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What are the functions of Magnesium?
facilitates Na/K-ATPase activity in cell membranes
PTH synthesis and release
Ca channel activity
What are the three ways that magnesium is lost in the horse leading to hypomagnesemia?
GI tract via malabsorption and diarrhea
Kidneys via fluid diuresis, diuretics, renal disease, and hypercalcemia which inhibits magnesium reabsorption
Skin via sweat
How do ruminants get hypomagnesemia?
dietary deficiency from grass tetany (high potassium of pasture blocks)
milk tetany from calves being fed a diet of milk low in magnesium
With which disorders is hypomagnesemia associated?
Diabetes mellitus (diuresis)
Third space syndromes (accumulation of fluid in the abdominal cavity of the GI tract)
What two electrolyte imbalances does hypomagnesemia cause?
secondary hypokalemia due to renal wasting of potassium
secondary hypocalcemia due to impaired PTH production and release
What are the clinical signs of hypomagnesemia?
(most are associated with the hypocalcemia and hypokalemia)
Tremors, fasciculations, ataxia
Cardiac arrythmias and possible arrest
Coronary artery spasms (in humans)
When will you see hypermagnesemia? What other electrolyte is this similar to?
hypermagnesemia is seen only when renal function is compromised; if the animal can urinate then is can get rid of excess Mg; this is similar to potassium
(Mg containing laxitives and antacids with a decreased GFR will increase Mg concentrations)
What two systems control Na balance? How does each work?
Osmoregulation - osmoreceptors in the hypothalamus sense increased osmolality and secrete ADH
Volume regulation - stretch receptors sense volume changes
What is the function of ADH? When is it released?
ADH acts on the collecting ducts to maximize water reabsorption
It is released when there is increased osmolality or markedly decreased plasma volume
What is the main regulator of Na balance?
*Na is reabsorbed at the distal tubule
What are the causes of hyponatremia?
Excess loss through GIT, renal, cutaneous, or 3rd space
Movement of H2O from intracellular to extracellular pull by hyperglycemia and mannitol
Increased intracellular water or increased vascular water (edema, CHF, cirrhosis, nephrotic syndrome)
Pseudohyponatremia seen with hyperlipidemia and hyperproteinemia
What are the third space syndromes that cause hyponatremia?
How do mannitol and hyperglycemia cause hyponatremia?
Mannitol administration causes intravascular movement of water which dilutes Na
Hyperglycemia acts in the same way
What is usually the cause of hypernatremia?
usually due to dehydration caused by inadequate water intake or excess water loss
*uncommon to see excess Na intake or retention
True or False: Chloride is secreted via type A intercalated cells to balance hydrogen secretion.
True; HCO3 gets brought into the body and Cl gets kicked out
What is the main cause of hypochloremia?
Cl parallels losses of Na, therefore all causes of hyponatremia are causes of hypochloremia
(GI sequestration, sweating, renal, 3rd space)
When will chloride loss be greater than Na loss?
sweating in horses
sequestration (GI obstruction)
acidemia (excrete Cl when H is excreted)
How do you correct chloride? What does this mean?
(measured Cl) x (mean Na / measured NA)
If corrected Cl is still below the reference interval selective loss of Cl should be susepcted
What is the main cause of hyperchloremia?
Cl generally parallels increases with Na, therefore causes of hypernatremia cause hyperchloremia
(dehydration caused by inadequate water intake or excess water loss)
How does aldosterone control potassium?
is controls the excretion of potassium at the renal tubules in exchange for Na
What are the two causes of hyperkalemia?
Redistribution (where there is no increase in total body potassium)
An increase in total body potassium via decreased excretion or iatrogenic
What is the mechanism behind redistribution of potassium during acidosis?
during acidosis there is surplus hydrogen extracellularly, hydrogen can enter the cells and kick out potassium to maintain electrical neutrality causing redistribution hyperkalemia
How does rhabdomyolysis cause redistribution hyerkalemia?
a defect in the resting membrane electrical potential Na gating and K distribution between the ICF and ECF
What three things can cause decreased renal potassium excretion resulting in hyperkalemia?
Hypoadrenocoticism (which usually secreted K in exchange for Na)
Anuric/aliguric renal failure
Urinary tract obstruction
What are the causes of hypokalemia?
decreased intake, increased excretion, increased renal flow in the distal nephron, vomiting, diarrhea, alimentary sequestation of H and Cl, hyperaldosteronism, horse sweat, salivation, low K IV fluids, redistribution shift from ECF to ICF, increased insulin, severe burns, renal loss
Explain how hypokalemia due to diarrhea might be masked.
loss of K and HCO3 by diarrhea can cause an acidosis which causes H to enter the cell and K move into the ECF
How does alkalemia cause redistibution hypokalemia?
if you have an alkalemia you have increased HCO3 in the blood, this will cause intrecellular H to move to the ECF in exchange for potassium, resulting in increased K in the ICF
What does the fractional excretion tell us?
normal fractional excretion suggests non-renal cause for electrolyte loss (suggests diarrhea)
What is an effective osmole? What is an ineffective osmole? Give examples of each.
Effective: a molecule/ion that can cause water to move toward it (ex. sodium)
Inneffective: will equiliberate itself between compartments without moving water (ex. urea)
What is the difference between osmolality and osmolarity?
