80 terms

Endocrine Exam VMD 459

Thyroid follicular hyperplasia associated with Decreased function of the thyroid gland
What are the major mechanisms responsible for thyroid follicular hyperplasia (Goiter)?
Iodine deficient diets, goitrogenic compounds (interfere with thyroxinogenesis), dietary iodine excess, genetic defects involved in the biosynthesis of thyroid hormones - inadequate thyroid hormone synthesis & decreased blood levels of T3 & T4
What is the overall effect of thyroid hormones?
To increase the Basal metabolic rate (BMR)
Common in adult dogs, rare in other animals
Clinical features of hypothyroidism
Reduced basal metabolic rate (obesity, sluggish), Skin and haircoat changes (alopecia, hyperpigmentation), reproduction decreases, lipidosis (hypercholestrolemia, atherosclerosis, hepatic, renal, corneal and glomerular lipidosis)
Common Causes of hypothryoidism
idiopathic follicular atrophy, lymphocytic thyroiditis
Uncommon causes of hypothyroidism
Bilateral nonfunctional thyroid tumors, severe iodine deficiency (goiter), hypothalmic or pituitary lesions are rare (secondary hypothyroidism)
Idiopathic Follicular Atrophy
Decreased TSH, progressive loss o follicular epithelium and replacement by adipose with inflam. response. Gross: smaller glands, lighter in color
Lymphocytic Thyroiditis
Immune based pathenogenesis - circulating thyroid specific autoantibodies. Irreversible change, no regeneration of follicles, but C cells unaffected. Gross: small, white
Non-functional Thyroid tumors
destruction of the thyroid gland - not very clinically significant - dogs & horses
Secondary Hypothyroidism
Arises from primary pituitary or hypothalamic lesion - but rare. Results in decreased TRH and/or TSH secretion
Why is it uncommon to have functional hyperthyroidism in the dog?
B/c of the rapid metabolism of T3/T4 in the dog
Describe feline hyperthyroidism
Excessive production of T3 & T4 with positive feedback inhibition to suppress both TRH & TSH secretion - leads to atrophic changes in residual normal follicles
What are secondary effects of hyperthyroidism
Congestive hypertropic cardiomyopathy with tachycardia and decompensatory Heart failure and saddle thrombi, liver dz, and hypertension secondary to HF
Nodular hyperplasia and Adenomas in the Horse
Common in older horses, lesions are inactive and found incidentally in horses
What is involved in total body calcium regulation?
The Parathyroid gland and Thyroid C cells
What is the function of Vitamin D and Parathyroid hormone (PTH)?
To increase total Calcium body levels
What is the function of Calcitonin?
To decrease total Calcium body levels
What is the function of bone in Calcium regulation?
Bone serves as a mineral sink to prevent excessive calcium form accumulating in the extracellular fluid but also provides a source of minerals to prevent hypocalcemia
Where and When is PTH secreted?
PTH is secreted by parathyroid chief cells in response to hypocalcemia - responsible for minute to minute calcium (and Phosphorus) regulation
Where is calcitonin secreted?
Calcitonin is secreted by the interstitial C cells (parafollicular cells) in thyroid interstitial space (works with PTH for minute to minute Calcium regulation)
Where does one get vitamin D?
Diet (active form) or synthesized in vivo from precursors . Responsible for long term skeletal integrity
Uncommon, mostly in dogs - Manifests as Hypocalcemia - excessive neuromuscular excitability = tetany (seizures), increased phosphorus
In ruminants = paresis
Excessive PTH production leading to Hypercalcemia
Prolonged hypercalcemia can lead to?
