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endoc
| Question | Answer |
|---|---|
| Which pathogenic mechanism of endocrine disease is the most important in animals | Hypersecretions. |
| Autonomous hypersecretion of a hormone can be caused in what 2 ways | Tumor or hyperplasia of the gland. |
| Acromegaly can result from an overabundance of growth hormone, due to a tumor located where | Pituitary gland (acidophil adenoma). |
| An adrenal cortical adenoma or carcinoma can produce excesses of which hormoneLeading to what type of clinical signs | Estrogen, feminization. |
| Norepinephrine can be produced in excess from what type of neoplasm | Pheochromocytoma. |
| What type of clinical sign can be seen with a pheochromocytoma | Hypertension. |
| What effect what an increase in T4/T3 hormone have | Increased basal metabolic rate. |
| An excess of which hormone would cause osteoscelrosis | Calcitonin. |
| A parathyroid gland chief cell adenoma would produce what type of lesion | Fibrous osteodystrophy. |
| An excess of which hormone causes hypoglycemia | Insulin. |
| In which location would the neoplasm be to affect insulin production | Pancreatic B cells (adenoma/carcinoma). |
| What causes secondary hyperfunction | A lesion in one organ secretes excess trophic hormone that leads to long-term stimulation and hypersecretion of hormone by the target organ. |
| An excess of ACTH can cause an overproduction of cortisol in which portion of the adrenal gland | Zonae fasciculate and reticularis of the adrenal cortex. |
| Secondary hyperactivity of an endocrine gland can also be caused by a disease of another organ, In the example of renal failure of this condition, what causes parathyroid stimulation | Decreased GFRhyperphophatemiadecline in serum calciumparathyroid stimulation |
| As destruction of the PCT cells continues, why is there continued parathyroid stimulation | Destruction of cells interfers with the metabolic activation of Vit D in the kidneysdecreased intestinal calcium absorptionhypocalcemiacontinued parathyroid stimulation |
| In this cascade of events, what happens to the skeleton | Mobilization of calcium from bonegeneralized demineralization of skeleton. |
| In what other way can hyperactivity of the parathyrois gland be caused | Nutritional (diet too low in calcium or too high in phosphorus) |
| Hyperactivity secondary to hormonal imbalances can be caused by what | Xenobiotic chemicals (foreign) |
| Non-endocrine neoplasms can cause hyperfunction of an endocrine gland by hypersecretion ofhomones or hormone-like factors, give an example of this in dogs | Parathyroid hormone-related peptide (PTH-rP) production by adenocarcinoma of apocrine glands of anal sacs in dogs (or lymphosarcoma in dogs and cats) |
| What is pseudohyperparathyroisism, or the humoral hypercalcemia of malignancy | Autonomous hypersecretion of PTH-rP from cancer cellsmimics PTHincreased mobilization of calcium from bone by osteoclastspersistent life-threatening hypercalcemia |
| If the rate of secretion of a hormone is normal, how might a hypersecretion of the hormone occur | Decreased degradation of the hormone, blood concentrations are increasedsimulates a hypersecretion |
| What chronic condition can cause a decrease in the rate of degredation of hormone | Chirrhosis of the liver, chornic renal disease |
| What effect would increased degradation of a hormone have | Increase degradation would stimulate further release |
| Hormone excess can also be caused by what other method | Iatrogenic |
| Exogenous corticosteroid administration can cause what type of disease of the adrenal gland | Cushing’s disease |
| Hypoglycemia can be caused by the administration of an excessive amount of which hormone | Insulin |
| Excess of administration of T4/T3 can cause what endocrine condition | Hyperthyroidism |
| What can result from an administration of progesterone to a dog to prevent estrus | Acromegaly from an indirect growth hormone excess |
| By what 3 ways can endocrine hypofunction occur | Destruction of secretory cells by a disease process, failure of development of an endocrine gland, a specific genetic/biochemical defect in the biosynthesis of the hormone |
| What type of injuries are adrenalitis and throiditis, that causes hypofunction | Immune-mediated |
| Failure of endocrine development includes the failure of the oopharyngeal ectoderm to differnentiate into which gland in dogs | Into the trophic hormone secreting cells of the adenohypophysis |
| This failure of development can lead to what type of condition n the dog | Dwarfism |
