due to incorrect sample handling)

hemolysis (especially in horses>pigs>some dogs)

thrombocytosis (platelets leak K+ during clotting)

hyperkalemia

hyponatremia

hypochloremia

hyperkalemia

hyponatremia

hypochloremia

without azotemia

1.)  look at pH

2.) has metbolic or respiratory component (or both) changed in the same direction as pH?

3.)  Look for compensatory change and determine whether or not it is appropriate (has metabolic or respiratory component changed in an opposite direction from pH?)

metabolic alkalosis ddx

excess adminstration of HCO3

loss of H+/Cl- rich fluid

gastric vomiting (loss to outside)

proximal GI obstruction (loss to stomach)

displaced abomasum (loss to abomasum and forestomachs)

heavy sweating in horses

paradoxic aciduria:  urine is acidic even though animal is alkalotic

Usually occurs with displaced abomasum or excess sweating in horses (occurs when dehydration is accompanied by alkalosis and low Cl-)

increased bicarb/less chloride for coupled Na aabsorption from proximal tubules, so more Na enters distal tubules, where Na reabsorption is coupled with K or H (when hypokalemia results, K is conserved and H is excreted)

low to normal pO2

hyperventilation

from hypoxemia (low pO2 stimulates hyperventilation, but CO2 diffuses much more readily than O2)

from stimulation of respiratory center (CNS dz, gram-negative sepsis, pain, excitement)

low pO2, high pCO2

decreased ventilation--inability to blow off CO2

airway obstruction

respiratory center depression

pulmonary disease (pneumonia, edema, etc)

restrictive diseases (pneumothorax, pleural effusion, etc)

addition of acid

ketoacidosis

lactic acidosis

ethylene glycol

renal failure (uremic acids)

loss of HCO3-

diarrhea (calf scours)

Addison's (impaired aldosterone-->decreased K+ and H+ secretion)

titrational (aka high anion gap) acidosis:  increased organic acids (bicarb titrates additional acid and is used up)

secretional acidosis:  normal anion gap, loss of bicarb

increases Ca, decreases P

Ca and P reabsorption from bone

increases Ca/decreases P reabsorption in kidneys

increases activity of Vitamin D

released in response to hypocalcemia

release inhibited by increased iCa, vit. D

What is the action of vitamin D?

increases Ca, increases P

increases Ca concentration by increasing absorption of Ca from intestine

enhances PTH action on bone and kidney

decreases Ca, decreases P

inhibits osteoclastic bone resorption

decreases renal tubular reabsorption of Ca and P

released in response to hypercalcemia

release is inhibited by hypocalcemia

acidosis increases ionized Ca

alkalosis decreases iCa

hypoalbuminemia (most common cause of decreases in total Ca, benign, iCa stays the same)

renal failure (decreased calcitriol formation by kidney. increased P)

pancreatitis

eclampsia

signs occur when ionized Ca is low

nervousness, anorexia, stilted gait

hyperventilation, numbness

generalized tetany, seizures

transient

post-prandial

dehydration

lipemia

young, growing dogs

Addison's

pathologic

humoral hypercalcemia of malignancy (most common)

primary hyperparathyroidism

idiopaathic hypercalcemia of cats

renal disease

vitamin D toxicosis

increased total Ca

increased iCa

decreased-normal P

increased PTH

undetectable PTHrp

normal to increased vit. D

increased Ca

normal to increased iCa

normal to increased P

decreased to normal PTH

undetectable PTHrp

decreased to normal vit. D

increased Ca

decreased to normal iCa

increased P

increased PTH

undetectable PTHrp

decreased to normal vit. D

increased total Ca

increased iCa

decreased to normal P

decreased PTH

increased PTHrp

normal to increased vit. D

increased total Ca

increased iCa

increased P

decreased PTH

undetectable PTHrp

increased vit. D

PTH:  decreases (decreasaed renal tubular reabsorption)

calcitonin:  decreases (inhibits PTH actions, increases movement into tissues)

vitamin D:  increases (stimulates absorption from intestine and kidney, inhibits PTH)

primary hyperparathyroidism

hypercalcemia of malignancy (PTHrp)

vitamin D deficiency

respiratory alkalosis

decreased intestinal absorption

renal tubular defects (e.g. Fanconi syndrome)

chronic renal failure in horses

decreased GFR (most common; prerenal or renal)

ruptured bladder or ureter, urethral obstruction

vitamin D intoxication

excessive P intake

primary hypoparathyroidism

increased loss (most common in small animals)

renal (diuresis, renal dz, hypercalcemia)

GI (malabsorption or diarrhea)

decreased intake (most common in ruminants)

lush pasture (high in K+, low in Mg--grass tetany)

older calves fed milk-only diets

prolonged anorexia

poor diet (especially if lactating)

prolonged IV fluid therapy or parenteral nutrition without Mg supplementation

PTH synthesis/release

facilitaates Na/K-ATPase activity in cells

structural role in bone formation

neruomuscular function

renal excretion is maain means of control

secondary hypokalemia (renal wasting of K)

impaired PTH production/release

neuromuscular/caardiac abnormalities

hyperexcitability

tremors, fasciculations, ataxia

frank tetany

cardiac arrhythmias/possible arrest

coronary artery spasms in humans

clinically less significant

iatrogenic

decreased renal excretion (decreased GFR/obstruction)