Flashcards in Test 2- Electrolytes Deck (64):
What is the major extracellular fluid ion?
Sodium. It is actively eliminated from cells via sodium pump. Major
influence on osmolalilty.
How is sodium regulated?
Through adequate intake (especially herbivores), renal tubular absorption via aldosterone, intestinal absorption, osmoreceptors that secrete ADH indirectly influence serum sodium concentration.
Sodium metabolism and plasma volume?
There is a balance between intake and losses. Urine, GIT, sweat all
affect plasma volume.
What are the 2 sodium balance regulated and interdependent systems:
Osmoreceptors in hypothalamus sense increased osmolalitly and secrete ADH
• Stretch receptors sense volume changes
What stimulates ADH?
ADH responds to increase osmolality and decrease in plasma volume. Acts on collecting ducts to maximize water reabsorption.
How are sodium and the RAAS related?
The RAAS is the main regulator of sodium balance. Sodium
reabsorbed in distal tubule.
• Aldosterone secreted in response to angiotensin, hyperkalemia and ACTH. Aldosterone conserves sodium and secretes potassium
What are causes of hyponatremia?
Loss of sodium in the GI, renal, cutaneous, 3rd spacing
• Shifts- plasma hyperosmolality (not due to sodium)
• Increase extracellular water- edematous states, CHF, cirrhosis,
• Decrease intake (herbivores)
What is the most common cause of hyponatremia?
Excess sodium loss. - Hypovolemia
• GIT- vomiting, diarrhea, saliva.
• Renal loss- hypoadrenocorticsism (addisons), (decrease
aldosterone- increase in potassium), ketonuria, prolonged diuresis.
• Cutaneous- sweating, burns
• 3rd spacing – sequestration of fluid (fluid in plasma moves into 3rd
space and plasma sodium decreases (peritonitis, ascites,
uroabdomen, chylothroax, Gi sequestration)
what is a fluid shift?
Osmotic shift form the ICF to the ECF. Common cause is hyperglycemia- for ever 100mg/dl increase in glucose there is approximately 2 mEq decrease in sodium. Mannitol can cause this as well
What are causes of increased extracellular water therefore leading to hyponatremia?
Primary polydipsia (psychogenic water drinking), excessive administration of sodium poor IVF, occasionally seen w/ edematous conditions; nephrotic syndrome, severe chronic hepatic or renal failure, congestive heart failure, psychogenic polydyspsia
What is cause of hyponatremia especially in herbivores (ruminants)?
Decreased intake- give a salt lick
What are consequences of hyponatremia if other osmotically active substances are not increased? (such as glucose, urea for example)
Hyposmolality, cellular edema (cellular overhydration)- If sodium level in blood lower than in the cell then you have water moving into the cell and the cells rupture
what are the 2 usual cause of hypernatremia?
Usually due to dehydration. Inadequate water intake (lack of
water supply, inability to drink, defective thirst mechanism) or pure water loss (panting/high fever/high stress, diabetes insipidis)
What is a less common source of hypernatremia?
Excess Sodium intake or retention- ingestion/ IV administration,
increased alodsteron(VERY RARE)
what is a major extracellular fluid anion that is important in transport of electrolytes and water that is involved in acid base metabolism?
What do you need to look at when evaluating chloride?
First look at sodium. Then look at Tc02
What if you have changes in NA and Cl and they are proportional?
Consider differentials that pertain to abnormalities in sodium(hypernatremia causes and hyponatremia cuases- remember Na and Cl move together)
What if you have changes in Na and Cl that are not proportional?
Consider acid base balance (Cl concentrations greater than
How is chloride regulated?
Based on electrochemical gradients. Corresponds to the active
transport of sodium.
What interferes w/ chloride transport?
Furosemide and Gi enterotoxins.Chloride is usually regulated secondary to sodium. Usually parallels sodium concentration.
What are causes of hypochloremia?
Generally parallels losses of sodium. All causes of decrease
sodium are causes of decrease chloride
What is the most common cause when chloride loss exceeds sodium loss?
Hypochloremic metabolic alkalosis- usually through gastric
secretions not resorbed by the small intestine: monogastric-
severe vomiting and ruminants- abomasal disorder, high Gi
• Also sweating in horses.
What is selective chloride loss?
When chloride loss exceeds sodium loss. (sever vomiting inruminaints. Leading to hypocholoremic metabolic alkalosis
What is the equation for calculated corrected chloride?
Cl- corrected = Cl measured x Na (mean normal)/ Na (measured)
o If corrected Cl is still below the reference interval, a selective loss of chloride is suspected.