| Give an example of a congenital defect of hormone biosynthesis | Dyshormonogenetic goiter in ruminants. |
| What causes secondary hypofunction | A destructive lesion in one organ intereferes with the secretion of trophic hormones and results in clinically detectable hypofunction in the target gland |
| Give an example of secondary hypofunction | Lesion in the pituitary gland causing reduced secretion of ACTH, hypofunction of the adrenal gland |
| Endocrine dysfunction can also result from a failure of target cell response, in what 2 ways | An alteration in hormone receptors or lack of adenyl cyclase in the cell membrane |
| Give an example of receptor cell failure | Insulin resistance in obese animals & humans (down regulation of receptors on the surface of target cells in response to chronic increase in insulin stimulated by hyperglycemia resulting from excessive food intake |
| What effect does lack of adenyl cyclase have on hormone target cell response | Creates a defect in cAMP-mediated signal transductioninability of target cell to respond |
| In ruminants, failure of the development of the pituitary can be due to what | Genetic aplasia or teratogenic plants |
| In these cases, why is prolonged gestation seen | Fetal cortisol mormally initiates partutition..in this case, the tareget organs are hypoplastic |
| Are endocrine neoplasms functional or nonfunctional | Both |
| What effect do functional neoplasms have | Produce trophic hormones that stimulate target organs (usually one taret organ) |
| Are the effects of a non-functional endocrine neoplasm benign | No, can be destructive to adjancent structures causing panhypopituitarism, diabetes insipidus and neuor disorders (CNS or cranial nerve dysfunction) |
| What type of neoplasma are seen more commonly in adults,In younger animals | Adults: adenomas, carcinomas,Younger: craniopharyngioma |
| From where does a craniopharyngioma originate | Rathke’s pouch |
| How are adenomas distinguished from nodular hyperplasia | Larger size and presence of a capsule |
| Which is the most common pituitary adenoma seen in horses | Adenoma of the pars intermedia (2nd in dogs) |
| In dogs, an adenoma of the pars intermedia, if inactive, can lead to what condition | Hypopituitaism and diabetes insipidus |
| If active, an adenoma of the pars ntermedia in a dog can cause what condition | Excessive ACTH secretion bilateral cortical hyperplasiahypercotisolism (Cushing’s disease) |
| In horses, compression of the hypothalamus by multinodular neoplasms leads to what clinical signs | PU/PD, polyphagia, muscle weakness, somnolence, intermittent hyperpyrexia, generalized hyperhidrosis and hyperthichosis/hirsutism |
| In these horses, plasma concentration of cortisol and immunoreactive ACTH (iACTH) can be elevated due to different processing of what polypeptide | POMC (proopiomelanocortin) |
| In dogs, functionally active ACTH-secreting adenomas are derived from which cells | Corticotrophs of the pars distalis/intermedia |
| In which breeds are these adenomas common | Aged boxers, boston terrier, dachshund |
| These ACTH-secreting adenomas lead to what condition | Cushing’s disease |
| What effect does the adenoma have on the adrenal gland, physically | Bilateral enlargement of the adrenal due to cortical hyperplasia; nodules of yellow-orange cotical tissue outside the capsule and extending down into and compressing the adrenal medulla |
| In dogs, cats , lab rodents and parakeets, what type of adenoma is endocrinologically inactive | Chromophobe |
| How does an inactive adenoma cause clinical signs | When it’s large enough to be space-occupying |
| What signs do clinically affected animals show with a chromophobe adenoma | Decreased spontaneous activity, incoordination, muscle weakness, collapse after exercise; in chronic casesblindness and dilated fixed pupils due to compression of the optic nerves |
| A craniopharyngioma is derived from where | A benign tumor derived from the epithelial remnants of the oropharyngeal ectoderm of the craniopharyngeal duct (Rathke’s pouch) |
| What effects does a cranipharyngioma have | Subnormal secretion of somatotropin (growth hormone) in younger animals; juvenile panhypopituitarism and dwarfism |
| Craniopharyngiomas can grow to be quite large and involve what other major structures | Cranial nerves, hypothalamus, thalamus |
| Clinical effects of this type of tumor include the lack of secretion of pituitary trophic hormones resulting in atrophy and subnormal functions of which target organs | adrenal cortex, thyroid, gonads and failure to attain somatic maturation due to a lack of growth hormone secretion |
