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211 Cards in this Set

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The hypothalamus produces what hormone and what does it stimulate?
Thyrotropin releasing hormone stimulates the release of TSH from the pituitary gland.
What does TSH stimulate?
The thyroid to produce and secrete T4 and T3 thyroid hormones.
What is the control of secretion on the pituitary gland?
Negative feedback of T4 and T3 act to decrease TSH from the pit gland.
TRH increases TSH from the pit gland.
What is serum TSH's level compared to T4?
Inversely proportional.
We measure T4 in the serum as 99% is bound to plasma proteins. Rank the hormones in order of metabolic activity starting with the most active thyroid hormone.
T3 > fT4 > T4
What are the three general actions of thyroid hormones?
1. Mediated via regulation of gene expression.
2. Increase basal metabolic rate and metabolism of carbohydrates, proteins, lipids.
3. Affect almost all organs in the body.
Which type (primary or secondary) of Canine Hypothyroidism is more common?
Primary destruction of the gland itself (95%)
What are the 4 types of primary hypothyrodism? How common are they?
1. Lymphocytic thyroiditis - autoimmune dz causing 50%
2. Idiopathic follicular atrophy causing ~50%
3. Neoplasia - rare
4. Congenital primary hypothyroidism - rare
Secondary hypothyroidism is destruction of what?
Destruction of TSH secreting cells.
What is the common signalment for canine hypothyroidism?
Young adult to middle age.
Purebred, mid to large size dogs.
What are the general clinical signs of canine hypothyroidism?
Dull, lethargic, weight gain, cold intolerance.

All due to decreased metabolic rate.
What are the dermatologic signs of hypothyroidism?
Alopecia around neck and tail progressing to bilaterally symmetrical over the trunk.
Dry, oily, or dermatitic seborrhea.
Hyperpigmentation.
Recurrent otitis externa and pyoderma.
Myxedema (tragic facial expresion).
What are the cardiovascular signs of hypothyroidism?
Bradycardia, weak pulses, muffled heart sounds.
Low voltage ECG complexes.
Decreased ventricular contractility.
What are the neuromuscular signs of hypothyroidism?
Peripheral neuropathy - generalized (ataxia/atrophy) or localized to facial or vestibular nerve.
CNS - CN abnormalities in 5,7,8. with ataxia and head tilt.
What are the reproductive clinicals signs with hypothyroidism?
Males NOT affected.
Females have prolonged anestrus, infertility, abortions or increased periparturient pup mortality.
This is only with severe and prolonged hypothyroidism.
Describe myxedema coma
Hypothermia w/o shivering, depression progressing to coma, bradycardia, hypotension, myexedema.
Chem profile shows low Na, glucose, and cortisol, and lipemia.
This is rare but life threatening.
What are the clinical signs with congenital hypothyroidism?
dull, lethargic, difficult to train, hypermetric, dwarfism due to epiphyseal dysgenesis, macroglossia (enlarged tongue), broad head.
What are the laboratory findings with hypothyroidism if you ran a chem profile?
Hypercholestrolemia.
Mild normocytic, normochromic anemia.
Mild hypoNa+ may occur.
Since hypercholesterolemia is common in 75% of hypothyroid dogs what are some other R/O for hypercholesterolemia?
Cholestatic liver dz
Diabetes mellitus
Pancreatitis
Cushings (hyperadrenocorticism)
Primary lipidemia
Post prandial hypercholesterolemia
Nephrotic syndrome with PLN
How is hypothyroidism diagnosed?
Clinical signs and thyroid function tests.
What would a hypothryoid dog's serum T4, fT4 and endogenous TSH tests come back as?
Serum T4 is decreased
Free T4 is decreased
TSH is increased
The most accurate hypothyroid test is?? Is it used often?
FT4 is the most accurate and avoids effects of various factors on protein binding in plasma.
It is measured by equilibrium dialysis and this is in limited availability throughout the US.
What tests do most practioners use for Dx of hypothyroidism?
Serum T4 in comparison to TSH.
How does one test for autoimmune thyroiditis?
Antithyroglobulin Ab is formed against thyroid follicle colloid protein in 40-50% of hypothyroid dogs.
What is the problem with Dx of autoimmune thyroiditis?
The antithyroglobulin Ab can be found in hypothyroid and euthyroid dogs. False positives are possible.
What are three factors affecting thyroid function tests?
Nonthyroidal illness
Drugs
Breeds
How does nonthyroidal illness affect thyroid function tests?
Decreased T4 is common in dogs with NT illness. TSH may be elevated. fT4 may not be affected but most cant test for fT4. Avoid testing when NT illness is present or if possible a low fT4 and high TSH indicated canine hypothyroidism.
How do drugs affect thyroid function tests?
May cause changes in thyroid hormones to mimic canine hypothyroidism.
Glucocorticoids, Pb, Clomipramine, and Sulfonamides.
What breeds can alter thyroid function tests?
Sight hounds - whippet/grey hound have normally low levels of T4.
What is the Rx for hypothyroidism in dogs?
Levothyroxine 2x a day.
What is the typical response to Rx of canine hypothyroidism?
Increased activity and attitude in 1-2w. CS should resolve w/in 2m of treatment except for dermatologic changes that may require several months.
Recheck in 8w with post pill testing.
What are the side effects of levothyroxine?
Thyrotoxicosis --> patient becomes hyperthyroid.
Signs = weight loss, increased appetite, hyperactive, PUPD, tachycardia. Confirmed by elevated serum T4. Stop Rx for 2-3d and reinstitute at lower dose.
What are the two causes of feline hyperthyroidism?
Adenomatous hyperplasia and carcinoma
What is the signalment for hyperthyroid cats?
old - 12-13yrs
What are the general clinicals signs for feline hyperthyroidism?
Weight loss despite good appetite (although the cat is generally overweight to begin with).
Polyphagia
Hyperactivity

