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34 Cards in this Set

  • Front
  • Back
In what zones of the adrenal cortex are glucocorticoids made?
zona fasiculata

zona reticularis
In what zone of the adrenal cortex are mineralocorticoids made?
zona glomerulosa
What are the effects of aldosterone of the kidney?
↑ tubular reabsorption of Na+

↑ tubular excretion of K+
What are the effects of cortisol?
antagonism of insulin: promote gluconeogenesis & glycogenesis, ↓ glucose uptake by insulin-sensitive tissues

↑ lipolysis

suppress wound healing, inflammation, & immune response
What zone of the adrenal cortex secretes sex hormones?
zona reticularis
What is the most common lesion associated w/ hypoadrenocorticism in dogs?
lymphocytic adrenalitis: destroys all 3 zones
What are causes of primary hypoadrenocorticism?
lymphocytic adrenalitis
-no regeneration of adrenal cortex --> require life-long therapy
-all 3 zones destroyed --> glucocorticoid & mineralocorticoid deficiency, electrolyte disturbances
-may be immune mediated
-end stage: “idiopathic
adrenal cortical atrophy”

necrosis +/- hemorrhage that destroys glands
-endotoxemia, DIC = adrenal cortical necrosis
-bacterial septicemia: Actinobacillosis (foals), Salmonella (horses)
-Waterhouse-Frederichsen: massive hemorrhage & necrosis of adrenal cortex (calves)
-viruses (fetuses, neonates): Herpes (IBR: cow, pseudorabies: pigs, equine rhinotracheitis)

granulomatous: rare
What are causes of secondary hypoadrenocorticism?
pituitary tumor that destroys ACTH producing cells --> secondary atrophy of ZF

rapid withdrawal of exogenous steroids: exogenous administration of steroids --> negative feedback to ACTH

overdose of Lysodren when treating Cushings --> massive adrenal cortical necrosis (ZG destroyed)

↓ ACTH --> atrophy of ZF & ZR --> glucocorticoid deficiency
ZG spared: only 10% dependent on ACTH for stimulation --> no mineralocorticoid deficiency or electrolyte disturbances

reversible: adrenal cortex will regenerate if causative agent removed
What is the most common lesion assoc. w/ hyperadrenocorticism in dogs?
functional pituitary tumor --> bilateral adrenal hypertrophy
What is the cause of primary hyperadrenocorticism?
functional adrenal tumor --> 1 big adrenal & contralateral atrophy

10-15% of dogs w/ Cushings

autonomous production of cortisol from functional adrenal cortical tumor (50% benign, 50% malignant)
What are causes of secondary hyperadrenocorticism?
functional pituitary tumor --> bilateral adrenal hypertrophy
-80-85% of dogs w/ Cushings
-80-90% of these are pituitary microadenomas --> ↑ ACTH production
-only 10-20% are pituitary carcinomas (if large enough, can produce CNS signs, ex. blidness)
-pituitary tumor is NOT responsive or only partially responsive to neg. feedback inhibition of ↑ cortisol --> continues to secrete ACTH

100% of horses w/ Cushings (tumor in pars intermedia)

most cats w/ Cushings: large pituitary tumor

iatrogenic: long term administration of steroids (may be #1 cause of Cushings in vet med)

idiopathic bilateral adrenal cortical hyperplasia: poodles, toys, minis, etc. (< 10% of all cases)
What causes the PU/PD in hyperadrenocorticism?
glucocorticoids antagonize ADH function on tubules (biochemical nephrogenic DI)

↑ GFR --> dilute urine

destruction of pituitary by tumor --> ↓ production of ADH
What is the pathway of thyroid hormone production?
thyrotropic releasing hormone (TRH) from hypothalamus stimulates thyroid stimulating hormone (TSH) from pituitary, which stimulates thyroid follicular cells to hypertrophy & undergo hyperplasia & produce more T3 & T4

a. produced by what cells?
b. secreted d/t...
c. function
a. C cells of thyroid
b. increased serum Ca, gut hormones
c. decrease serum Ca conc.
What are lesions assoc. w/ hypothyroidism in dogs?
lymphocytic thyroiditis: 90% of cases in dogs
-end stage: “idiopathic follicular collapse”
-gland destroyed w/ no regeneration: requires life-long tx

functional thyroid tumor: RARE
-thyroid tumors that cause NO functional problems are common in older horses & dogs

secondary: pituitary lesion --> ↓ TSH (uncommon)
What is the most common lesion of hyperthyroidism in cats?
thyroid adenoma: COMMON in cats

rarely metastasizes
thyroid tumors in dogs

a. prevalence
b. biologic behavior
c. functional effects
a. common
b. 80% of thyroid tumors in dogs are carcinomas (larger tumors more likely to be malignant; mets: invade lungs before lymph nodes)
c. ↑ T4 likely d/t hypothyroidism w/ presence of Abs to thyroid Ags that cross react w/ assay rather than thyroid tumor
How is total serum calcium distributed in the body?
ionized: ~45% (biologically active fraction)
protein-bound: ~50% (most bound to albumin)
complexed: ~5%
What are ddx for hypocalcemia w/ hyperphosphatemia?
renal dz (common)

