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  1. anterior pituitiary hormone release
    • releases indirect hormones (trophic hormones).
    • Negative feedback loop
  2. posterior pituitary hormone release
    • direct hormones produce effect in target organ.
    • Vasopressin (ADH, kidney)
    • oxytocin (uterus and mammary gland/milk letdown. Neurohormonal reflex)
  3. Tropic hormones
    • secreted by anterior pituitary, indirect-acting hormones (cause secretion of second hormone that causes effect)
    • TSH (thyroid stimulating hormone)
    • ACTH (adrenocorticotropic hormone) (cortisol)
    • LH (luteinizing hormone) (ovaries/testes, ovulation and testosterone)
    • FSH (follicle-stimulating hormone) (ovaries/testes, follicles and spermatogenesis)
    • LTH (prolactin) (mammary gland, milk production)
    • GH (growth hormone, somatotropin)(body growth, mammary gland)
  4. neurohormonal reflex
    • udder stimulation, stimulation of uterus/vagina during parturition and stimulation of cortex/stimulation for lactation/nursing/milking
    • cause oxytocin release, which causes milk letdown.
  5. Adrenal cortex
    • produces steroids, mainly from cholesterol
    • glucocorticoids and mineralcorticoids
  6. Glucocorticoids
    • steriods produced from adrenal cortex zona fasciculata and zona reticularis.
    • Major is cortisone, cortisol.  
    • Secretion regulated by ACTH from anterior pituitary
    • Carbohydrate, fat and protein metabolism
  7. Mineralcorticoids
    • steroids produced from adrenal cortex zona glomerulosa
    • major is aldosterone, acts in kidney to increase sodium reabsorption and potassium secretion. 
    • Secretion regulated by: renin-angiotensin pathway, hyperkalemia, ACTH stimulation
  8. hyperadrenocorticism
    • Cushing's disease, common in dog, rare in cat, complex in horse. 
    • Increased secretion of glucocorticoids.  
    • Can be pituitary dependant, adrenal dependant, iatrogenic
  9. Hypothalamic-pituitary axis
    CNS feels stress, tells hypothalamus to release corticotropin releasing hormone, which tells anterior pituitary to release ACTH, which tells adrenal cortex to release cortisol, whose presence in blood tells anterior pituitary to stop releasing ACTH
  10. PDH
    • pituitary dependant hyperadrenocorticism.
    • 80% of dogs have this form.  90% of those are microadenoma (tiny, benign, active tumor).  Macroadenoma causes seizures
    • secretes ACTH all the time, regardless of Cortisol levels
    • Adrenals get bigger.
  11. adrenocortical neoplasia
    • adrenal tumor on one gland. That gland produces cortisol constantly, ACTH never released due to cortisol levels in blood, other adrenal shrinks in disuse atrophy. 
    • More common in large-breed dogs
    • Can be removed with surgery, give and taper steriods to wake up atrophied gland
  12. Iatrogenic hyperadrenocorticism
    • Glucocorticoid administration leads to constant cortisol in blood, ACTH never released, adrenals never make cortisol, disuse atrophy, get very small.  
    • Taper steroids
  13. Clinical signs of hyperadrenocorticism
    • PU/PD (cortisol increases GFR and inhibits ADH release)
    • Polyphagia
    • symmetrical alopecia
    • pendulous abdomen (weak belly muscles from protein breakdown)
    • enlarged liver (increase in ALP, possibly ALT)
    • Muscle weakness and wasting (visible vertebrae)
    • panting
    • fragility syndrome in cats (fragile skin)
    • calcinosis cutis (calcium lesions on skin)
    • neurological signs from macroadenoma (dull listless attitude, stupor, anorexia, aimless walking, circling, ataxia, seizures)
  14. Hyperadrenocorticism hemogram
    Steroid leukogram (lymphopenia, eosinopenia, mature neutrophilia, monocytosis, mild polycythemia)
  15. hyperadrenocorticism UA
    • specific gravity ~ 1.020 in dogs, maybe more dilute due to suppression of ADH (suppressing immune as concentration fights UTI)
    • UTI in 50% of dogs
    • Proteinuria in 50% of dogs, mild, UPC 2-3
  16. hyperadrenocorticism blood chemistry
    • mild hypercholesterolemia
    • increased ALP
    • increased bile acids (mild)
    • mild hyperglycemia
    • hyperlipidemia
  17. 5 diagnostic tests for hyperadrenocorticism
    • urine cortisol/creatinine ratio
    • ACTH stimulation test
    • Low dose dexamethasone suppression test
    • high dose dexamethasone suppression test
    • abdominal ultrasound (size of adrenals, scan for tumor)
  18. urine cortisol/creatinine ratio
    • a rule-out. Use voided sample so animal is less stressed for accuracy
    • Increased suggests cushings but not diagnostic.  