All due to increased metabolic rate.
What are the GI signs for feline hyperthyroidism?
Diarrhea with increased volume of soft feces due to increased food intake and GI motility.
Vt due to rapid intake of food and the direct effects of T4 on the CRTZ.
What are the hepatic signs of feline hyperthyroidism?
Elevated serum hepatic enzymes - ALT, ALP
Due to Hypoxia, CHF, and direct toxic effect of thyroid hormones on the liver.
What are the renal signs of feline hyperthyroidism?
PUPD due to increased renal blood flow from increased cardiac output. This may decrease BUN and Creat.
What are the skeletal system signs of feline hyperthyroidism?
Increased bone turnover and hyperPhosphatemia.

Also see elevated ALP
What are the cardiovascular signs of feline hyperthyroidism?
Increased CO, increased HR and stroke volume.
Increased adrenergic responsiveness.
Direct effect of thyroid hormones on heart cause LV hypertrophy.
Heart murmur or gallop.
Tachycardia.
Heart failure and sinus tachycardia (uncommon)
Systemic arterial hyerptension.
Erythrocytosis due to increased Ep production and direct effect of thyroid hormones on bone marrow.
On PE of a feline with suspected hyperthyroidism what would you typically find?
PUPD, Polyphagia, weight loss, unkept coat, thin, palpable thyroid (bilateral in 75%), panting.
Some common lab findings with feline hyperthyroidism are...
Elevated liver enzymes (ALT, ALP 2-3x normal)
increased BUN and creat due to minimal urine concentrationand increased GFR.
Diagnosis of feline hyperthyroidism is done how?
Clinical signs and elevated T4. A single elevated T4 in a cat with compatible signs is diagnostic.
How can nonthyroidal illness affect T4 test? A fT4 test?
NT illness can decrease T4 and and increase fT4.
Free T4 by equilibrium dialysis would be what in a hyperthyroid cat?
Increased. This is more sensitive than serum T4
What do you do if hyperthyroidism is suspected in a cat but basal T4 is normal?
Free T4 or repeat T4.
Can do T3 suppression test but not common to do.
Radionuclide imaging with technetium pertechnetate scan.
What are the treatments for feline hyperthyroidism?
Antithyroid drugs - Methimazole
Iodine compounds for short term management.
Ethanol injection to destroy thyroid tissue.
Radioactive Iodine Rx.
Surgery.
How does Methimazole work for hyperthyroid Rx?
It inihibits the incorporation of iodine into tyrosine residues on the thyroglobulin molecule.
Basically it inhibits synthesis of thyroid hormones.
Give orally or transdermal.
What are the side effects of methimazole?
Occur w/in the first 2-3m of treatment.
Anorexia, Vt, lethargy.
Transient eosinophilia, lymphocytosis, leukopenia, agranulocytosis, thrombocytopenia, hemolytic anemia.
Hepatotoxic with liver enzyme elevation and icterus.
What is a complication for ethanol injection to Rx feline hyperthyroidism?
Extra-thyroid injection can cause damage to surrounding structures resulting in laryngeal paralysis.
If available, what is the treatment of choice for feline hyperthyroidism?
Radioactive iodine Rx. Iodine 131 is taken up by adenomatous thyroid gland and follicular cells are destroyed. No real side effects and its 98% effective!
What Sx can be done to Rx feline hyperthyroidism?
Bilateral thyroidectomy. Problems are surgical and anesthetic risks - horners syndrome, laryngeal paralysis, hypoparathyroidism.
Why is renal failure a concern with hyperthyroid Rx?
All treatments can decrease renal blood flow due to decreased cardiac output when a euthyroid state is reached. As T4 decreases, GFR will decreased as will BUN and Creat. A cat can be managed in chronic kidney disease for years! Not so with hyperthyroidism!
What does the medulla of the adrenal gland produce?
Catecholamines
What does the cortex of the adrenal gland produce?
Steroid hormones
What are the three zones of the adrenal cortex and what do they produce?
Zona glomerulosa - mineralocorticoids (aldosterone)
Zona fasiculata - glucocorticoids (cortisol)
Zona reticularis - minor glucocorticoids and weak sex steroids.
Where are the corticosteroids produced by the adrenal gland metabolized and excreted in dogs and cats?
Metabolized in the liver for both dogs and cats. Urinary excretion for dogs, biliary excretion for cats.
What is the major glucocorticoid hormone?
Cortisol
What are the functions of glucocorticoids?
Affects on metabolism:
1. increase liver gluconeogenesis
2. Decrease peripheral glucose utilization
3. Protein catabolism
4. Increase lipolysis
How are glucocorticoids regulated?
Stress increases hypothalmic secretion of CRH.
CRH stimulates ACTH release from the pituitary.
ACTH stimulates the adrenal cortex to produce cortisol.
Cortisol has negative feedback on hypothalamus and pituitary.
What is the major mineralocorticoid hormone?
Aldosterone.
Cortisol and corticosterone have slight mineralocorticoid activity.
What are the functions of aldosterone?
Maintain electrolyte balance.
Maintain extracellular water volume.
Increases renal Na retention.
Increases renal K secretion.
Increases renal tubular H+ secretion.
Minor increase in intestinal Na resorption.
How is aldosterone secretion controlled?
Plasma K+ concentration directly affects aldosterone and when K+ is high, aldosterone is secreted.
Hypotension stimulates aldosterone secretion through the renin/angiotension system.
Minor effect of reduced Na via renin/angio system to stimulate aldosterone secretion.
What are the major catecholamines that the adrenal medulla produce?
Most is epinephrine. Also norepinephrine.
What do the catecholamines do?
Blood vessel constriction (raises BP).
Increased cardiac rate and strength.
Inhibits GI motility.
Mydriasis.
Increases metabolic rate.
What are the two general types of canine hyperadrenocorticism?
Pituitary dependent (excess ACTH by pituitary tumor)