Osmolality is solute per kg of pure water
Osmolarity is solute in moles per liter of solution
What are the osmotically active solutes in serum that can be measured?
Na, Cl, HCO3, proteins, glucose, and ethylene glycol, methanol, paraldehyde, mannitol, radiographic contrast medium
What is the clinical significance of an increased osmole gap?
this means that there is an increase in an osmotically active molecule in blood which is not measured on the serum biochemical profile (ie. ethylene glycol, methanol, paraldehyde, mannitol, radiographic contrast media)
What does it mean when there is not difference between calculated osmolarity and measured osmolality, but there is an increase measured osmoality?
this means that there is a normal osmole gap with an increased measure osmolality indicating increased Na and markedly increased urea or glucose
What does it mean when there is not difference between calculated osmolarity and measured osmolality, but there is an decrease measured osmoality?
this means that there is a normal osmole gap with a decreased measured osmolality indicating decreased Na and possibly a decrease in urea or glucose
What does it mean when there is a difference between calculated osmolarity and measured osmolality with an increase in measured osmolality?
there is an increased osmole gap which indicated ethylene glycol or some other non calculated osmole
What influences blood volume?
movement of electrolytes and water due to intake, losses, retention, or shifts between ICF and ECF
What is the major constituent of plasma osmolality (ECF)? What is the major constituent of ICF?
*plasma sodium is influenced by potassium
How should hypothalamic osmoreceptors respond to hyperosmolality? How should they respond to hypoosmolality?
Hyperosmolality: induce thirst and release of ADH
Hypoosmolality: decreased H2O intake and increased renaal H2O loss
What is release of ADH directly influenced by?
Na concentration and blood volume (hypersomolality/hypernatremia and hypovolemia)
When is RAAS activated?
when there is decreased renal perfusion (usually due to decreased blood pressure), hypotension, volume depletion, and increased sympathetic activity
How does aldosterone work?
it acts at the collecting duct to reabsorb Na in exchange for potassium or hydrogen
How does atrial natriuretic factor work?
it is released when there is an increase in central venous pressure and promotes sodium loss in urine to induce diuresis, causes vasodilation and inhibits release of aldosterone
What is hypertonic dehydration?
when water loss is in excess of electrolyte loss
Sodium and Cl will be increased
What are some causes of hypertonic dehydration?
What is isotonic dehydration?
when water loss is equivalent to electrolyte loss
Serum sodium and chloride do not change
What are some causes of hypotonic dehydration?
vomiting (loss of Na, Cl, K, +/- HCO3)
3rd space loss
heat stress ans sweating in horses
What are some problems with hypotonic dehydration?
fluid may shift from vasculature into cells cause cells to swell
cerebral edema (when the concentration of Na is < 115-120, especially if rapid change)
osmoreceptors are not stimulated and ADH is not released
may have medullary washout
True or False: ADH reduces hyperosmolality by controlling Na reabsorption/K and H excretion; while aldosterone reduces hyperosmolality by controlling water movement.
ADH controls water movement
Aldosterone controls Na reabsorption and K and H excretion
What 4 things determine pH?
2) Addition or removal of acids (lactate, ethylene glycol, loss of H)
3) Strong ion movement (Na, Cl, K)
4) Serum proteins, phosphate, and other weak acids
For a blood gas analysis, what type of blood is being collected and what type of tube is used? What gases are analyzed?
you will collect arterial blood in a heparinized tube
you will analyze the pO2, pCO2, HCO3, and pH
*this should be done in 5 min, otherwise it should be put on ice
What is the pathogenesis behind respiratory acidosis?
(CO2 + H2O --> H + HCO3)
Respiratory Acidosis: hypoventilation; increases CO2 which drives the equation to the right, increasing H and decreasing pH
What is the pathogenesis behind respiratory alkalosis?
(CO2 + H2O <-- H + HCO3)
Respiratory Alkalosis: hyperventilation; decreases CO2 which drives the equation to the left, decreasing H and increasing pH
What is the pathogenesis behind metabolic acidosis?
(CO2 + H2O --> H + HCO3)
Metabolic Acidosis: loss of bicarb through diarrhea, salicary loss, or the generation of organic acids drives the equation to the right, increasing H and decreasing pH
What is the pathogenesis behind metabolic alkalosis?
(CO2 + H2O <-- H + HCO3)
Metabolic Alkalosis: increase in bicarb due to a loss or sequestration of acid or increase in Cl drives the equation to the left, decreasing H and increasing pH
What is one of the biggest clues to a mixed acidosis? What other clues might you see?
Main clue: a normal pH
Others: compensation exceeds or falls short of expected level, also look at anion gam, Cl behavior, and strong io difference (SID)
*normal compensation is not a mixed acid-base disorder
What will you see with an appropriate compensation in an acid-base disorder?
the opposite system should be slightly above or slightly below the reference interval
basically ask yourself "did the opposite system move in the appropriate direction?"
True or False: The body's compensation to an acid-base disorder usually returns the pH to normal.
False; compensation rarely returns the pH completely to normal
True or False: Respiratory compensation happens quickly (hours) and metabolic compensation happens slowly (days).
