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What are the functions of Magnesium?

facilitates Na/K-ATPase activity in cell membranes
bone formation
PTH synthesis and release
nerve conduction
Ca channel activity
phosphorus transport

What is the main means of control of handling magnesium?

renal excretion

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)
Hyperaldosteronism (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
Frank tetany
Cardiac arrythmias and possible arrest
Coronary artery spasms (in humans)
Eating disorders

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 are the clinical signs for hypermagnesemia?

Heart dysfunction
GI upset

What three things affect plasma volume?

urine, GIT, and sweat

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?

RAAS (renin-angiotensin-aldosterone-system)
*Na is reabsorbed at the distal tubule

What three things does aldosterone get secreted in response to?


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?

GI sequestration

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

What is the major extracellular fluid anion?


Where is most of the chloride reabsorbed?

the proximal tubule

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

True or False: Chloride is usually regulated secondary to Na, and parallels Na concentration.


What two drugs can interfere with chloride transport?

Furosemide and GI enterotoxins

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)

What are the major intracellular cations?

potassium and sodium

What is the main regulation for potassium?

renal excretion

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

What condition can cause HCO3, K, and Cl to all be low?


3rd space syndromes can cause hyperkalemia. What is the exception?


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

How does insulin spike (glucose bolus/excitement) cause redistribution hypokalemia?


What does the fractional excretion tell us?

normal fractional excretion suggests non-renal cause for electrolyte loss (suggests diarrhea)

How does water move in the body?

Across lipid bilayers and through aquaporins

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

How do you calculate the osmole gap?

Osmole gap = (measured osmolality) - (calculated osmolality)

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

True or False: Hydration status is equal to vascular blood volume.


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?

ECF: sodium
ICF: potassium
*plasma sodium is influenced by potassium

True or False: Blood volume is largely related to Na concentration.


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?

diabetes insipidus
diabetes mellitus
osmotic diuretic
osmotic diarrhea
water deprivation

What is isotonic dehydration?

when water loss is equivalent to electrolyte loss
Serum sodium and chloride do not change

What are some causes of isotonic dehydration?

renal disease
excess vitamin D

What is hypotonic dehydration?

when electrolyte loss is greater than water loss

What are some causes of hypotonic dehydration?

secretory diarrhea
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?

1) pCO2
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 does a hyperchloremia with normal sodium suggest?

a metabolic acidosis

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

What are the unmeasured cations?

Ca, Mg, and gammaglobulins

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?

dead-space rebreathing
airway obstruction
respiratory center depression (drugs/disease)
pulmonary disease
restrictive 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?

displaced abomasum
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) fluorescence
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)

True or False: Ethylene glycol is an anion.

False; it is an osmole

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?

Dogs: adenocarcinomas
Cats: adenomas

What is the breed predilection for dogs with adenocarcinoma?

beagles, boxers, golden retrievers

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 is the most common canine endocrinopathy?

Canine hypothyroidism

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
fasting hypercholesterolemia
fasting hypertriglyceridemia
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)

What does PTH regulate?

Increases calcium and decreases phosphorus

True or False: Hyperparathyroidism is in more than 70% of hyperthyroid cats.


True or False: Dogs and cats both tend to get a parathyroid adenoma rather than a carcinoma.


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?

stress leukogram
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 sodium level is diagnostic of hyposdrenocorticism?

less than 23

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

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