Adrenal dependent (adrenal tumor)
What is the signalment for PDH?
Older dogs with male and female equally represented. Common breeds are min poodles, dach, bostons, silky terrier.
What is the signalment for ADH?
Older dogs with 65% female. 50% are over 20kg but no real breed predilection.
The majority of PDH dogs have a functional pituitary tumor. What are the other few causes of PDH?
Idiopathic with speculation that it may be food induced, a microscopic pit tumor, or another tumor producing ACTH.
What type of tumor is most common with ADH?
60% adenocarcinoma arising from the adrenal cortex.
40% adenoma.
Are ADH tumors unilateral or bilateral?
Most are unilateral and because of negative feedback on the pituitary by excess cortisol being produced by the tumor, there is atrophy of the contralateral adrenal cortex.
What are the effects of excess cortisol?
Diuresis and PU. Cortisol inhibits vasopressin secretion and increases GFR.
Protein catabolism leading to muscle wasing and weakness with a potbelly.
Inhibits inflammation and immune fct which can predispose to infection.
Increased hepatic gluconeogenesis and peripheral insulin resistence leading to increased hepatic glycogen deopsition and increased lipolysis.
Polyphagia.
What are the common clinical signs of cushings?
PUPD
Pendulous abdomen
Bilaterally symmetrical alopecia
Hepatomegaly
Lethargy
Polyphagia
What is a recommended plan for DX of hyperadrenocorticism?
CBC, Chem, UA to rule out other diseases.
ACTH stim test or LDDS.
High Dose dex suppression test.
Abdominal U/S and radiology.
What is commonly seen on the CBC for cushings patients?
Eosinopenia
Lymphopenia
Mature neutrophilia
---Stress leukogram

Occasional erythrocytosis
What is the common biochemical results of cushing patients?
Increased ALP
Hypercholesterolemia
Increased ALT
Mild hyperglycemia (hyperadrenocorticism can cause secondary diabetes mellitus)
What is seen on a UA of a cushings dog?
Proteinuria
Bacteriuria (often w/o pyuria [WBC])
Variable SG
Abdominal Rads show what with cushings dogs?
Hepatomegaly
Calcinosis cutis
Dystrophic mineralization (renal pelves, gastric mucosa)
ADH dogs have soft tissue adrenal mass +/- mineralization of gland.
The ACTH stim test is the most specific test for ID of hyperadrenoC. Is it sensitive as well?
Yes. The ACTH stim test is the best but some don't use due to cost.
What is a postive result with the ACTH stim test?
Post-ACTH cortisol is > ref range.
What is a positive result for the LDDS test?
Cortisol at 8h post dexamethasone is >1ug/dL or greater than the ref. range.
There is failure for suppression to hold for 8 hours.
How a Urine Cortisol/Creat ratio be used in testing for hyperadrenocorticism?
It's very sensitive but needs a second confirmatory test.
How do you differentiate PDH from ADH?
High dose dex suppression test - where cortisol is suppressed in most PDH but still elevated in ADH.