How can you tell an acute metabolic compensation from a chronic metabolic compensation?
the acute case will happen in less than 48 hours and you will see immediate titration of HCO3 and ICF buffers
the chronic case will happen in more than 48 hours and you will see change in the excretion of H, Cl, and HCO3
What is appropriate compensation for a metabolic acidosis?...For a metabolic alkalosis?
Acidosis: 0.7 decrease in pCO2 for each 1 unit decrease in HCO3
Alkalosis: 0.7 increase in pCO2 for each 1 unit increase in HCO3
What is appropriate compensation for a respiratory acidosis?...For a respiratory alkalosis?
Acidosis: 1.5 increase in HCO3 for each 10 units increase in pCO2
Alkalosis: 2.5 decrease in HCO3 for each 10 units decrease in pCO2
True or False: pCO2 is metabolic in origin and is a good estimate of bicarb.
False; pCO2 is respiratory; TCO2 metabolic and is a good estimate of bicarb
If you do not have a blood gas machine how can yo identify a metabolic acidosis or alkalosis?
look at TCO2
if it is decreased you most likely have a metabolic acidosis
if it is increased you most likely have a metabolic alkalosis
What are the unmeasured anions? Do they affect the anion gap?
albumin, lactate, ketones, ethylene glycol, phosphate, sulfate, oragnic acids
yes, they will cause an increase in the anion gap
Which components are considered when calculating the anion gap?
Na, K, Cl, and HCO3
(Na + K) - (Cl + HCO3)
True or False: An increased anion gap is suggestive of an alkalosis and an decreased anion gap is suggestive of an acidosis.
an increased anion gap = acidosis
a decreased anion gap = alkalosis
What is titrational acidosis? What does this do to the anion gap?
a decreased HCO3 with a normal Cl
due to the accumulation of unmeasured anions (organic acids: ketones, lactate, sulfates, phosphates, uremic acids, and EG metabolites)
Increases the anion gap
What is a secretional acidosis? What does this do to the anion gap?
there is a loss of bicab due to secretion of bicarb rich fluids (saliva, diarrhea) causing an increase in chloride retention
Normal anion gap
What will happen to the anion gap in a metabolic acidosis? What is this caused by?
the anion gap will be normal due to increased HCO3
this is caused by loss of Cl rich fluid, gastic vomiting, high GI obstruction, and sweating in horses
What will happen to the anion gap in a mixed metabolic acidosis/alkalosis? Give two examples of when this happens?
You will see an increased anion gap due to a decrease in chloride with normal or slightly increased bicarb (but not enough to close the gap)
this can happen when you have a GI obstruction with lactic acidosis or renal failure with vomiting
What can cause a respiratory acidosis?
respiratory center depression (drugs/disease)
alkalemia from metabolic alkalosis
(basically anything that causes decreased ventilation)
What can cause a respiratory alkalosis?
decreased pO2 (which leads to hyperventilation)
CNS disease (stimulation of the respiratory center)
gram negative sepsis
(basically anything that causes increased ventilation)
What can cause a metabolic acidosis?
addition of an organic or exogenous acid (renal failure, ketoacidosis, lactate, ethylene glycol)
loss of HCO3 (diarrhea, loss of saliva)
Addison's disease (aldosterone normally causes Na retention and promotes K and H secretion)
What can cause a metabolic alkalosis?
loss of H through vomiting, obstruction, sequestration, diuretics, hypokalemia, secondary to respiratory acidosis
excess HCO3 through administration
hypokalemia (shifts H from ECF to ICF)
What electroyte imbalances and anion gab disturbance might you see with hypochoremia?
chloride is normally lost proportional with Na through alimentary or renal loss
also seen in a metabolic acidosis with an increased anion gap
What can cause hypochloremia?
upper GI abomasal atony (bovine renal failure)
How can you tell if there is greater loss of Cl than Na?
use the corrected Cl equation
[(mean Na/patient Na) x patient Cl]
if Cl is till below the reference rage then there is grater loss of Cl than Na
What is paradoxical aciduria?
When there is hypovolemia, hypochloremia, and alkalosis causing the animal to produce an acid urine
Explain the mechanism behind paradoxical aciduria.
there is volume and Na depletion -> RAAS kicks in to reabsorb Na in exchange for H and K -> also have bicarb reabsorption without chloride reabsorption
What are the 6 ways to diagnose ethylene glycol toxicosis?
1) test kit
2) calcium oxalate crystals in urine
4) increased serum osmolality with increased serum osmole gap 1 hr post ingestion (>20 = suggestive; >30 = diagnostic)
5) increased anion gap (3-6 hrs post ingestion)
6) increased fractional excretion of sodium (3 hrs post ingestion before onset of azotemia)
Why might you see hyperphosphatemia with ethylene glycol toxicity?
some anti-freeze include a rust factor that contains phosphate
What is the mechanism for the release of T3 and T3 form the thyroid gland?
the hypothalamus releases TRH which causes the pituitary to release TSH which then causes the thyroid gland to release T3 and T4
Where are T3 and T4 produced? What is their function?
T4 is produced by the folicular cells (in the thyroglobulin) of the thyroid gland but the majority of T3 is produced from T4 inside cells
They both function to inhibit secretion of TSH from the pituitary
Which forms of thyroid hormone are capable of entering cells? What are the other types?