• Normally hydrogen and chloride are secreted into the stomach and sodium and bicarb are put into the plasma. Sodium and bicarb reunite w/ Chloride and hydrogen in the duodenum (not the case w/ a duodenum obstruction so it can lead to a hypochloremic metabolic alkalsosis net gain of bicarb as pH increases. Net loss of chloride
what is paradoxical aciduria w/ selective chloride loss?
Volume depletion, chloride depletion. (kidney resorbed sodium to
correct dehydration b/c of the vomiting occurring and resorbs bicarb instead of chloride (electroneutrality) resulting in an exacerbated alkalosis (more bicarb). But to keep electrical neutral- the bicarb is absorbed rather than the chloride. So becomes even more alkalemic and aciduric.
Is hyperchloremia common?
No, uncommon. It normally is a result of paralleled increase in
sodium (same causes of hypernatremia.
• Hyperchloremic metabolic acidosis (GIT loss of bicarb, proximal and distal renal tubular acidosis.
• Alkalemic/ bicarb excess- bicarb excreted in the distal nephron. Generates H+ and Cl follows H+ into plasma (maintain electroneutraliitiy)
- a major intracellular cation that is associated w/ IC osmotic pressure and IC fluid volume. Critical in resting membrane potentials, carbohydrate metabolism and electron transport.
What are clinical signs of abnormal serum k+ concentrations?
Cardiac dysfunction- can be life threatening, and skeletal muscle dysfunction
How is potassium regulated?
Adequate intake, renal excretion (promoted by aldosterone, K+
exchanged for sodium), sweat, Gi Loss
What are causes of hyperkalemia?
• Failure of renal excretion- most common.
• Redistribution- inorganic acidosis, insulin deficiency, muscle
trauma: rhabdomyolysis, massive hemolysis
• Increase intake- parenteral administration of potassium
Most common cause of hyperkalemia
Hyperkalemia- renal failure of excretion. Most common cause of hyperkalemia
What are causes of failure of renal excretion?
Oliguria/anuria, urethral obstruction, ruptured urinary bladder, hypoadrenocrticism (decreased aldosterone), drugs that decrease K+ excretion- spironolactone
How is hypoadrenocorticism associated w/ hyperkalemia?
Decreased aldosterone associated w/ K+ retention and sodium loss.
• A low Na:K ratio =
What are examples of redistribution that cause hyperkalemia?
Inorganic acidosis, insulin deficiency, severe muscle trauma (rhabdomyolysis, seizures)
• Redistribution is a major mechanism behind hyperkalemia. In an acidosis. H and K balance maintains electroneutralitiy
between ICf and ECF. When increase in proton, the cells will take up proton and then to maintain electroneutrality puts potassium int the ECF.
What do you have to be concerned about w/ giving high K+ IV fluids?
Hyperkalemia- increased potassium
Hyperkalemia- increased potassium
• Generally in vitro not in vivo. ! EDTA tubes
• Marked thrombocytosis: leakage of intracellular potassium
• Hemolysis: K + released from RBC
Separate the serum quickly- horses, pigs, most cattle, some sheep. Akitas, some Japanese dog breeds. Mice rats, monkeys ! these animals have high intracelluarl potassium concentrations.
what does hypokalemia usually indicate?
• Marked depletion of cellular potassium.
• Decreased intake or low K+ IV fluids
• Loss (alimentary- vomiting, diarrhea, abomasal disorders
• Renal- diuresis, Cushing’s, renal failure in cats
• Horse sweat
• Redistribution- alkalemia, insulin injection
what are consequences of hypokalemia?
If K+ concentration is
What occurs w/ potassium during diarrhea?
Potassium and bicarb loss via the GIT track leads to an acidosis and protons enters the cells and potassium leaves the cells- may bask the hypokalemia actually present so serum K levels can be normal! potassium supplementation may be indicated despite normal serum potassium
How can an alkalosis cause hypokalemia? (redistribution hypokalemia)
Increase in bicarb outside cell yields proton to move outside of the
cell and to keep elecrtoneutrality potassium will move back into the
cell yielding a hypokalemic state.
How does insulin cause a redistribution hypokalemia?
Insulin spike (glucose bolus or exciement or injected insuil) puts potassium in the cell and puts proton out in the cell
what is fractional excretion of electrolytes?
Relates to fractional excretion of creatinine. Expressed as a
percentage. Shows kidney involvement in electrolyte losses.
Normal Fractional excretion suggests non renal cause for
electrolyte loss such as diarrhea
What does water balance depend on?
Adequate intake, renal and GI function, losses in sweat and
respiration, neural control
What is osmolality?osmolarity?
osmolalility= [solute] per kg of solvent (mOsm/kg)- 1 osmole of solute added to 1 kg (1L) of water
• osmolarity= [solute] per liter of solution (mOsm/L) 1 osmole of solute placed in a beaker and water is added to make the 1 L.