    • normal rules out cushings (<13)
  19. ACTH stimulation test
    • Test of choice.  Evaluates ability of adrenals to increase cortisol levels in response to ACTH.  
    • Take baseline sample, administer exogenous ACTH (cosyntropin), take post sample at 60 minutes.  
    • In cat, take again at 90 minutes.  
    • In horse, take at 2 and 4 hours instead
  20. exaggerated response to ACTH stim test
    • >20ug/dl.  Hyperadrenocorticism, ADH or PTH.
    • bilateral adrenocortical hyperplasia or responsive tumor
  21. mild response to ACTH stim test
    8-20 normal.  Negative feedback should stop much response
  22. diminished response to ACTH stim test
    • < 8 iatrogenic cushings or addisons
    • atrophied adrenals produce less cortisol due to chronic admin of exogenous glucocorticoids.
  23. Low Dose Dexamethasone Suppression Test (LDDST)
    • confirms spontaneous Cushings, changes with stress.  Good for second opinion after ACTH.
    • Take baseline blood sample, administer dexamethasone IV (0.01mg/kg in dog, 0.1mg/kg in cat), take 4 and 8 hour samples
  24. Low dose dexamethasone suppression test, no change
    • no response indicates iatrogenic (maybe addisons), cortisol levels already suppressed due to atrophy
    • exogenous glucocorticoids already caused adrenal atrophy, produce less cortisol, so ACTH levels are suppressed normally.  
    • Dex does not decrease ACTH secretion or cortisol level
  25. Low dose dexamethasone suppression test, lack of suppression
    • adrenal-dependant hyperadrenocorticism (cortisol levels stay high) (probably).  Could be pituitary tumor (30%).
    • nonspecific result, does not differentiate between PDH and ADH, do abd ultrasound, HDDST or check endogenous ACTH
  26. Low Dose dexamethasone suppression test, 4hr suppression, 8 hr escape
    suggests pituitary tumor (70%).
  27. Low Dose dexamethasone suppression test, suppression
  28. Ultrasound differentiating between PDH and ADH
    • PDH: bilateral hyperplasia or normal adrenals, but same on both sides
    • ADH: unilateral adrenal enlargement, other is hypoplastic or undetectable
  29. High Dose Dexamethasone Suppression Test
    • differentiates between PDH and ADH
    • no suppression in ADH
    • PDH suppression is dose-dependant (high will eventually suppress, no escape)
    • Baseline bloods, administer 0.1-1.0mg/kg in dog, 1.0mg/kg in cat, take 8 hour post sample.
  30. High Dose Dexamethasone Suppression Test no suppression
    • adrenal dependant hyperadrenocorticism
    • 25% of pituitary dependant willalso not be suppressed (unclear why)
  31. High Dose Dexamethasone Suppression Test suppression
    75% of pituitary dependent hyperadrenocorticism or normal.
  32. Endogenous ACTH concentration
    • Distinguishes ADH from PDH in dogs, must be tested IMMEDIATLY, ACTH not stable
    • ADH: low ACTH level, 60% undetectable plasma ACTH
    • PDH: high ACTH levels
    • Measure single baseline plasma ACTH concentration.  Not routine test.
  33. Treatment of pituitary dependant Hyperadrenocorticism
    • Traditional: Lysodren/mitotane to erode adrenal cortex (type of chemo, can kill cortex and create Addisons, easier to treat).  Watch for Addisonian crisis of VDA/lethargy
    • Trilostane: inhibits enzyme in cortisol production.  Most react minorly, occasional idiosyncratic addisonian reaction
    • Ketoconazole: antifungal, interferes with androgens/estrogen. Not useful
    • L-Deprenyl (inhibits dopamine breakdown. Not useful
  34. Treatment of adrenal-dependent hyperadrenocorticism
    adrenalectormy surgery.  Can try to use mitotane/Lysodren to kill tumor, but usually not useful
  35. Treatment of iatrogenic hyperadrenocorticism
    taper steriods off.