Free T4 and free T3 are the unbound forms that enter cells
>99% is bound to protein
fT4 enters cells and is converted to T3
What functions of the body do T4 and T3 increase?
Increased metabolic rate, O2 consumption, HR, bone formation and resorption, catabolism of muscle and fat, protein synthesis, and erythropoiesis
True or False: It is common for cats to get hypothyroidism and for dogs to get hyperthyroidism.
False; cats get hyperthyroidism and dogs get hypothyroidism
Which thyroid neoplasms are most common in dogs? Which ones are more common in cats?
What is the most important clinical sign with feline hyperthyroidism? What will you find upon physical exam? What will you see in a biochemical profile?
Clinical signs: weight loss (most common); also polyphagia, PU/PD, restlessness, vomiting, diarrhea, skin/hair changes
Physical exam: palpable thyroid, tachycardia, and hyperactivity
Biochem Profile: increased ALT and ALP with an adequate concentration of urine, and increased tT4
90% of hyperthryroid cats will have increased tT4. What should you look for in those that don't?
measure fT4, if it is in the upper reference limit then they have hyperthyroidism
What are the causes of primary hypothyroidism? What are the causes of secondary hypothyroidism?
Primary:lymphocytic thyroiditis or idiopathic thyroid atrophy
Secondary: pituitary destruction or suppression
What are the clinical signs for canine hypothyroidism?
signs are variable
you may see weight gain with non increase in appetite, bilateral truncal alopecia with no pruritis, lethargy, hyperkeatosis, and myxedema
What laboratory abnormalities might you see with canine hypothyroidism?
mild normocytic normochromic non regenerative anemia
decreased fT4 and tT4, increased TSH, and the presence of thyroglobulin autoantibodies
What is Euthyroid Sick Syndrome?
decrease in tT4 (with normal or decreased fT4 and normal TSH)) in an animal that does not have a thyroidal illness; it is caused by non-thyroidal illnesses or drugs (phenobarbitol, glucocorticoids, sulfonamides, furosemide)
How would you diagnose a primary hyperparathyroidism?
1) rule out other causes of hypercalcemia
2) measure PTH (high to increased)
3) look for hyperphosphatemia
*if there is hypercalcemia but the problem is not parathyroid function, you will see decreased PTH
What hormones are secreted from the neurohypophysis? What hormones are secreted from the adenohypophysis?
Neurohypophysis: antidiuretic hormone (ADH) and Oxytocin
Adenohypophysis: adrenocorticotropic hormone (ACTH), TSH, somatotropin, MSH, FSH, LH, and prolactin
What does antidiuretic hormone do?
adjusts body water to keep it in balance with sodium concentration by:
increasing water intake via a thirst mechanism
increased water conservation
What is central diabetes insipidus? What is nephrogenic diabetes insipidus? What is the result of both conditions? What is the major differential?
Central: deficiency in ADH
Nephrogenic: there is no response to ADH, hypercalcemia, or drug induced
Results in PU/PD, low USG
DDx: psychogenic polydipsia
What two tests would you do to differentiate between central and nephrogenic diabetes insipidus? What would you be looking for with each test?
1) Response to Desmopressin (ADH) - administer ADH, if the urine is concentrated it is CDI; if the urine is not concentrated it is NDI
2) Modified Water Deprivation Test - dehydrate the animal to see if they release ADH and/or if the kidneys respond to it
What animals should you refrain from doing a Modified Water Deprivation Test on?
animals with renal disease, azotemia, or dehyration
True or False: Many hyperadrenocoticism patients do not have increased cortisol, therefore basal cortisol is not a useful test.
What are the etiologies for canine hyperadranocoticism?
Iatrogenic (high doses of glucocorticoids)
Pituitary adenoma (most cases)
Funtional adrenal tumor (can be an adrenal carcinoma or adenoma)
What dogs are predisposed to hyperadrenocoticism? What are the commonly affected breeds?
middle aged to older females (uncommon in dogs less than 6 years)
Breeds: Poodles, German Shepherds, Dachshunds, Labs, and Terriers
What are the clinical signs associated with canine hyperadrenocoticism?
PU/PD, heat intolerance, panting, polyphagia, abdominal enlargement, lethargy, truncal alopecia, calcinosis sutis, pyoderma/acne, hypeglycemia, anetrus, testicular atrophy, (fat distribution, protein catabolism, gluconeogenesis)
What are the laboratory abnormalities of a dog with hyperadranocoticism?
increased ALP, ALT, and cholesterol
USG less than 1.015
UIT with or without neutrophils (possible pyelonephritis and renal failure)
What is a screening test? What screening tests are done for hyperadranocoticism?
Identifies animals that potentially have a disease for further assessment with more specific tests
ALP activity: This tests for an increase in ALP activity which is suggestive HAC
Urine cortisol:creatinine ration: normal dog is < 10x10^-6 which is suggestive of hyperadrenocorticism
When might you see induction of steroid ALP?
7 days of increased serum corticol can lead to induction of steroid ALP
*if sALP is not elevated it is unlikely that there is an excess of cortisol or glucocorticoids
What is a confirmatory or diagnostic tests? Give examples.
discriminate between animals with screening test results suggestive or a particular disease and those that have another disease causing similar signs
Examples: LDDS and ACTH stimulation test
What are the LDDS confirmatory and diagnostic test?