Endogenous ACTH concentration.

U/S to see large adrenals if ADH and not if PDH.

LDDS will differentiate 50% of cases.
Rx and Px of PDH?
Trilostane that inhibits production of cortisol.
Mitotane that kills the adrenal cortex.

PX is that the patient is never cured, only medically managed. 70% alive at 1 yr, 50 at 2yr, 20 at 4yr.
Rx and Px of ADH?
Surgery - afterwards pt will be hypoadrenal and you have to supplement cortisol.

Mitotane.
Ketoconazole that inhibits enzymes but can be hepatotoxic.
Trilostane.

PX - 50% of adenocarcinomas are inoperable. Immediate post op survival with adenoma is 60-100%, 20-100% with adenocarcinoma.
What is addisons disease in the dog?
Canine Hypoadrenocorticism.
What is the difference between primary and secondary addisons?
Primary is most common and is caused by immune destruction of adrenal cortices. There is glucocorticoid and mineralocorticoid deficiencies.

Secondary is caused by pituitary failure (neoplasia) and glucocorticoid deficiency only.
What is the signalment for Addisons?
Young adult dogs around 2.5-6.5yrs.

Mostly females with intact more common than spayed females.

If in males it's normally a castrated male.

Can occur in any breed.
What does a glucocorticoid deficiency cause?
Weakness and lethargy with an inability to deal with stress and hypoglycemia.
What does a mineralocorticoid deficiency cause?
Severe Na loss.
Hypovolemia.
K+ retention leading to hyperK
Decreased acid excretion from kidneys.
Excxess colonic Na and water loss --> Hypovolemia and diarrhea.
What are the effects of hyperkalemia from a mineralocorticoid deficiency?
Excess K has a negative cardiac inotropic effect and cardiac arrhythmias are common.

Peaked T wave, prolonged PR interval, wide QRS, bradycardia, AV block.
What are the common clinical signs of Addisons?
Anorexia
Lethargy and depression
Vt.
Weakness
Dehydration
What is a common Dx plan for hypoadrenocorticism?
CBC
Chem
UA
ECG
Basal cortisol concentration (to rule in addisons but can't r/o)
ACTH stim test - main test
Hypoadrenocorticism has what typical CBC results?
Lack of a stress leukogram (different from cushings)
Lymphocytosis and eosinophilia.
What are the common Biochemical abnormalities with Addisons?
Na/K ratio <27:1
HyperK
Increased BUN and Creat
HypoNa
HyperP
HyperCa
Although the SG is variable with Addisons, most are hyposthenuric, isosthenuric, or hypersthenuric?
Isosthenuric. 90% are less than 1030
Basal cortisol and ACTH stim test can lead to DX of Addisons. What are positive results?
Basal cortisol <1ug/dl
Post ACTH cortisol is undetectable

Normally both would be detectable in a healthy animal.
Therapy for acute crisis with hypoadrenocorticism includes what?
Correct hypovolemia and electrolyte imbalances.
Perform ACTH stim test.
Replace glucocorticoids and mineralocorticoids.
Keep NPO 24hr.
What is the long term management of Hypoadrenocorticism?
Mineralocorticoid replacement with oral fludrocortisone or injectible DOCP.

Glucocorticoid replacment with oral prednisolone.
Px of Addisons?
Excellent! Normal life span with medically managed.
The pars distalis portion of the pituitary gland produces what?
Growth hormone (somatotropin)
Adrenocorticotrophic hormone (ACTH)
TSH
Prolactin
FSH
LH
What controls the secretion of pars distalis pituitary hormones?
The hypothalamus hormones.
What hormones are produced in the hypothalamus?
Corticotropin releasing hormone (CRH)
Thyrotropin releasing hormone (TRH)
GnRH
Growth hormone releasing hormone (GRH)
Somatostatin
True or false: Hormones of the pars distalis have negative feedback on the hypothalamus.
True.
What does the pars nervosa of the pituitary produce?
Neurons originate in the hypothalamus and extend into the PN. It produces oxytocin and vasopressin (ADH).
What is the physiology of vasopressin - ADH?
Hypothalamus receptors detected increased osmolality and increase ADH, decreased osmolaltiy and decrease ADH.