  36. hyperadrenocorticism in cats
    • very rare. 
    • Different from dogs: associated with diabetes mellitus, relentless weight loss leading to cachexia, fragility syndrome in skin
    • Also seen: hyperglycemia, glucosuria, hypercholesterolemia, increase in ALT
    • Don't see: stress leukogram, increase in ALP, urinary abnormalities
  37. Diagnostic tests for hyperadrenocorticism in cats
    • urine cortisol/creatinine ratio (screen)
    • ACTH stim (60 and 90 mins)
    • LDDST (0.1mg/kg)
    • HDDST (1.0mg/kg)
    • abdominal ultrasound
    • NOT endogenous ACTH
  38. Results of diagnostics for hyperadrenocorticism in cats
    • urine cortisol/creatinine like dogs
    • dex tests more variable than dogs due to diabetes.  Test at 4, 6 and 8 in HDDST, increase at 8h is suggestive of Cushings, increases at 4 and 6 support diagnosis, probably
  39. Differentiation of PDH v ADH in cats
    • HDDST: suppression = PDH. No suppression needs more testing
    • Abdominal ultrasound: PDH bilateral adrenals, larger or normal, ADH unilateral enlargement and hypoplasia
  40. Diagnosis of hyperadrenocorticism in cats
    • clinical signs, physical exam, abdominal ultrasound, and tests.  
    • Put it all together.  No real definitive.
  41. Treatment of hyperadrenocorticism in cats
    • ADH: adrenalectomy 
    • PDH: bilateral adrenolectomy with post-surgery medications.  Can attempt medical management, but problematic.
  42. cachexia
    severe muscle wasting
  43. Primary hypoadrenocorticism
    • glucocorticoid and mineralcorticoid deficiency
    • Immune-mediated destruction of adrenal gland
    • clinical signs begin with 90% of adrenals destroyed, wax and wane and start slowly.
    • Mineralcorticoid deficiency: abnormal electrolyte concentrations lead to cardiac problems
    • Glucocorticoid deficiency: GI signs
  44. Secondary hypoadrenocorticism
    • "Atypical Addisons"
    • Glucocorticoid deficiency, mineralcorticoids normal (aldosterone), electrolytes normal.
    • GI signs
    • Reduced ACTH from pituitary, not adrenal damage.  Lesion in pituitary or hypothalamus.  
    • Long-term admin of exogenous glucocorticoids or megestrol acetate
  45. Clinical signs of Hypoadrenocorticism
    • Vague, waxing and waning except in Addisonian crisis (shock, cardiac arrest, bradycardia from hyperkalemia)
    • Lethargy, anorexia, episodic VD, weight loss, weakness/depression, dehydration
  46. Hemogram of hypoadrenocorticism
    • normocytic, normochromic nonregenerative anemia of chronic disease
    • eosinophilia
    • lymphocytosis
  47. Chemistry of Hypoadrenocorticism
    • *Hyperkalemia, hyponatremia (Na:K < 27:1), though normal in secondary
    • prerenal azotemia (dehydration)
    • hyperphosphatemia
    • hypercalcemia
    • hypoglycemia (not always)
  48. UA of hypoadrenocorticism
    USG < 1.020
  49. Tests/diagnosis of hypoadrenocorticism
    • Hx, exam, clinopathologic findings
    • basal cortisol screening test, <2 ug/dL (not diagnostic, just a R/O)
    • definitive: ACTH stim test, post ACTH cortisol <2 ug/dL. Can't increase
  50. differentiating 1 vs 2 hypoadrenocorticism
    • Electrolytes: N:K < 27:1 = primary; Normal is early primary or secondary
    • Baseline ACTH concentration (RUSH to lab), most reliable.  High = primary, Low = secondary.
  51. Treatment of Addisonian crisis (primary hypoadrenocorticism)
    • Emergency.  