• osmolality does not equal osmolarity.
What is an effective osmole?
Osmotically active- molecule/ion that can cause water to move toward it. In serum, effective osmoles are sodium, chloride, bicarb, proteins, glucose, ethylene glycol
How is serum osmolality measured?
By freezing point depression –dogs- normal 300 mOsm/kg. cat 310 mOsm/kg
• Osmolarity be estimated from a calculation
o Osmolality = 2[Na] + [BUN]/2.8 + [glucose]/18
What is the osmole gap?
Osmole gap= measured osmolality- calculated osmolality
What does an increased osmole gap indicates?
An increase in an osmotically active molecule in blood; that is not measured on the serum biochemical profile
• Ex- toxins! ethylene glycol, methanol, paraldehyde. Mannitol or radiographic contrast medium
o If the osmole gap is less than or eequal to 30 ! normal
o If osmole gap is greater than 30! there is an unaccounted
￼What if there is no difference between claclated osmolarity and measured
￼osmolality but there is an increased in measured osmolality?
Normal osmole gap w/ increased measured osmolality there is increased sodium or markedly increased urea or glucose.
￼What is there is no difference between clacluated osmolality and measured
￼osmolality but there is no decrease in measured osmolality?
Normal osmole gap w/ decreaed measured osmolality - there is a decrease in sodium concentration even a marked decrease in UN or glucose can only cause a minor decrease in osmoaltiy
￼What if there IS a difference between calculated and measured osmolality w/
￼an increase in measured osmolality?
There is increase in the osmole gap and signifies the presence of unmeasured osmole (ex ethylene glycol
Remember- hydration status is indicative of the vascular blood volume.
What does low body water or high plasma osmolality lead to?
Leads to increase thirst and decrease renal water excretion
What does excess body water or low plasma osmolality lead to ?
Leads to increase renal water excretion
Water balance—hydration! blood volume. Water follows solute concentration gradients. Proximal tubule, intracellular fluid versus extracellular fluid
Blood volume is influenced by movements of electrolytes wand water – how?
• Increae or decrease intake, losses, retention, shifts (ICF in or out to
• Regulated by sensing of plasma osmoalilty, blood pressure
Sodium is a major constituent of plasma osmolality (ECF) and is actively controlled. Increase in sodium leads to increase ECF, decreased sodium leads to decrease ECF.
Potassium is a major in ICF but plasma sodlium is influenced by potassium. If total body potassium decreases than sodium will move into cells to maintain electroneutralitiy
What does hyperosmolaltiy and hyposomolatity due to the hypothalamic osmoreceptors?
Hyper- stimulates thirst and release ADH (ADH directly rleaed by influenced of sodium cocnetration in blood and blood volume- therefore hyperosmolality and hypovolemai)
• Hypoosmolality- decreased water intake and increased renal water loss
What stimulates release of aldosterone?
Plasma volume, hyperkalemia, angiotensin II, ACTH, acts on
collecting ducts (Na resorption, exchanged for K+ or H+)
What is ANF?
Atrial natriuretic factor. It is released when there is increase increase central venous blood pressure causing loss of sodium in urine and diuresis, or vasodilation. It inhibits aldosterone release.
• Increased osmolality stimulates thirst centers
What laboratory evidence demonstrate dehydration?
Polycythemia/erythrocytosis; increased plasma proteins (panhyperproteinemia), increased USG, dehydration can be hypertonic, isotonic, hypotonic (water loss, electrolyte loss)
What do you need to look at when evaluating hydration?
Clinical signs, body weight, PCV/TP, USG, BUN, creatinine (serial evals may be important)
What is hypertonic dehydration?
When sodim an chlrodie are both elevated (water loss exceeds electrolyte loss)
o Diabetes insipidius, diabetes mellitus, osmotic diuretics, osmotic diarrhea, water deprivation
What is isotonic dehydration?
When sodium and chloride are w/in the reference interval. Water loss is equivalent to electrolyte loss
o Causes- renal dz, diarrhea
What is hypotonic dehydration?
Look at sodium and chlrodie- both decreased- hypotonic dehydration. Electrolyte loss is greater than water loss! causes: secretory diarrhea, vomiting (Na, Cl, K w/ our w/ot bicarb), 3rd space loss, heat stress and sweating in horses (often Cl- losses are greater than sodium losses)
What are problems associated w/ hypotonic dehydration?
Fluid shifts from vasculature into cells. Vascular volume decreases further and cells swell- cerebral edema (occurs when sodium is