| Disturbances of water metabolism (PU/PD etc) can occur from the interference with the synthesis and release of what hormone | ADH |
| A large craniopharyngioma can cause what other ADH related condition | Diabetes insipidus |
| What type of neuro issues might be seen in the presence of a cranipharyngioma | Deficits in cranial nerve functions and CNS dysfunction |
| Dogs with pituitary dwarfism also have a shorter lifespan due to what other secondary endocrine dysfunctions | Hypothyroidism, hypoadrenocorticism |
| Name the 2 forms of diabetes insipidus | Hypophyseal and nephrogenic |
| In the hypophyseal form, lesions that interfere with the synthesis or secretion of ADH compress or cause destruction of what structure | Pars nervosa |
| What type of lesions can affect the pars nervosa | Neoplasm, granuloma, cyst, trauma |
| Where is ADH produced | Supraoptic nucleus |
| The nephrogenic form of DI is a hereditary defect resulting in what | Lack of adenyl cyclase in the plasma membrane of the epithelial cells of the distal tubules & collecting ductscells fail to respond to ADH |
| Both forms of DI lead to what clinical signs | PU/PD, urine of low osmolality |
| Administration of exogenous ADH will lead to a rapid increase in urine osmolality (above that of plasma) in which form of DI | The hypophyseal form, not the nephrogenic form ; used for differential dx |
| Cushing’s syndrome is the name given to what condition | Hypercortisolism |
| Cushing’s is common in which species | Older dogs and sometime horses; rare in other species |
| Primary hyperadrenocorticism accounts for 10-15% of cases and is usually caused by what | Cortical neoplasm, esp adenoma |
| Secdondary hyperadrenocorticism accounts for 80% of cases, What is the pathogenesis of this cause | Bilateral cortical hyperplasia due to increased ACTH from pituitary tumor (pituitary dependent hyperadrenocorticism, PDH) |
| What accounts for the cause of the other 5-10% of cases of hyperadrenocorticism | Pharmacological (iatrogenic), over administration of glucocorticoids |
| Clinical signs of Cushing’s disease are from the effects of corticosteroids and include what | Gluconeogenic, lipolytic, protein catabolic, decreased protein synthesis and anti-inflammatory |
| PU/PD are seen in response to what | Hyperglycemia |
| Polyphagia can be seen as a result from what | Direct effect and/or tumor effect on the hypothalamus |
| Why is hepatomegaly seen as a clinical sign of Cushing’s | Steroid hepatopathy, increased glycogen in hepatocytes |
| Muscle atrophy and weakness will be seen as which clinical sign | Pendulous abdomen |
| What type of skin lesions are seen in Cushing’s | Dermal atrophy, bilateral symmetric alopecia |
| What pathognomonic lesionis seen in the skin | Calcinosis cutis (dystrophic mineralization) |
| Hyporadrenocorticism is also known as what | Addison’s disease |
| Primary hypoadrenocorticism is a result of what | Bilateral idopathoic adrenal cortical atrophy |
| Addison’s occurs more frequently in which dogs | Young to middle-age females, may be autoimmune/inherited |
| Which portion of the adrenal cortex is destroyed in Addison’s | All 3 layers |
| This destruction leads to a deficient production of which cortical hormones | All |
| A deficiency of which cortical hormonesa can be fatal | Mineralcorticoids |
| How can hypoadrenalcorticism by caused iatrogenically | Sudden withdrawl following prolonged excessive administration of synthetic steroids |
| Secondary hypoadrenocaroticism is a result of ACTH deficiency from destructive pituitary lesions leading to trophic atrophy of the 2 inner zones of the adrenal cortex,which hormones are NOT affected | Mineralcorticoids, no electrolyte imbalance |
| In dogs, what are some of the general clinical signs seen as a result of deficient production of any corticosteroids | Lethargy, stress intolerance, bradycardia (specific ECG changes), anorexia, vomiting and diarrhea leading to dehydration/emaciation |
| Affected dogs can present in what distressed state | Circulatory failure (cardiogenic/hypovolemic shock) |
| Synthesis & secretion of minerlacorticoids is reduced leading to electrolyte imbalances What is the hallmark sign of this condition | Hyponatremia/ hyperkalemia |
| Less potassium is exreted by the kidneys,The resulting hyperkalemia has what effect | Cardiovascular disturbances (bradycarida, weakness, shock) |
| In long standing cases, what is the condition of the skin | May be hyperpigmented due to an excess of pituitary MSH that develops reciprocally to a decrease of inhibitory cortisol (reduced neg feedback) |