Vascular baroreceptors and stretch receptors detect decreased BP and increase ADH, increased BP and decrease ADH.
How does vasopressin (ADH) act on the kidney?
It increases renal tubular permeability to water and causes the urine to be concentrated.
There are MANY causes to the problem "failure to thrive." What is a good Dx plan?
Gather Hx: diet, litter size, managment and competition for food, presence of dysphagia, underlying disease signs?

PE: heart murmurs, cleft palate, nasal dc. Can do esophagram, rads, echo.

Fecal: deworm empirically

Can do STLI for chronic small bowel diarrhea is signs present.

CBC, Chem, UA with bile acids.
After other causes of failure to thrive are ruled out how can you confirm pituitary dwarfism?
Serum thyroxine and TSH.
Serum ACTH and ACTH stim.
Serum GH before and after xylazine or GHRH for stimulation.
What is canine acromegaly most commonly caused by?
Hyperprogesteronemia which stimulates mammary cells to produce growth hormone.
What is the common signalment for canine acromegaly?
Most common in older bitch in luteal phase of estrus. 4-11yrs.
What are the clinical signs of canine acromegaly?
Excessive oropharyngeal tissue that can lead to stridor.
PUPD
Fatigue
Abdominal enlargment
XS skin folds
Mammary tumors
Vaginal dc
Increased interdental spaces
What can you use to Dx acromegaly?
Signalment and CS.
Elevated ALP and glucose.
Increased serum somatomedin.
What is the Rx for canine acromegaly?
Spay
W/D progesterone therapy
Progesterone receptor antagonists (not in US)
Insulin if needed for secondary diabetes
What are some r/o for PUPD?
Drugs - corticosteroids, Pb
Renal dz/failure
Diabetes mell
Liver dz
Pyometra
HyperCa
Hyperadrenocorticism
Hyperthyroidism
HypoK
Hypoadrenocorticism
Acromegaly
Polycythemia
Renal glucosuria
Central diabetes insipidus
Nephrogenic diabetes insipidus
Psychogenic polydipsia
What is a diagnostic plan for PUPD?
Differentiate from pollakiuria.
Hx
UA 3x.
Chem, CBC
When evaluating PUPD and your SG comes back as hypersthenuric, isosthenuric, or hyposthenuric, what can these values tell you?
SG >1030 with normal glucose and protein you should be thinking psycogenic PD, liver dz, or hyperadrenocorticism.

With Isosthenuria 1008-1012 this renal failure, consider test to measure GFR (nuclear scintigraphy), and creat clearane test.

With hyposthenuria <1008 think hyperadrenocorticism, liver dz, pyometra, CDI, NDI, psychogenic, hyperCa.
How does the water deprivation test work?
Deprive water
Give ADH
50+% increase in urine osmolality after giving ADH = CDI
Urine not concentrated after ADH = NDI

Note - a concentrated urine with deprivation with little or no response to ADH points to psycogenic polydipsia.
How does the ADH response test work?
Measure water consumption at home for 2d.
Begin Rx with DDAVP (synthetic ADH) in eye or oral and measure water consumption.
Take USG.

Marked reduction in urine volume - CDI.
No response to DDAVP - think other causes of PUPD.
What is Nephrogenic Diabetes Insipidus?
Renal tubules do not respond to ADH.

Most cases are acquired.
Pyometra, pyelonephritis, Cushings, Addisons, hyperCa, hypoK, hyperthyroidism.
To help Dx NDI you do a modified water deprivation test. What does this entail?
Deprive water until pt. loses 5% of body weight.
Measure USG - urine not concentrated with deprivation in NDI.
No response to ADH administration with NDI.
Rx NDI?
Treat the underlying condition.
Idiopathic? Use Chlorothiazide diuretics or salt restriction.
What do the chief cells of the PT gland secrete? The C-cells?
Chief secrete parathyroid hormone.
C-cells produce calcitonin.
What are the acute effects of PTH?
Acute - increase Ca release from bone pool, increase renal Ca resorption and P excretion.
What are the long term effects of PTH?
Mobilization of Ca and P from stable gone.
Increases Ca and P GI absorption indirectly by increasing active form of Vit D.
The net effect is to increase plama Ca and decrease plasma P.
How does the concentration of Ca affect PTH?
Low ionized Ca stimulates secretion of PTH. High Ca inhibits PTH.
What are the actions of Calcitonin?
Decreases Ca and P mobilization from bone.
Increases movement of P into bone.
Increases renal excretion of Ca and P.

Net effects - decreases plasma Ca and P.
How does Ca concentration affect Calcitonin?
Hypercalcemia stimulates release of calcitonin. Low Ca inhibits calcitonin.
What are the actions of Vit D?
Increase Ca and P GI absorption.
Promotes movement of Ca and P from bone.