    • Correct hypotension, hypovolumia, electolyte imbalance (decrease K and Ca, increase Na), metabolic acidosis (give0/9% NaCl with sodium bicarb), vascular integrity (worried about DIC)
    • Provide immediate water-soluble glucocorticoids (desamethasone sodium phosphate), IV until orals given
    • Desoxycorticosterone pivalate (Percortin) if mineralcorticoids needed
  52. Maintenance treatment of Hypoadrenocorticism
    • Mineralcorticoid supplementation: Desoxycorticosterone pivalate (Percorten) IM every 25-30 days
    • Fludrocortisone acetate PO BID (mineral and gluco)
    • Glucocorticoid supplementation: Hydrocortisone (closest to endogenous) BID then tapered down to lowest effective.
    • Administer in times of stress!  50% on Fludrocortisone only need hydro in stress
  53. Treatment of secondary hypoadrenocorticism
    • administration of glucocorticoids (forever)
    • sometimes can gradually taper and discontinue exogenous glucocorticoids or megestrol acetate.  
    • Monitor electrolytes so secondary doesn't progress to primary
  54. Thyroid-produced Hormones
    • T3 (20%) Triiodothyronine (4x more potent than T4)
    • T4 (80%) Thyroxin
  55. Thyroid hormones function
    • Regulates basal metabolism
    • Increase O2 consumption/heat production
    • small amts glycogen storage, large amts glycogenolysis.  Increases gluconeogenesis.
    • increase absorption of glucose and uptake by cells
    • **enhances effects of sympathetic nervous system (tachycardia, etc)
    • increases CO, force of contraction, HR
    • increases blood volume
    • Normal growth and development
  56. Causes of Primary hypothyroidism
    Most common form, includes destruction of thyroid gland, immune-mediated or idiopathic.
  57. Causes of Secondary hypothyroidism
    • problem in pituitary gland causing impaired TSH secretion
    • Second most common
  58. Causes of tertiary hypothyroidism
    • problem in hypothalamus causing deficiency in thyrotropin releasing hormone
    • Very rare
  59. Clinical signs of hypothyroid
    lethargy, fatigue, cold intolerance, weight gain with poor appetite, bilaterally symmetrical alopecia (usually trunk, not itchy), dry skin and hair, reproductive problems
  60. Thyroid stimulation
    hypothalamus produces thyrotropin releasing hormone, pituitary produces thyroid stimulating hormone, then thyroid produces T3 and T4, which come back to stop the pituitary and hypothalamus.
  61. Lab results of hypothyroidism
    • hypercholesterolemia***
    • hyperlipidemia
    • mild normocytic, normochromic nonregenerative anemia (sometimes)
  62. T4
    • 80% of thyroid hormone secreted.  >99% exists bound to plasma proteins as a buffer
    • and reservoir. 
    • The rest is free T4, which can enter cells and is active. Diagnostically significant levels.
    • When fT4 enters cell, becomes T3
  63. Thyroid gland function assessment
    • Screening test is T4 concentration (too little T3)
    • Thyroid panel includes T4, fT4 and TSH concentration, definitive diagnosis
  64. first screening test for hypothyroidism
    • baseline serum T4 concentration.  Includes T4 and fT4 in circulation.  Decreased indicates hypothyroid but is not definitive.  Other things can decrease T4 (drugs, illness, random fluctuations, aging)
    • Can also do free T4 baseline serum, a little less effected by illness or drugs.