| What is the appearance of the adrenal gland in a case of Addison’s | Cortex is reduced to 1/10 or less of its normal thickness, consists primarily of the capsule; medulla makes up bulk of the gland |
| What is the most commone neoplasm of the adrenal medulla in animals | Pheochromacytoma |
| In which species do Pheochromocytoma occur most | Dogs and cattle (often concurrent thyroid C cell tumor in bulls and humans) |
| What is a parganglioma | An extraadrenal pheochromocytoma occurring in the abdomen (infrequently) |
| Pheochromocytomas are large and often invade adjacent structures such as what | Vena cava |
| Pheochromocytomas tend to metastasize to where | Liver, regional lymph nodes, lungs |
| Pheochromocytomas are rarely functional, but when they are, can cause tachycardia, edema, cardiac hypertrophy attributed to what | Catecholamine secretion |
| Arteriolar sclerosis and widespread medial hyperplasi of arterioles have been reported in dogs with pheochromocytomas with what clinical sign | Paroxysmal hypertension |
| An application of Zenkers solution (potassium dichromate or iodate) will turn a freshly cut surface of a pheochromocytoma what color | Dark Brown in 5-2 0 mins |
| What is the term for a nonneoplastic, noninflammatory enlargement of the thyroid gland due to increased TSH secretion | Goiter |
| Pathogenetic mechanisms of a goiter include an iodine deficient diet or excess dietary what | Iodide (causes thyroid hyperplasia) |
| Brassica and Crucifera plants are considered goitrogenic compounds because they interfere with what | Thyroxinogenesis |
| The overall result of these mechanism is inadequate thyroxine synthesis which leads to decreased blood levels of which hormones | T4/T3 |
| This decreased blood level of T4/T3 is detected by the hypothalamus and pituitary gland which in turn do what | Increase secretion of TSH |
| This increase of TSH leads to what condition in the thyroid follicularcells | Hypertrophy and hyperplasiagoiter |
| In which species is hyperthryroidism seen most | Aged cats (in assoc with adenomas and multinodular hyperplasia)Dogs (due to thyroid neoplasia) |
| Clinical signs of hyperthyroidism include what kind of serum T4/T3 concentrations | Marked increase |
| What general clinical signs are seen | Restlessness, increased activity and weight loss in spite of voracious appetite (polyphagia), PU/PD, hyperexcitability |
| What responde do affected animals have to high ambient temps | Intolerant |
| What cardiac manifestations of hyperthyroidism can occur | Tachycardia, dysrhythmias |
| What other cardiac condition can be caused by hyperthyroidism | Secondary hypertrophic cardiomyopathy |
| Thyroid neoplasm can result in hyperthryroidism, based on the cells capability to synthesize what | T4/T3 |
| Which species is more efficient in the excretion of thyroid hormones | Dogs |
| In which species is hypothryroidism most commonly seen | Dogs, horses |
| Name 4 etiological causes of hypothyroidism | Idiopathic follicular collapse/atrophy, lymphatic thyroiditis, bilateral nonfunctional follicular cell neoplasm, chronic pituitary lesions, severe iodine-deficient goiter |
| What general clinical signs are see in hypothyroidism | Reduction in basal metabolic rate manifested as lethargy, weight gain, muscular weakness, slow reflexes |
| What type of skin lesions are seen | Hyperkeratosisincreased scaliness (seborrhea), bilateral symmetrical alopecia |
| Normally, T4 stimulates the anagen phase of hair growth, what do the reduced levels of T4/T3 favor | The telogen or resting phase, hairs are easily dislodged from the follicle |
| Hyperpigmentation of the skin is seen due to what | Increased number of melanocytes in the basal layer |
| What is myxedema | Accumulation of mucin (glycosaminoglycans + protein) making skin soft and scaly |
| What effects does hypothyroidism have on the reproductive system | Lack of libido, infertility (reduction in sperm count due to atrophy of spermatogenic epithelium in testes, abnormal or absent estrus cycles, reduced conception rates |
| How can hypothyroidism results in atherosclerosis | Hypercholesterolemia due to decreased rate of lipid metabolism w/decreased intestinal excretion of cholesterol & conversion of lipids into bile acids |
| Cows feed a high calcium diet prior to partuition may be affected with this hyporparathyroid condition | Parturient paresis (milk fever) |
| What is the general response of the parathyroid gland in this disease | Parathyroid glands have been inactive and don’t respond adequately to the sudden Ca loss in milk., esp in the face of anorexia and increased calcitonin secretion prepartum |