primary hypoparathyroidism (rare)
What are ddx for hypocalcemia w/ normo- to hypo-phosphatemia?
hypoalbuminemia (#1), renal failure (incl. EG toxicity), 1º hypoparathyroidism, milk fever (cow), eclampsia (bitch), pancreatitis, blister beetle poisoning (horse), nutritional 2º hyperparathyroidism, endurance racing (horse), hypomagnesemia
How does renal dz cause hypocalcemia?
↓ reabsorption of Ca from tubules d/t loss of tubular cells
↓ conc. of vitamin D d/t destruction of renal cells that produce vitamin D
↑ conc. of P that reciprocally --> ↓ Ca
soft tissue deposition of Ca x P (mineralization)
hypoalbuminemia d/t ↓ GFR
if cause of renal failure is EG toxicity --> Ca complexed w/ oxalate --> often SEVERE hypocalcemia
primary hypoparathyroidism

a. most common lesion
b. results
a. lymphocytic parathyroiditis (RARE): occurs in dogs only
b. immune mediated stimulus --> infiltration of lymphocytes & plasma cells --> destruction of PT gland
eventually, all PT glands will be destroyed --> conc. of PTH in serum will be undetectable --> cannot maintain serum Ca w/in RR
What are ddx for hypercalcemia w/ hypophosphatemia?
hypercalcemia of malignancy, 1º hyperparathyroidism, renal failure (HORSES only)
What are ddx for hypercalcemia w/ normo- to hyper-phosphatemia?
1º hyperparathyroidism, hypercalcemia of malignancy, vitamin D toxicosis, hypoadrenocorticism, renal disease, blastomycosis, young animals (esp. large breed dogs), idiopathic (cats), bone lesion (rare)
primary hyperparathyroidism

a. lesions
b. results
a. PT adenoma (seen in dogs, rare in cats), 1º PT hyperplasia may be more common than adenoma in cats
b. inc. PTH --> inc. serum Ca
hypercalcemia of malignancy

a. cause
b. associated tumors
a. tumor cells produce a protein very similar to native PTH (PTH-rp) that stimulates essentially the same biological functions: hypercalcemia & hypophosphatemia via stimulation of receptors on renal epi, osteoblasts, MPs
b. LSA, apocrine gland adenocarcinoma of anal sac, multiple myeloma in dogs, gastric SCC in horses
What causes renal secondary hyperparathyroidism?
↓ in serum Ca --> stimulation of PT glands
What causes nutritional secondary hyperparathyroidism?
d/t insufficient Ca or too much phosphorous in diet (ex. all meat diets for carnivores, excessive grain diets in horses)
What are ddx for hypoglycemia?
β-cell neoplasm, insulin overdose, sepsis, neonatal, starvation, small dog, hunting dog, endurance horses, Addison’s, ketosis, artifact (failure to separate serum), pregnancy toxemia
B cell tumors (insulinomas)

a. species most commonly affected
b. biologic behavior
c. results
a. dogs, ferrets, sometimes cats
b. tumors are invariably malignant in dogs & mets 1st go to regional ln’s & liver (despite benign cytologic & histologic appearance)
patient’s glucose conc. can be managed relatively well w/ diet & prednisone & may extend dog’s life for several years (it’s the hypocalcemia, not the tumor, that kills)
c. secrete excessive quantities of insulin --> life-threatening hypoglycemia
What are ddx for hyperglycemia?
diabetes mellitus
↑ blood catecholamine (epi) conc.
↑ blood glucocorticoid conc.
postprandial hyperglycemia
EG toxicosis (~50%)
cattle: epi & glucocorticoid induced hyperglycemia is common!
lipemia often interferes w/ glucose measurement (often present in patients w/ DM)
Type I DM

a. cause
b. % of dogs & cats w/ DM
c. most common lesions in dogs
d. most common lesion in cats
e. other possible lesions
a. absolute insulin deficiency
b. ~100% of dogs, 50-70% of cats w/ DM
c. recurrent pancreatitis (#1), immune mediated destruction of islets
d. islet amyloidosis
e. vacuolation of islets, lymphocytic inflammation of islets, islet cell aplasia
Type II DM

a. cause
b. % of dogs & cats w/ DM
a. insulin is present but does not produce its functional effect
insulin secretion in response to hyperglycemia is sluggish: inappropriately slow
peripheral tissues respond to insulin slowly (insulin resistance)
b. rare in dogs, 30-50% of cats w/ DM (many of these cats CAN be tx w/ insulin)

a. cause
insulin is present but does not produce its functional effect b/c of insulin antagonists in circulation
antagonists include glucocorticoids (#1), growth hormone, progesterones, glucagons
dogs may have this type, esp. w/ Cushing’s or in diestrus
cats w/ islet amyloidosis: amylin is co-secreted w/ insulin & is a competitive inhibitor of insulin

Type III probably precedes Types I & II
β-cell hypertrophy in an attempt to ↓ serum glucose conc. --> degeneration of β cells --> vacuolation & necrosis of islet cells from “exhaustion” --> Type I