  65. Things that decrease T4 in euthyroid dogs
    • concurrent illness (Non-Thyroidal Illness in dogs, Euthyroid Sick Syndrome in cats)
    • drugs
    • random fluctuations
    • Aging decreases production
  66. Baseline endogenous canine TSH concentration (with T4, fT4 readings), expected findings for hypothyroid or other
    • Hypothyroid: decreased T4, decreased fT4 and increased TSH with appropriate hx and exam. Supports diagnosis
    • Normal levels of T4, fT4 and TSH RULES OUT hypothyroid
    • Decreased all three could be secondary (or tertiary, but rare)
  67. Treatment of hypothyroid
    • Soloxine
    • Thyro Tabs
    • (synthetic Leothyroxine, human drug is no good)
  68. Iatrogenic hypothyroidism
    • most common cause in cats (from treating their hyperthyroid)
    • bilateral thyroidectomy, radioactive treatment, overdose of anti-thyroid drugs
  69. Naturally occurring adult-onset primary hypothyroidism in cats
    • RARE
    • Congenital much more common
  70. Congenital primary hypothyroidism causes
  71. Hyperthyroidism in cats
    • Multisystemic disorder, excessive production and secretion of T3 and T4
    • Caused by thyroid tumor (usu benign)
    • Can be unilateral or bilateral, or start uni and become bi
  72. Clinical signs of hyperthyroidism
    • weight loss (cachexia in cats) with polyphagia
    • restlessness/hyperactivity, vocalizing
    • hair coat changes, alopecia, mats, no or excessive grooming
    • PUPD (can be concurrent renal disease)
    • V/D
  73. Physical exam findings in hyperthyroidism
    • palpable thyroid mass
    • tachycardia, heart murmur, gallop rhythm, premature beats, dropped beats
    • hyperactive
    • dehydrated
    • cachectic appearance, thin
    • aggressive
    • hypertension
  74. Lab results of hyperthyroid
    • CBC usually normal, possible slight polycythemia
    • Can see stress leukogram
    • mild to moderate increased ALT
    • increased T4 and fT4
  75. Diagnosis of hyperthyroid
    • Take Hx and clinical signs, PE into account
    • Increased serum T4, if high enough.  Other wise add fT4. Both high supports.
    • high fT4 with low or normal T4 indicates euthyroid sick syndrome in cats or non-thyroid illness in dogs
  76. Methimazole
    • Hyperthyroid drug that stabilizes, anti-thyroid.
    • Can be long-term, no contraindications
    • Consistency BID required
    • tumor keeps growing
    • mild reactions like GI, facial pruritus, lymphocytosis, eosinophilia, leukopenia
    • Severe immune-mediated hypersensitivity like agranulocytosis, thrombocytopenia, hepato- or renal toxicity.
  77. Thyroidectomy
    • treatment for hyperthyroid. 
    • Complications: ectopic thyroid tissue located elsewhere, metastatic carcinoma may have spread, removal of parathyroid, cardiac arrhythmias/failure (cats already often have hypertrophic cardiomyopathy)
    • Disadvantages: anesthetic risk, Post-op complications (Ca, heart), potential for iatrogenic hypothyroidism (take one at a time)
  78. Radioactive Iodine
    • Treatment of choice for hyperthyroidism
    • Advantages: ectopic tissue and thyroid carcinoma gone, no anesthesia, no loss of parathyroids
    • Contraindications: CRF (maintains increased sympathetic tone, so GRF decreased), CHF (hypertropic cardiomyopathy), evidence of metastasis
    • Disadvantages: go somewhere special, expensive sometimes twice, prolonged hospitalization, hazard to humans, iatrogenic hypothyroidism
  79. Science diet y/d
    • for treating hyperthyroid, reduced iodine diet, changes thyroid levels in 3 weeks.  
    • avoids daily meds, not a great treatment but cheap and easy for owner
    • Tumor continues to grow
    • High in carbs, gain weight, risk diabetes
  80. Hyperthyroidism in dogs
    • caused by thyroid tumors, adenoma or carcinoma, only 10% active causing hyperthyroidism.
    • Clinical signs: swelling/mass in neck, polyphagia with weight loss, hyperactivity, PUPD (renal?), panting, behavior change/aggression
    • Diagnosis: high T4 and fT4, no TSH seen.  Needs surgery
  81. Three ways to introduce glucose to body
    • diet
    • glycogenolysis
    • gluconeogenesis
  82. Glycogen
    intracellular storage form in liver of glucose
  83. 4 ways glucose levels are maintained
    • glycogenolysis/gluconeogenesis
    • peripheral tissue utilization (muscle, CNS, etc)
    • intestinal digestion and absorption of carbs
    • hormonal influence from pancreas and adrenals (insulin, glucagon, glucocoriticoids, catecholamines)
  84. insulin
    • made by: beta cells of pancreas
    • net effect: lower blood glucose concentrations by shifting glucose, fatty acids and amino acids to their storage forms (glycogen, triglycerides and proteins).
