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Goiter

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)

Hypothyroidism

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

Hypoparathyroidism

Uncommon, mostly in dogs - Manifests as Hypocalcemia - excessive neuromuscular excitability = tetany (seizures), increased phosphorus
In ruminants = paresis

Hyperparathyroidism

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

Pseudohyperparathyroidism

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

ACTH

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

Adrenalitis

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

Panhypopituitarism

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

Pheochromocytomas

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?

Myxedema

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?

Pheochromocytoma

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

Hypopituitarism

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

Genetic

Cattle breeds: Jersey, Guernsy, Swedish Red, Holstein, Ayrshire
Failure of Adenohypophysis development --> lack of fetal tropic hormone secretion --> prolonged gestation (~ 2 months)

Infectious

Teatrogenic viral infections --> infect mother --> cross the placenta --> fetus susceptible --> congenital malformations of CNS --> disrupts fetal hypothalmic-hypophyseal axis --> prolongs gestation

Toxic

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

Atrophy

compression by tumors (nonfunctional tumors of the pituitary) or Vit. A deficiency in neonatal ruminants

Necrosis

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

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