Low Dose Dexamthasone Suppression Test (LDDS) - glucocorticoids are administered and the amount of ACTH secretion is observed (in an HAC dog you will not see decreased ACTH and therefore continuous secretion of corticol (>1.5ug/dl) -> no suppression
What is the ACTH stimulation test?
a base line cotisol level is taken followed by an injection of ACTH and plasma cortisol is measured after an hour; in an HAC dog you will see hypersecretion of cotisol (>20ug/dl)
*can be used to rule out iatrogenic HAC
What is a differentiating test? Give examples.
in the case of hyperadrenocotocism, discriminate between pituitary dependent and adrenal based disease
Examples: LDDS, HDDS, endogenous ACTH measurement
How does LDDS function as a differentiating test?
if may cause suppression of ACTH if you have a pituitary tumor, but adrenal tumors will not be suppressed; therefore if cortisol levels drop below 1.5ug/dl or half the baseline value ->pituitary tumor
if cortisol levels are greater than 1.5ug/dl or are not suppressed to at least half the baseline value -> adrenal tumor
How does HDDS function as a differentiating test?
use when LDDS does not distinguish between pituitary or adrenal tumors
obtain baseline cortisol -> inject 0.1mg/kg dex as 4 and 8 hours
if cortisol levels drop below 1.5 ug/dl -> pituitary tumore
if cortisol levels are greater than 1.5 ug/dl -> adrenal tumor
How does an endogenous ACTH measurement function as a differentiating test?
plasma is collected early in the morning
if ACTH is high or high-normal -> pituitary tumor
if ACTH is low or low-normal -> adrenal tumor
True or False: Hypoadrenocorticism is primarily immune-mediated destruction of adrenal cortices.
Who is most susceptible to hypoadrenocoticism?
this disease is rare in animals but is more common in female mixed breed dogs greater than 5 yrs
can also be seen in Great Danes, Poodles, West Highland Whites
What are the electrolyte imbalances seen with hypoadrenocoticism?
Hyponatremia, Hypovolemia, Hypotension
Hypovolemic crisis = Addisonian Crisis
What are the presenting complaints associated with hypoadrenocoticism? What will you find during the physical exam?
Presenting: poor appetite/anorexia, lethargy, depression, thin, vomiting/ regurgitaion
PE: lethargy, depression, thinness, weakness, dehydration
What signs contribute to the hypovolemic crisis seen with hypoadrenocoticism?
dehydration, shock, collapse, bradycardia, weak femoral pulse, hypothermia
What are the common laboratory findings for hypoadrenocoticism?
mild-moderate normocytic normochromic non-regenerative anemia typically with no stress leukogram, pre-renal azotemia, increased UN (due to GI hemorrhage), hypoglycemia
True or False: If an animal is in Addisonian crisis the best thing to do is rehydrate them.
False; assess the situation, rehydration can dilute RBCs to life-threatening levels
What is the the test of choice for the diagnosis of hypoadrenocoticism?
ACTH stimulation test (administer ACTH to see if the animal produces cortisol)
if baseline cortisol is less than 1.2 ug/dL and after an hour is less than 1.8 ug/dL -> diagnostic for hypoadrenocoticism
What are the three reasons enzymes might pass into plasma?
injury to tissues or increased production or elimination from the body is decreased
How is enzyme activity measured?
because enzymes catalyze biochemical reactions, their activity is measured by the disappearance of substrate or the formation of product
What is the biological half life of enzymes?
the duration of enzyme activity after passage into the blood
What is the concept behind leakage enzymes? Give examples of "leakage enzymes."
Enzymes escape from the cell as a result of injury to cell membranes or organelles
Ex) ALT, AST, SDH, GLDH, CK
What are induced enzymes? What are their increases usually due to? Give examples of "induced enzymes."
these are enzymes that are attached to membranes; they rarely increase due to cell injury
increases are usually due to increased production
Ex) ALP, GGT
How are leakage enzymes and induced enzymes related?
loss of leakage enzymes may induce production which would increase induced enzymes
induced enzymes may also rise after acute injury
What are the sources of Alkaline Phosphate (ALP)? Which one is most important? Why?
Sources: liver, intestine, placenta, and kidney
The liver is most important because it has the longest half life (3 days); ALP from other sources are only around for 6 minutes
What is the difference in the detection of GGT in the liver and GGT in the kidney?
injury to renal epithelial cells results in leakage of GGT into the lumen and therefore is increased in urine but normal in serum
injury to hepatocytes results in leakage of GGT into blood vessels which will cause increase serum levels
True or False: Increase in enzymes can be used to assess the severity of tissue damage.
False; you cannot assess the magnitude or severity of tissue damage based on the increase of enzymes but you can get the feel for the distribution (generalized vs localized)
Which enzymes are strictly muscle specific? What other enzymes other enzymes can be indicative of muscle problems?
muscle specific: creatine kinase
Where else can CK also be found?
nerves and brain
*however injuries to these areas do not raise serum CK
What organs have the highest activity of Aspartate Aminotransferase (AST)?
skeletal and cardiac muscle
What three conditions will you have on your DDx list just by seeing increased CK?