Net effect - increases plasma Ca and P.
What are the main causes of hypercalcemia?
Growth (puppies) - bone activity.
Hypercalcemia of malignancy - PTHrP or bone infiltration by tumor.
Renal failure (hemoconcentration, reduced GFR)
Addisons (hemoconcentration)
Primary hyperparathyroidism
Hypervitaminosis D
Hemoconcentration (increased Albumin)
What tumors are associated with hyperCa++
Most common associated tumors are lymphoma, anal sac adenoC, myeloma.
How is Ca related to albumin?
Calcium is 40% bound to albumin. When albumin is low, you can have low Ca.
How does hyperCa++ affect the body?
It inhibits ADH action causing PUPD.
Ionized Ca affects cell membrane activity and can lead to neuromuscular, renal, and cardiovascular dysfunction.
Mineralization of soft tissues - heart and kidney.
What are the clinical signs of hyperCa??
Those of an underlying dz.

PUPD
Anorexia
Lethargy
Weakness
Cardiac arrhythmias
Seizure/muscle twitches.
What causes a high Ca with a normal or low P?
Malignancy
Feline idiopathic hyperCa
Primary hyperparathyroidism
Differentiate primary renal failure from secondary renal failure due to hyperCa.
With primary renal failure - ionized Ca is almost always normal. Azotemia and hyperP are severe. Other signs of small kidneys, anemia, and Vt are present.

With secondary renal failure from hyperCa - high ionized Ca, mild azotemia, mild hyperP.
Aggressive therapy for hyperCa is?
Aggressive therapy needed with azotemia, dehydration, Ca x P >70 or Ca >16.

IV 0.9% NaCl
Furosemide to increase Ca excretion
Avoid thiazides because they reduce Ca excretion.
Corticosteroids
Calcitonin
Pamidronate disodium IV infusion with NaCl over 2 hours.
Maintenance therapy for HyperCa is?
Oral glucocorticoids
Oral furosemide
Injectible Calcitonin
How does pH affect Ca?
Acidosis increases ionized Ca.
Alkalosis decreases ionized Ca.
What are the common causes for hypoCa?
Hypoalbuminemia
Renal failure (xs P from low GFR)
Ethlyene glycol
Puerperal tetany
Acute pancreatitis
Hypoparathyroidism
Phosphate enema
What does hypoCa do to the body?
Neuromuscular dysfunction as it's necessary for NT release.
Destabilizes nerve cell membranes.
What are the clinical signs of hypocalcemia?
Restless
Tremors
Seizures
Muscle fasciluation
Weak
Anorexia
Ataxia
Facial rubbing
Panting
Small capsular cataracts
Rx for Hypocalcemia?
IV 10% Ca gluconate to effect.
Follow with continuous IV Ca gluconate.
Alternatively - SQ Ca gluconate diluted with saline.
Hypocalcemia, hyperP, azotemia rule outs?
Acute renal failure
Chronic renal failure
Hypocalcemia, HyperP, no azotemia rule outs?
severe hypoMg, primary hypoparathyroidism.
Common causes of hyperPhosphatemia.
Bone growth
Azotemia
Primary hypoPTH
Vit D intoxication
Phosphate administration IV or enema.
When hypophosphatemia is noted you might see what clinical signs?
Hemolysis
Rhabdomyolysis
Coma
Cardiomyopathy
NOTE - Usually no signs of low P are seen with Hypercalcemia or malignancy and primary hyperPTH.
NOTE - Usually no signs of low P are seen with Hypercalcemia or malignancy and primary hyperPTH.
HypoP is sometimes associated with what?
Diabetic ketoacidosis during therapy.
Enteral nutrition of anorexic cats.
What is Puerperal Tetany associated with?
Hypocalcemia with pregnancy or lactation.
When does puerperal tetany occur?
one to 3 weeks post partum.
What is the common signalment for puerperal tetany?
large dogs mostly in the last 1/3 or pregnancy.
Since the signs of puerperal tetany are the same as hypocalcemia how can you Dx it?
Clinicals signs, history, and measured low Ca and P. Response to therapy also confirms.
Puerperal tetany Rx?
IV Ca gluconate followed by continuous Ca IV drip or SQ. Wean pups/kittens.
Vitamin D intoxication is associated with what?
Rodenticides and psoriasis ointment.
What are the clinical signs of Vit D intox?
lethargy
anorexia
vt
shock
Very high Ca and P
Azometia
What is the Rx for Vit D intox?
IV fluids, furosemide, calcitonin, palmidronate.
Define anagen, catagen, telogen.
Anagen - the period of hair growth
Catagen - the transition phase
Telogen - the resting phase of the hair cycle
What are some extrinsic factors that influence the hair cycle?
Hormones (adrenal, gonadal, pituitary, pineal, thyroidal)
Photoperiod
General State of Health
Ambient temperature
What are some intrinsic factors that influence the hair cycle?
Growth factors and cytokines.
Alopecia X is what type of alopecia?
Acquired alopecia due to an endocrinopathy
What PE findings will there be with an alopecia X patient?
PUPD
Pendulous abdomen
Testicular asymmetry/cyrptorchidism
Vulvar enlargement
CHange in activity level
Weight gain
What is the clinical approach to pruritis with alopecia X?
If pruritis is absent pursue the pattern of hair loss, presence of inflammation and lesions.