vomiting, anorexia, PU/PD, muscular weakness, metastatic mineralization, fibrous osteodystrophy
Causes of hyperparathyroidism
Primary Hyperparathyroidism (adenoma/carcinoma)
Nutritional secondary Hyperparathyroidism
Renal secondary hyperparathyroidism
Pseudohyperparathyroidsim (humoral hypercalcemia of malignancy)
Primary Hyperparathyroidism (PH)
functional adenomas and Carcinomas of parathyroid gland --> increased PTH
A single parathyroid gland is enlarged, the other 3 are atrophied
Nutritional Secondary Hyperparathyroidism
Dietary imbalance of Calcium and phosphorus or diet deficient in Vitamin D - all result in hypocalcemia and increased PTH --> Parathyroid Chief cells hypertrophy and hyperplasia
Renal secondary Hyperparathyroidism
Elevated PTH in response to chronic hypocalcemia - all four parathyroid glands undergo chief cell hyperplasia
Lymphosarcoma and perianal gland adenocarcinomas make PTH-like peptide (PTHrP) which elicits Calcium resorption from renal tubules and activates osteolysis of bone
Parturient Hypocalcemia
Milk Fever "dairy cows" = paresis
Thyroid C cell tumors
Think Dairy Bulls
Adrenal Gland
Normal cortex/medulla ratio of 2:1
Zona glomerulosa
Mineralocorticoids - Aldosterone - affect ion transport of renal tubular and sweat gland epithelial cells with excretion of Potassium and retention of sodium and chloride
Lack of mineralocorticoid secretion
Addison's dz - lethal retention of Potassium and loss of sodium
Zona fasciculata
80%, secretes glucocorticoids - Cortisol and Corticosterone - effects on carbohydrate, lipid, protein and metabolism, suppress inflammatory and immune responses
Zona Reticularis
5%, secretes sex steroids (progesterone, estrogens, androgens) and cortisol
Corticotropin - secreted by adenohypophysis = principal regulator of adrenal cortical growth and secretory activity
Adrenal Medulla
Epinephrine/Norephinephrine synthesis - vascular drainage from adrenal cortex - Cortisol levels control conversion of NE to Epi
Hemorrhage of adrenal cortex
Occurs in newborn animals - birth trauma or stress, or in wild animals (extreme exertion), or in all animals from terminal phase of stress response or as a result of toxemia
Mineralization of Adrenal Cortex
Common in cats - cause unknown - clinically not a problem
Adrenal Cortex - Amyloid deposition
Occurs within the cortex - occurs in all species, cortices may be widened and have regions that are grossly "translucent" - does not result in cortical dysfunction
Infectious/parasitic - leads to inflam./necrosis
Ex: Histoplasma, Coccidioides, Toxoplasma, Cryptococcus, Aspergillus, Viral infections: equine herpes virus, bovine herpesvirus and porcine - can destroy cortical tissue.
Idiopathic adrenocrotical atrophy
Most common lesion in dogs with Addison's Dz (hypoadrenocorticism) - bilaterally symmetrical cortical atrophy - affects all 3 layers, cortex is 1/10 the normal thickness and deficient production of ALL classes of corticosteroids. Medulla is normal in size, the patients have elevated serum K+ and decreased Na+ = characteristic Na/K ratio for diagnosis
Also cortical atrophy, but they do not have the typical electrolyte abnormalities associated with addison's dz
Clinical features of Hypoadrenocorticism (Addison's dz)
severe hyperkalemia --> bradycardia and hypernaturia and hyperchloriduria with decreasing blood levels of Na+ and Cl-. Leads to hypoglycemia and increased insulin sensitivity. Hyperpigmentation of the skin (Increased release of ACTH), low plasma cortisol levels. PU/PD, hypovolemia, hypercalcemia, may have shock
Cortical Nodular Hyperplasia
Aged animals (dog, cat, horse, cow) - on the capsule, cortex and medulla. Multiple nodules that are yellow - must distinguish from cortical adenomas
Cushings Disease
Hyperadrenocortisolism - most common in aged dog/horse and results in increased cortisol production
Causes of hypercortisolism
Functional pituitary adenoma, or adrenocortical tumor, iatrogenic steroids, idiopathic cortical hyperplasia, non-adrenal gland tumors with ACTH-like activity
Functional pituitary adenoma
secretes ACTH autonomously leading to diffuse bilateral adrenal cortical hyperplasia, mainly of zona fasciculta and often with compression atrophy of the zona glomerulosa - most common cause of cushings in dogs
Functional Adrenocortical tumors
Adenomas or Carcinomas - contralateral cortex may be atrophied due to the negative feedback inhibition of pituitary ACTH secretion by increased cortisol levels. Can be local invasion of the aorta or vena cava and widespread metastases
Idiopathic cortical hyperplasia
Occurs mainly in poodles - affects the zona fasciculata without lesion in the pituitary
Lesions associated with hypercortisolism in the dog (sustained excess glucocorticoids)
Muscle atrophy, hepatomegaly (pendulous abdomen), mineralization in other tissues, involution of lymphoid tissues (increased susceptibility to bacterial infections), skin lesions (alopecia)
Adrenal gland pathology in ferrets
Excessive estrogenic steroid production by adrenal cortex - maybe result of early gonadectomy - signs: bilateral symmetrical hair loss, vulvar swelling, PU/PD, palpable abdominal mass, non-regenerative anemia
most common tumor in adrenal medulla of animals - mainly cattle, horse, dog.
