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34 Cards in this Set
- Front
- Back
In what zones of the adrenal cortex are glucocorticoids made?
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zona fasiculata
zona reticularis |
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In what zone of the adrenal cortex are mineralocorticoids made?
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zona glomerulosa
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What are the effects of aldosterone of the kidney?
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↑ tubular reabsorption of Na+
↑ tubular excretion of K+ |
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What are the effects of cortisol?
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antagonism of insulin: promote gluconeogenesis & glycogenesis, ↓ glucose uptake by insulin-sensitive tissues
↑ lipolysis suppress wound healing, inflammation, & immune response |
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What zone of the adrenal cortex secretes sex hormones?
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zona reticularis
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What is the most common lesion associated w/ hypoadrenocorticism in dogs?
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lymphocytic adrenalitis: destroys all 3 zones
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What are causes of primary hypoadrenocorticism?
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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 |
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What are causes of secondary hypoadrenocorticism?
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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 |
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What is the most common lesion assoc. w/ hyperadrenocorticism in dogs?
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functional pituitary tumor --> bilateral adrenal hypertrophy
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What is the cause of primary hyperadrenocorticism?
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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) |
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What are causes of secondary hyperadrenocorticism?
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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) |
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What causes the PU/PD in hyperadrenocorticism?
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glucocorticoids antagonize ADH function on tubules (biochemical nephrogenic DI)
↑ GFR --> dilute urine destruction of pituitary by tumor --> ↓ production of ADH |
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What is the pathway of thyroid hormone production?
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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
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calcitonin
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. |
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What are lesions assoc. w/ hypothyroidism in dogs?
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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) |
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What is the most common lesion of hyperthyroidism in cats?
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thyroid adenoma: COMMON in cats
rarely metastasizes |
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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 |
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How is total serum calcium distributed in the body?
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ionized: ~45% (biologically active fraction)
protein-bound: ~50% (most bound to albumin) complexed: ~5% |
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What are ddx for hypocalcemia w/ hyperphosphatemia?
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renal dz (common)
primary hypoparathyroidism (rare) |
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What are ddx for hypocalcemia w/ normo- to hypo-phosphatemia?
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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
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How does renal dz cause hypocalcemia?
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↓ 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 |
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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 |
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What are ddx for hypercalcemia w/ hypophosphatemia?
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hypercalcemia of malignancy, 1º hyperparathyroidism, renal failure (HORSES only)
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What are ddx for hypercalcemia w/ normo- to hyper-phosphatemia?
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1º hyperparathyroidism, hypercalcemia of malignancy, vitamin D toxicosis, hypoadrenocorticism, renal disease, blastomycosis, young animals (esp. large breed dogs), idiopathic (cats), bone lesion (rare)
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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 |
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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 |
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What causes renal secondary hyperparathyroidism?
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↓ in serum Ca --> stimulation of PT glands
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What causes nutritional secondary hyperparathyroidism?
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d/t insufficient Ca or too much phosphorous in diet (ex. all meat diets for carnivores, excessive grain diets in horses)
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What are ddx for hypoglycemia?
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β-cell neoplasm, insulin overdose, sepsis, neonatal, starvation, small dog, hunting dog, endurance horses, Addison’s, ketosis, artifact (failure to separate serum), pregnancy toxemia
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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 |
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What are ddx for hyperglycemia?
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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) |
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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 |
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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) |
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Type III DM
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 |