If pruritis is present, do a skin scraping, skin cytology, and dermatophyte culture.
What cytotoxic agent can cause hair loss?
Cyclophosphamide
What 4 conditions cause alopecia after clipping?
Hypothyroidism
Hyperadrencorticism
Alopecia X
Post-clipping alopecia
The sexual status of dogs can influence hair loss. How so?
Sertoli cell tumors
Ovarian cysts
Lack of cycling due to hypothryoidism and hyperadrenocorticism

All of these cause alopecia.
What are the clinical signs of Alopecia X?
Bilateral symmetrical hair loss originiating in frictional areas.
Primary hairs are lost first. "puppy like coat"
Alopecia X must be ruled in by exclusion. What are some tests that need to be done to rule out certain diseases that cause alopecia?
ACTH Stim
Histopathology
Skin scraping
TSH and T4 measurement

NOTE - a urine C/C ratio may be increased over a 10 day study in dogs with alopecia X.
What 6 hormones are screened in an adrenal panel?

Which is important with alopecia X?
Cortisol
Estradiol
Androstenedione
17- Hydroxyprogesterone
Progesterone
Aldosterone

17Hydroxyprogestone is sometimes increased in dogs with alopecia X.
What are some treatments for Alopecia X?
Melatonin - Give for 3 months before evaluating response.

Trilostane - Hair re-growth occurred within 4-8 weeks, but may take up to 6 months
What are the two forms of acanthosis nigrans?
Hereditary form: primary idiopathic acanthosis nigrans of dachshunds.

Secondary form: due to intertrigo, endocrinopathies, or hypersensitivities
What are the clinical signs of primary acanthosis nigrans?
Dachshund < 2 year old
Axillary hyperpigmentation, followed by lichenification, seborrheic changes, and alopecia.

With chronicity, lesions spread along ventrum and secondary pyoderma, Malassezia, and pruritus are common.
How is acanthosis nigrans diagnosed?
Exclusion. Clinical signs and histopathology (hyperpigmentation and hyperplasia - although nonspecific)
What is the treatment for acanthosis nigrans?
Controllable but not curable disease – in early cases benign neglect.
Symptomatic therapy - anti-seborrheic shampoos, or topical glucocorticoids (for focal lesions)

For more advanced cases - oral glucocorticoids, oral vitamin E, or melatonin
What is male feminization syndrome associated with?
Reported to occur in 24-57% of dogs with Sertoli cell tumor. Sertoli tumors are most often associated with cyrptorchidism.

Seminomas and interstitial cell tumors can also secrete estrogen and cause feminization syndrome.
What is the signalment and clinical signs associated with male feminization syndrome?
Middle-aged to older dogs.

Lesions: bilateral symmetric, non-pruritic alopecia. Pruritis occurs only is there is secondary pyoderma. Hyperpigmentation may occur. Linear preputial dermatosis.

Sites: perineum, ventrum, chest, neck and flanks.

Pendulous prepuce, gynecomastia, enlarged nipples, cryptorchid or mass in scrotal testis. Prostate may be enlarged and infected also.
What is Linear preputial dermatosis?
Narrow strip of erythema, hyperpigmentation, and scaling along the
ventral midline from the prepuce toward the scrotum.
What is the treatment for male feminization syndrome?
Bilateral castration.
Clinical response is usually seen within 3 months.
Remission followed by relapse indicates functional metastases.
Cisplatin as a single agent can be tried for cases associates with metastases.