    • Increases glucose uptake and storage in all cells but RBC, neurons and renal tubular epithelial
    • Promotes glycogen production in liver
    • Increases uptake of amino acids and K+ into cell
  85. Glucagon
    • Made in: alpha cells of pancreas
    • net effect: increase glucose concentration in blood
    • Liver: decrease glycogen synthesis and increase glycogenolysis, increase gluconeogenesis
    • stimulate insulin release so glucose can be used
  86. Glucocorticoids and carbohydrate metabolism
    • from adrenal cortex, primarily cortisol, in response to stress
    • Net result: increase in hepatic glycogen, increase blood glucose (stress hyperglycemia)
    • Action: stimulates hepatic gluconeogenesis, increases hepatic glycogen,
    • lipolysis, redistributes fat into abdomen and liver (hepatic lipidosis)
    • Inhibits protein synthesis and enhances catabolism, releasing amino acids.
    • Anti-insulin: inhibit glucose uptake and metabolism in peripheral tissues (esp muscle and adipose
  87. Epinephrine and carbohydrate metabolism
    • net effect: increases blood glucose especially in liver
    • actions: promotes glycogenolysis and gluconeogenesis, stimulates glycogenolysis in skeletal muscle
    • inhibits insulin secretion, stimulates glucagon secretion
    • Promotes lipolysis for free fatty acids
    • Sympathetic response, increased HR, CO, bronchodilation
  88. somatotropin in carbohydrate metabolism
    from anterior pituitary, increases blood glucose and reduces glucose uptake by myocytes and adipocytes
  89. Effects on blood glucose of insulin, glucagon, cortisol, epinephrine
    • insulin lowers blood glucose
    • rest increase blood glucose, have anti-insulin effect
  90. physiologic hyperglycemia
    • No glucosuria
    • postprandial hyperglycemia: carb digestion increase blood glucose.  Returns to fasting levels within 4 hours in monogastric animal.
    • Stress, excitement or fright: Epi and NorEpi release stimulates glycogenolysis and GH release, decreases insulin release, increases glucagon, stimulates ACTH which increases cortisol and therefore hyperglycemia
    • Steriod-associated hyperglycemia: glucocorticoids produced by "stress" stimulate gluconeogenesis, insulin resistance, increase blood glucose.  Cortisol is anti-insulin, increases glucagon.
  91. Who has greatest hyperglycemia values
    cats, 300mg/dL.  No glucosuria indicates physiologic, not pathologic.
  92. Steroid-associated hyperglycemia
    glucocorticoids produced by "stress" stimulate gluconeogenesis, insulin resistance, increase blood glucose.  Cortisol is anti-insulin, increases glucagon.
  93. Excitement or Fright hyperglycemia
    Epi and NorEpi release stimulates glycogenolysis and GH release, decreases insulin release, increases glucagon, stimulates ACTH which increases cortisol and therefore hyperglycemia
  94. Postprandial hyperglycemia
    carb digestion increase blood glucose.  Returns to fasting levels within 4 hours in monogastric animal.
  95. Pathologic hyperglycemia
    Diabetes mellitus
  96. Diabetes Mellitus
    • group of metabolic diseases causing hyperglycemia from defects in insulin secretion, insulin action or both
    • Insulin deficiency (insulin-dependant): disorders that cause a progressive loss of beta cells
    • insulin resistance (non-insulin dependant): disorders in which there is insulin antagonism by hormones.  Common in cats, adult humans
  97. Type I Diabetes Mellitus
    • Dogs
    • insulin-dependant
    • Beta cell destruction, usually immune-mediated
    • leads to absolute insulin deficiency
  98. Type II Diabetes Mellitus
    • Obese cats, start at II and become I
    • non-insulin dependant
    • inadequate compensatory insulin secretory response
    • caused by defects in insulin secretion
    • post-insulin receptor defects in target cells
  99. Clinical signs of Diabetes Mellitus
    • PUPD
    • Polyphagia
    • weight loss
    • V/D
    • neuropathy (walking on hocks)
    • cataracts
    • dehydration (here and below, DKA)
    • anorexia
    • lethargy
    • coma
    • death
  100. DKA
    • diabetic ketoacidosis
    • decreased glucose utilization (from diabetes) leads to hyperglycemia and glucoseuria
    • body metabolizes storage, fats then protein
    • hepatic catabolism of fat to fatty acids and ketones
    • ketones build up, causing ketonuria (1), ketonemia (2), metabolic acidosis/ketoacidosis.  Metabolizing protein adds to acidosis/muscle wasting
  101. Diagnosis of diabetes mellitus in: 
    • dogs: blood glucose over 180mg/dL
    • cats: blood glucose over 200-280mg/dL
    • Both: GLUCOSURIA (stressed cats get hyperglycemia without glucosuria)
  102. Fructosamine
    • Representative of glucose level over preceding 2-3 weeks.