1) Skeletal muscle injury (necrosis, IM injections, trauma, exercise, downer horses and cattle)
2) Cardiac muscle injury (more in people)
3) Muscle breakdown (catabolism) (commonly seen in severely anorexic cats)
What are the kinetics of creatine kinase?
increases rapidly after injury (peaks at 6-12 hrs)
has a very short half life (2-4 hrs)
can return to normal within 24-48 hrs after acute injury
How does enzyme activity of AST compare to CK after injury?
AST has a slower increase and a longer duration than CK
CK peak = 6-12 hrs
AST peak = 24-36 hrs
CK half life = 2-4 hrs
AST half life = 12 hrs
CK return to normal = 24-48 hrs
AST return to normal = 72 hrs
True or False: Alanine Aminotransferase (ALT) is liver specific and has nothing to do with muscle.
False; ALT is considered "liver specific" but can be increased in SEVERE muscle damage (skeletal muscle = 5% of liver ALT activity)
How does myoglobinuria relate to muscle injury?
myoglobin is released from dead or dying muscle during severe acute injury
myoglobin have a low molecular weight and is not protein bound, therefore it readily passes through the glomerulus and is excreted in urine
How can you distinguish between myoglobin and hemoglobin in urine?
a dipstick test will be positive for hemoglobin in both myoglobin and hemoglobin
1) an ammonium sulfate precipitation test will precipitate hemoglobin but not myoglobin and the dipstick test will remain positive
2) you can also check serum; if serum is spun down and cleared, it is myoglobin; is not cleared it is hemoglobin
3) anemia is suggestive of hemoglobin
4) increased CK is suggestive of myoglobin
How much liver function has to be lost for an animal to be in liver failure?
70-80% (failure to eliminate and synthesize substances
True or False: Liver enzymes are neither specific for the cause of liver disease nor predictive of the outcome.
What enzymes are indicative of hepatocellular injury?
Alanine Aminotransferase (ALT)
Aspartate Aminotransferase (AST) (a significant amount comes from muscle as well)
Sorbitol Dehydrogenase (SDH)
Glutamate Dehydrogenase (GLDH)
True or False: ALT is always liver specific.
False; you can see elevated levels with SEVERE muscle damage
How long after injury will you see ALT?
increases by 12 hrs post injury and peaks by 24-48 hrs
*half life is 72 hrs in dogs and 6 hrs in cats
What can 2X elevated levels of ALT indicate in young dogs? What should you measure?
can be indicative of portocaval shunts
should measure bile acids
True or False: In large animals increased ALT is indicative of liver damage.
False; there is more ALT in the muscle of large animals than in the liver; therefore ALT is not useful to evaluate the liver
What enzyme is useful for evaluating the liver in large animals?
SDH is usually used in large animals
(GLDH can also be used)
*both are liver specific in large animals
True or False: Both focal and diffuse hepatic necrosis cause laboratory changes.
False; only diffuse necrosis (greater than 60-80%) causes laboratory changes (increase leakage and induced enzymes and bile acids)
What cells produce alkaline phosphatase? What are increased levels indicative of?
produced by osteoblasts (-> high in young animals)
elevated levels indicative of cholestasis and corticosteroids
True or False: ALP is not induced by steroids in cats because cats do not get steroid hepatopathy.
False; ALP is not induced by steroids in cats but they DO get steroid hepatopathy
What enzyme is better for looking at hepatocellular damage in cats?
GGT (except for hepatic lipidosis)
If you see an increase in ALP without hyperbilirubinemia, what will you suspect?
steroid or anticonvulsant medication induction
When will you see increases in gamma glutamyl transferase (GGT)?
cholestasis, steroids, and hepatic injury
(not with anticonvulsant therapy)
What are the laboratory findings for cholestasis?
mild increase in leakage enzymes
marked increase in induction enzymes
moderate to marked increase in serum bilirubin
moderate to marked increase in bile acids
What would you suspect with increased enzymes in an old dog? What would you suspect in a middle aged dog? What about a young dog?
old dog: nodular hyperplasia
middle aged dog: chronic hepatitis
young dog: portocaval shunt (do bile acid), or portocaval hypoplasia
What are non hepatic disease associated with elevation in enzymes?
hypothyroid, pancreatitis, hypoxia
What are the causes of vacuolar hepatopathy?
hypoxia, infectious disease, metabolic disease, GI disease, neoplasia, cardiovascular disease, nutritional abnormalities, inflammatory disorders, benign nodular hyperplasia in old dogs
What are the substances removed by the liver?
What is indicated by an increase in bile acids?
Deviation of portal circulation (portosystemic shunt or cirrhosis)
Decrease in hepatocyte uptake (inflammation, necrosis, steroid hepatopathy, decreased functional hepatic mass)
Decreased bil excretion with subsequent regurgitation into blood (cholestasis, bile duct leakage)
True or False: In chronic liver disease, >60% of dogs are hyperalbuminemic.
False; they will be hypoalbuminemic
Why might you only see a minor decrease in globulin with chronic liver disease?
because globulin is also synthesized by lymphoid tissue
True or False: Ammonia is decrease and BUN is increase in liver failure.