Dogs with estrogen-induced bone marrow suppression have a poor prognosis.
What do the alpha cells of the pancreas produce?
Glucagon
What do the beta cells of the pancreas produce?
Insulin. These are the majority of the cells in the pancreas.
What do the D cells of the pancreas produce?
Somatostatin
What do the F or PP cells produce in the pancreas?
Pancreatic polypeptide
What does insulin secretion cause?
Glucose to move itno cells.
Glycogen, fat, and protein storage.
What does glucagon secretion cause?
Inhibits insulin secretion.
Stimulates glycogenolysis and gluconeogenesis.
Increases blood glucose.
Prevents hypoglycemia with high protein low carb meals. Also causes fatty acid mobilization.
What does increasing blood glucose due to glucagon?
It inhibits glucagon.
B cell paracrine fuction (GABA) turns off glucagon.
With type 1 DM how is glucagon affected with increased blood glucose?
Glucagon is elevated in type 1 DM.
After most nutrients from a meal have been absorbed and metabolized or stored what happens to blood glucose, insulin, and glucagon?
Blood glucose drops
Insulin drops
Glucagon increases.
What is the major stimulus for glucagon increases?
Hypoglycemia.
Glycogenolysis and gluconeogenesis also increase as glucagon increases.
What happens to insulin , glucagon, and fatty acids during prolonged fasting?
Insulin secretion is minimal.
Glucagon secretion is increased.
Fatty acid mobilization is increased and most are converted in the liver to ketones.
How is the nervous system affected by hypoglycemia?
Glucose is the only major energy source for nervous tissue.
The immediate response to hypoglycemia is to release glucagon and epinephrine.
The slower response is to increase secretion of cortisol and growth hormone.
What are the pathophysiologic causes of hypoglycemia?
Artifact of sample handling.
Increased flucose usage by insulinoma or large tumors.
Reduced glucose production from severe hepatic disease, transient juvenile hypoglycemia or hypoadrenocorticism.
Combination of increased usage/decreased production with sepsis and hunting dog hypoglycemia.
What are the clinical signs of hypoglycemia?
The CS result due to neuroglycopenia.
Sympathetic stimulation occurs first - tachycardia, nervousness, trembling, panting.
Neuro signs second - bizarre behavior, weak, dementia, collapse, seizure, coma.
What is a good Dx plan for hypoglycemia?
Review HX and signalment.
PE (sepsis? large tumor?)
CBC
Chem
Liver fct test
Rads
ACTH stim test
Simultaneous glucose and insulin (insulinoma)
What is an insulinoma?
Insulin secreting islet cell tumor of the pancreas.
Occurs in old dogs (uncommon) and ferrets (common).
Also malignant
What is the pathophysiology of an insulinoma?
Excess insulin causes hypoglycemia. This cause sympathetic stimulation and neuroglycopenia brain dysfunction (seizure).
What is a good Dx plan for insulinomas?
CBC, chem UA
simultaneous insulin/glucose - low glucose with high insulin suggests insulinoma.
Rads/US for metastasis or other tumors.
Laparotomy to remove mass and confirm.
What are the chemical abnormalities with insulinomas?
Hypoglycemia
Occasional increase ALP, ALT
Occasional increase bilirubin
Occasional decreased K
What are the treatment options for insulinomas?
Sx
Medical management - multiple small meals, pred, diazoxide
What is the PX for insulinomas?
Nearly all metastasize regarless of histopath.
Average survival 10-14m.
Range is 1-40m though!
What is the signalment for transient juvenile hypoglycemia?
Miniature and toy breeds
6w to 6m
Eventually outgrow by 6m
What are the reasons behind transient juvenile hypoglycemia?
High glucose need due to large brain/liver ratio.
Immature gluconeogenic and glycogenolytic systems.
Small muscle mass and fat stores.
RX for transient juvenile hypoglycemia?
IV 1-2ml/kg 50% glucose diluted to 25%.
Glucose can also be rubbed on the MM is vascular access cannot be obtained.
Treat cerebral edema if seizures exist - mannitol, O2, Pb.
What is neonatal hypoglycemia?
This occurs commonly when neonates <1m are sick for any reason.
Rx with SQ 1/2 strength LRS with 2.5% glucose and warm animal.
Can also give via stomach tube 5-10% glucose.
Describe type 1 DM?
Type 1 - juvenile onset with autoimmune destruction of beta cells causing an absolute insulin deficiency. This is insulin dependent DM.
THis is more common for dogs to get.
Describe type 2 DM?
Adult onset with a multifactorial cause including insulin resistance and abnormal insulin secretory patterns although total insulin secretion may be normal or increased.
There is a relative insulin deficiency. This is more common for cats to get.
What is the pathophysiology behind diabetes mellitus?
Hyperglycemia.
Glucosuria occurs when renal threshold is exceeded and leads to osmotic diuresis and PUPD.
Fatty acid mobilization occurs because of lack of insulin and cells need energy.
Liver metabolizes FA to ketones which results in acidosis and ketonuria.
Na and K lost due to diuresis.
There is a negative energy balance in spite of Polyphagia.
What are the major clinical signs of DM?
PUPD
Weight loss despite polyphagia
Bilateral cataracts that happen overnight
Hepatomegaly
Obese
Muscle wasting
Dermatologic changes.
What is good client education for DM?
Its lifelong management
insulin injections 1-2x d
feeding consistency crucial
constant exercise
What is the common signalment for canine DM?
More females than males.
If males, more likely castrated.
Most >7yr
Secondary diabetes can occur in the dog with was diseases?
Hyperadrenocorticism
Hypersomatotropism
Progesterone therapy
DX of uncomplicated DM is done how?
Chem - hyperglycemia >300
Glucosuria
Ketonuria
Fasting lipema