    • Normal is 225-375 umol/L (cats <300)
    • good for screening in cats or diabetes monitoring
    • Excellent control = 350-400 umol/L
    • good control = 400-450 umol/L
    • fair control = 450-500 umol/L
    • poor control = >500umol/L
  103. Treatment of diabetes mellitus
    • type I, dogs: insulin injections (NPH, vetsulin, levemir)
    • type II, cats: high protein low carb diet and weight loss
    • type I, cats: insulin injections (PZI, glargine)
    • Monitoring: BG curves, Fructosamine, urine ketodiastix.  Watch for negautive glucoseuria (insulin too high) or positive ketones in urine (insulin too low)
  104. Sign that insulin dose is too low
    ketones in urine
  105. Sign that insulin is too high
    negative glucoseuria
  106. glargine
    • insulin for cats, human recombinant, intermediate to long-acting, U-100, SQ.
    • Peak-less insulin.  Very steady, no highs or lows.  
    • Puts 30% of newly-diabetic cats into remission
  107. Dog insulin is molecularly similar to
    pork insulin.
  108. Cat insulin is molecularly similar to
    human or cow insulin
  109. Concentration of insulin
    • measured in units, physiologic activity rather than weight.
    • U-100 (100U per ml) for humans
    • Vets also have 40U for smaller volumes.
    • Must use syringes that correspond with the drug.
  110. Humulin R
    • regular human recombinant insulin, short-duration, only one that can be given IV, IM and SQ.  
    • Rapid onset, good for ER or DKA patients
  111. Humulin N, NPH
    human recombinant insulin, intermediate duration, given SQ to dogs, primarily.
  112. Vetsulin
    Pork insulin, tends to work best in dogs.  Intermediate-duration, U-40, SQ
  113. PZI Vet
    Beef (90%) and pork (10%) insulin, used mostly in cats, intermediate-duration, U-40, SQ.
  114. Insulin use and storage
    • refrigerate, shelf-life 28 days, but up to 6 months in fridge
    • do not use with discoloration or precipitate
    • Resuspend before giving, roll bottle to not destroy proteins.
    • Alternate injection sites, use low-fat areas
    • Feed prior to administration (hypoglycemia adverse effect). Also tremors, seizures, etc. Keep Karo on hand.
  115. Decreased insulin antagonists, pathologic
    Hypoadrenocorticism leads to hypocortisolemia, decreased gluconeogenesis, increased insulin sensitivity in target cells
  116. Increased insulin secretion, pathologic
    (Pancreatic B-Cell neoplasia)
  117. Hypoglycemia
    • Blood glucose < 60 mg/dL
    • Caused by: increased glucose utilization, decreased glucose production or both
  118. Decreased gluconeogenesis, pathologically
    • hepatic insufficiency/failure
    • starvation
    • neonatal or juvenile hypoglycemia
  119. Decreased glycogenolysis, pathologically
    glycogen storage disease
  120. Increased glucose utilization, pathologic
    • lactation
    • exertion (Iditarod)
  121. Pathogenesis leading to hypoglycemia, unknown causes
    • sepsis (bacteria use up glucose?)
    • pregnancy
  122. Pharmacologic or toxic causes of hypoglycemia
    • insulin OD
    • ethanol (drunk)
  123. Clinical signs of hypoglycemia
    • Blood glucose < 45mg/dL
    • seizures
    • weakness
    • collapse
    • restlessness
    • nervousness
    • hunger
    • muscle fasciculations
    • ataxia
    • Less commonly, lethargy, blindness, bizarre behavior or coma
  124. Hypoglycemia causes in puppy or kitten
    • idiopathic
    • starvation
    • liver insufficiency (PSS)
    • sepsis
  125. hypoglycemia causes in young adult dog or cat
    • liver insufficiency
    • hypoadrenocorticism
    • sepsis
  126. hypoglycemia in older dog or cat
    • liver insufficiency
    • beta-cell neoplasia
    • hypoadrenocorticism
    • sepsis
Card Set:
2013-11-19 01:18:55
Clin Path

Endocrine in Clinical Pathology
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