False; the liver converts ammonia to urea, therefore in liver failure ammonia will be increased and BUN will be decreased
What two things cause decreases in cholesterol?
not taking in dietary cholesterol (starvation, malabsorption, maldigestion) or liver failure
Which coagulation factors does the liver produce? How else does the liver effect coagulation factors? What happens if factor activities are less than 30%?
I, II, V, VII, IX, X
Bile flow is also necessary for absorption of vitamin K dependent factors (II, VII, IX, X)
At less than 30% -> prolonged clotting time, aPTT, and PT
What will you see with an early portosystemic shunt?
enzyme activity may be normal or increase
bile acids increased
microcytic anemia (maybe)
What will you see with a late portosystemic shunt?
Liver failure leading to decreased albumin, BUN, glucose, cholesterol, and coagulation factors
marked increase in bile acids, cholestasis (inceased bilirubin and ALP), and microcytic anemia
What are you thinking when you see a markedly increased ALP with a normal (or mildly increased) GGT?
phenobarbitol or hepatic lipidosis
What is a common etiology for chronic hepatitis?
Infectious (lepto, ICH)
Drugs (primidone, phenobarbitol, some NSAIDS)
What are the most common breeds for chronic hepatitis? Which ones are associated with copper?
Copper associated: Bedlington terriers, West highland whites, skye terriers, dobermans, dalmations, and labs
Non copper associated: cocker spaniels and standard poodles
True or False: You will see laboratory abnormalities before you see clinical abnormalities in chronic hepatitis patients.
When should you take a glucose sample from an animal?
during fasting (except in non ruminants) unless there are symptoms of hypoglycemia
How are ruminants different in their sources of glucose?
they do not have intestinal absorption and used volatile fatty acids for gluconeogenesis
How is blood glucose regulated by insulin?
secreted by the pancreatic islet cells to lower glucose by increased uptake, inhibiting liver gluconeogenesis, and promoting liver glycogen storage
How is blood glucose regulated by glucocorticoids?
increases blood glucose by promoting hepatic gluconeogenesis, inhibiting insulin binding, and inhibiting insulin action
How do catecholamines regulate blood glucose?
(epinephrine and norepinephrine)
increase hepatic glycogenolysis, inhibit insulin secretion, stimulate glucagon secretion, and inhibit insulin action
How does glucagon regulate blood glucose?
secreted by pancreatic islet alpha-cells to increase hepatic gluconeogenesis and glycogenolysis, and inhibit insulin binding and action
How does growth hormone regulate blood glucose?
increases blood glucose by inhibiting cellular glucose uptake, inhibiting insulin action, and increasing hepatic gluconeogenesis
What lab error can cause hypoglycemia?
failure to remove the serum from clot within 30 minutes (should collect in a fluoride/gray top tube to inhibit glycolysis)
What are some conditions in the body that can cause hypoglycemia?
beta-cell tumore (insulinoma)
hepatic failure (decreased glucogenesis and glycogenesis)
neonatal/juvenile hypoglycemia (inadequate glycogen and protein stores)
ketosis/pregancy toxemia (neg energy balance)
xylitol (giving gum to a dog)
Ackee fruit (Jamaican vomiting sickness)
What neoplasms other than insulinoma can cause hypoglycemia?
Discrete cell tumors (lymphocytic leukemia, lymphoma, plasma cell tumor)
Epithelial tumors (hepatocellular, mammary, pulmonary, calivary carcinomas, hepatomas)
Connective tissue tumors (leiomyosarcoma, leiomyoma)
At what level of blood glucose will you see a drop in insulin? If insulin does not drop what will you think?
if blood glucose is less then 60 mg/dl insulin should drop
if insulin is still high at this point think insulin producing producing tumor (insulinoma)
What are the most common causes of hyperglycemia?
cateholamines from exertion, fear, or pain (may reash 400 mg/dl in cats)
panreatitis (increased glucagon production)
hormone imbalance (GH/acromegaly, glucadonoma, hyperadrenocorticism, pituitary tumor
ethylene glycol toxicosis
Megestrol acetate in cats
cattle with milk fever, moribund animals, and proximal duodenal obstruction
How does ethylene glycol cause hyperglycemia?
the first metabolite of ethylene glycol is aldehyde which prevents glucose uptake by cells
also causes stress and azotemia
What is the blood glucose renal threshold for dogs, cats, horses, and cattle? What happens when the threshold is exceeded?
Dogs: 180-220 mg/dl
Cats: 290 mg/dl
Horses: 180 mg/dl
Cattle: 100 mg/dl
when the threshold is exeeded you will have glucosuria
What can excess glucose lead to?
Hyperadrenocoticism can lead to excessive insulin release, beta-cell exhaustion and atrophy which can lead to resultant diabetes mellitus
True or False: Ruminants can have incredibly high blood glucose levels ranging from 600-1000 mg/dl with duodenal obstruction.
What is the major form of diabetes mellitus in dogs? What is the major form in cats?