Bulls - they develop with the calcitonin secreting C cell tumors of the thyroid gland - chromaffin cells secrete NE leading to hypertension and resultant arteriolar medial hyperplasia
Chemoreceptor Organs
Extra adrenal paraganglia - multifocally embedded within the wall of the aorta and carotid arteries (aortic and carotid bodies) - organs responsible for assessing blood pH, CO2, O2 levels and regulate respiration and circulation
Tumors of aortic and carotid bodies
Adenomas or Carcinomas - referred to as Chemodectomas or paragangliomas - slow growing, most common in brachycephalic dogs and are non-functional
Neoplasia of the thyroid gland epithelium in the dog
Most commonly results in carcinomas of the thyroid follicular epithelium
What dermatopathy is unique to hypothyroidism in the dog?
Excessive levels of maternal dietary iodine in the mare results in decreased fetal plasma levels of thyroid hormones resulting in?
Goiter - follicular hyperplasia
In lymphocytic thyroiditis in dogs....
there is irreversible destruction of thyroid follicular epithelium
local invasion of the canine vena cava is a common finding with?
In functional hypercortisolism in the dog due to an adrenocorticotrophic hormone (ACTH) secreting tumor of the adenohypophysis you would expect?
Hepatic lipidosis and hepatomegaly and muscle atrophy
Fatal hyperkalemia is expected with...
Adrenal cortical necrosis and hemorrhage in newborn lambs with cold stress, in bacterial endotoxemia in horses, with widespread adrenalitis and necrosis due to herpes virus infection, granulomatous adrenalitis from fungal infections
In adenohypophyseal aplasia in Jersey, Guernsey and Swedish red cattle, the prolonged fetal gestation results from a primary failure of
ACTH production
the dorsal growth into the brain of pituitary tumors
occurs in horses & dogs
Juvenile panhypopituitarism (Pituitary dwarfism in dogs)
Failure of differentiation of Rathke's pouch - failure of oral ectoderm - failure of adenohypophysis - German Shepard Dogs (autosomal recessive) - dwarfism (GH deficiency) and other hormones drastically reduced. Both ACTH and Cortisol levels are normal
Primary dz in the pituitary - congenital or degenerative
Secondary dz in the hypothalamus - destruction or modulation of trophic hormone releasing factors OR negative feedback suppression by plasma levels of thyroxine or other glucocorticoids (iatrogenic)
failure of FETAL endocrine function (Think Ruminants)
Genetic, Infectious, Toxicologic
Cattle breeds: Jersey, Guernsy, Swedish Red, Holstein, Ayrshire
Failure of Adenohypophysis development --> lack of fetal tropic hormone secretion --> prolonged gestation (~ 2 months)
Teatrogenic viral infections --> infect mother --> cross the placenta --> fetus susceptible --> congenital malformations of CNS --> disrupts fetal hypothalmic-hypophyseal axis --> prolongs gestation
Veratrum Californicum "skunk cabbage" - inhibits neural tube development when sheep ingest 9-14 days during gestation --> results in prolonged gestation
Degenerative Changes in the pituitary
Atrophy, Necrosis, Diabetes Insipidus
compression by tumors (nonfunctional tumors of the pituitary) or Vit. A deficiency in neonatal ruminants
Thromboemboli, abscess from traumatic injury in the oral cavity
Diabetes Insipidus
Neurogenic - syndrome from lesions in the neurohypophysis (decreased ADH), PU/PD, lesions - hypothalamus, infundibular stalk, pars nervosa
ACTH - secreting Adenoma (Pituitary Dependent Cushings)
Excess Cortisol Production, trophic stimulation of the Adrenal gland
Common breeds: Boxers, dausands, Boston terrier
Can lead to secondary neuro signs or diabetes Insipidus
Uniform bilateral hyperplasia and hypertrophy of adrenal cortex (reticularis & fasiculata) from ACTH production
Adenomas of Pars Intermedius (Horse)
Increase incidence with age - most common pituitary tumor in horses
Equine Cushings - loss of dopaminergic inhibition
Clinical signs = increased POMC, MSH, ACTH, compression of overlying hypothalamus
Sleepy, glucosuria, hyperglycemia, long hair coat
three pathogenic mechanisms of hyperadrenocorticism that result in bilateral adrenocortical hyperplasia
Pituitary dependent (functional corticotroph adenoma), Idiopathic cortical hyperplasia, Non-adrenal gland tumors with ACTH-like activity
How does equine cushings differ from canine cushings?
Equine cushings results in part from damage to the hypothalamus