Dogs: type I (immune mediated beta-cell destruction -> no insulin production)
Cats: type II (decrease insulin production)
What is Fructosamine? What is it used for?
a glycated protein (protein + glucose) that increases with hyperglycemia
used for diagnosing diagnosing diabete mellitus (more sensitive in cats)
used to rule out transient hyperglycemia (more sensitive in dogs)
used for monitoring glycemic control
What is glycated hemoglobin? How does it compare to fuctosamine?
formed in erythrocytes as a result of a reaction between glucose and hemoglobin
it can detect hyperglycemia over a longer period of time than can frutosamine
What are some common laboratory abnormalities associated with diabetes mellitus?
dehydration, increased PCV, total protein, glucosuria, ketonuria, osmotic diuresis, low specific gravity, electrolyte loss, increased plasma osmolality
What is ketonuria and ketonemia a sign of?
altered lipid metabolism seen with disorders of negative energy balance (diabetes mellitus, starvation, pregnancy, toxemia, bovine ketosis)
How does treatment of diabetes mellitus with insulin and fluids cause dramatic hypokalemia? What other electrolyte has this similar process?
lack of insulin and acidosis causes a shift in potassium to the ECF, when insulin and fluids are given it drives all the available potassium that has accumulated outside the cell back inside causing hypokalemia
The same thing happens to phosphorus (could lead to hemolysis)
How is the IV glucose test conducted? What other test should you do with this one?
fast for 12-24 hours, give 0.5 g glucose / kg body weight, collect blood and 5 minute intervals; normal animals will have normal blood glucose levels within 60 minutes
You should also measure serum glucose by obtaining a fasting blood sample, normal animals should not go below 70 mg/dl glucose within 24 hours of fasting (animals with insulin secreting tumors will go below 60 mg/dl glucose in 8-10 hrs)
What is the normal level blood glucose for fasted dogs?
70-100 mg/dl glucose and 5-20 micro units/ml insulin
What is a normal reaction for a normal cat or dog after glucose administration for an IV glucose tolerance test? When will you suspect insulin dependent diabetes mellitus?
Dogs: insulin increases 5-10X at 5 minutes and returns to baseline by 60 min
Cat: insulin increases 2-3X at 5-15 minutes and returns to baseline by 120 min
Insulin dependent diabetes mellitus is indicated when there is a low baseline serum insulin with little to no increase
What is used to detect pancreatic injury?
serum amylase, serum lipase, peritoneal fluid amylase/lipase, trypsin-like immunoreactivity (dogs and cats only), pancreatic lipase immunoreactivity
What does it mean when amylase it greater than 3-4X the upper end of normal?
suggestive of pancreatic injury
What does it mean when lipase is greater than 2X the upper end of normal?
suggestive of pancreatic damage or dogs receiving steroids
What happens to lipase and amylase in dogs given corticosteroids? Which drug causes the most change in lipase?
lipase goes up but amylase may stay normal or decrease
Dexamethoasone can cause up to a 5X increase in lipase
What other system besides the pancreas can show increases in amylase and lipase?
you may see an increase in both with renal failure or prerenal azotemia
True or False: When amylase/lipase serum levels are high than pancreatic levels you should consider pancreatitis.
False; you should consider pancreatitis when peritoneal levels are higher than serum levels
At what stage of pancreatitis will you see increases in TLI's (trypsinogen)? What is an increase in TLI's also a sign of?
only in the early stages because it is cleared rapidly
increases TLI's can also be due to decreased GFR, malnourishment, Dexmethasone (with azotemia)
What level of PL is suggestive of pancreatic inflammatory disease in cats? What level in dogs?
Cats: >12 ug/L
Dogs: >400 mg/L
What are some other abnormalities seen with pancreatitis?
increased liver enxymes
True or False: Amylase is the main enzyme for determining pancreatitis in cats.
False; amylase is of no value in cats
What are the main clinical signs of a cat with feline pancreatitis?
anorexiam lethergy dehydration, weight loss, hypothermia, icterus, fever, abdominal pain, dierrhea, and palpable abdominal mass
What are the laboratory findings of feline neucrotixing pancreatitis?
anemia, hemoconcentration, neutrophilia, neutropenia, increased ALT, AST, ALP, and increasted bilirubin
What would cause the fecal occult test to be positive? What ultimately determines that?
when there is 20-50% sensitivity
determined by the amount of pseudoperoxidase activity
What can cause a false negetive fecal occult blood?
high vitamin C intake, high fluid content of diluted blood, blood nor uniformly distributed in the sample, and reading error
What indicates bacterial overgrowth in a fecal cytology?
homogeneity (fecal matter should be heterogenous)
What is exocrine pancreatic insufficiency? How is this different from malabsorption? What are the clinical signs?
inadequate food digestion
in malabsorption the food is digested by disease prevents absorption
clinical signs: weight loss, poorly formed stools, and increased fecal volume
What will you see with malabsorption?
voluminous, poorly formed, gray feces with hypoproteinemia (protein losing enteropathy)
Where is folate absorbed? Where is vitamin B12 absorbed?
Folate: in the proximal small intestine (jejunum)
Vitamin B12: in the distal small intestine
What will you suspect with a decrease in folate and a normal vitamin B12?
proximal small intestinal defect
What will you suspect with a normal folate and a decrease in vitamin B12?
distal small intestinal defect
What is the connection between intrinsic factor, viatmin B12 and the pancreas in cats?
the pancreas secretes intrinsic factor which is essential for the absorption of vitamin B12, if EPI causes a decrease in IF, you should also see a decreases in B12
Where organ system other than the pancreas can you have intrinsic factor secretion.
the stomach secretes IF
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