| With the onset of lactation, how does the cow develop paresis | Hypocalcemia, hypophosphatemia |
| What type of diet would reduce the incidence of parturient hypocalcemia | Low in calcium with doses of Vit D |
| Functional neoplasms of chief cells produce what condition | Hyperparathyroidism |
| What types of neoplasm cause hyperparathyroidism in dogs | Parathyroid adenomas (older dogs) and parathyroid carcinoma (rare) |
| Functional tumors produce excess PTH in spite of negative feedback by increased blood calcium, Mineral is removed from the skeleton and bone is replaced by an immature fibrous connective tissue,What is the name for this condition | Fibrous osteodytsrophy |
| What clinical malady can this lead to | Lameness from fractures |
| What are some of the clinical signs of hyperparathyroidism | Anorexia, vomiting, constipation, depression, PU.PD, weakening of bones, generalized muscular weakness due to decreased neuromuscular excitability |
| What blood parameters would you look for to dx hyperparathyroidism | Total blood Ca, phosphorus and circulating concentrations of parathyroid hormones |
| Secondary hyperparathyroidism is more common and can be secondary to what 2 conditions | Nutritional imbalance, renal disease |
| In which species is nutritional imbalance 2nd dary parathyroidism seen | All species but esp cats, dogs, horses, non human primates, birds, reptiles |
| What type of diet can cause the condition in horses | High grain/poor quality roughage or all-bran diet (Miller’s disease) |
| In dogs and cats the condition is brought on by what type of diet | |
| All meat | |
| A disturbance in mineral homesostasis is induced by a diet consisting of what | |
| Low Ca content, excess oxalate or P with normal or low Ca, inadequate Vit D | |
| The resulting hypocalcemia of these diets stimulates secretion of PTH with what kind of changes to the chief cells | |
| Hypertrophy and hyperplasia | |
| Secondary hyperparathyroidism due to renal disease is seen in which species | C ats and dogs |
| In renal disease, a reduced GFR will result in what level of phosphate, Having what effect on blood Ca levels | Hyperphosphatemia, lowers blood Ca levels |
| What effect do these conditions have on Vit D | Impaired activation |
| Prolonged hypocalcemia leads to what condition of the chief cells | Hypertrophy and hyperplasia, resulting in bilateral enlargement of the parathyroids |
| What effect does the excess PTH have on bone | Excessive bone resorption, marked proliferation of fibroblasts and generalized fibrous osteodystrophy. |
| What happens to the bones of the skull | Become swollen, are soft and pliable (big head in horses, rubber jaw in dogs and cats) |
| Pseudoparathyroidism is caused by secretion of parathyroid related protein, which mimics PTH, from where | Tumor cells, acts to causes hypercalcemia and hypophosphatemia |
| The release of these PTHrp and other humoral factors from tumors that create the hypercalcemia is called what | Humoral hypercalcemia of malignancy (HHM) |
| Hypercalcemia is induced by the metastases of what type of tumor | Solid neoplasm mets to bone, grow locally producing hypercalcemia by bone resorption |
| Increased concentrations of serum ionize calcium are induce clinical signs in which systems | GI, nueormuscular, cardiovascular, rneal |
| Inceased circulating concentrations of PTH-rP have been observed in what type of tumors of female dogs | Adenocarcinoma of the aprocine glands of the anal sac |
| The increased PTH-rP results in what conditions | Persistant hypercalcemia and mils phosphatemiagenerlaized muscular weakenss, anorexia, vomiting, bradycardia, depression, PU/PD |
| In dogs and cats, what other condition can cause increase circulating PTH-rP | Lymphosarcoma |
| In this situation, hypercalcemia is a result of what | Production by neoplastic cells of humoral substances, and/or from physical disruption of trabecular bone by lymphosarcoma in the bone marrow |
| Define diabetes mellitus | A metabolic disorder that results from a diminished availability of insulin for normal function of many cells of the bodypersistant hyperglycemia |
| What is the pathogensis of DM, from the onset of hyperglycemia | Glucose unable to enter some tissueshyperglycemiamobilization of fat for energyketosisacidosiscoma |
| How is Type I DM characterized | Destruction of beta cells with progressive and eventual complete loss of insulin secretion |
| Destruction of beta cells can be due to what | Toxins, immune mediated, viruses (FMD in cattle), cytokines, injury by free radicals, atrophy/hypoplasia/comgenital aplasia of islets, neoplasia, acute pancreatic necrosis with necrosis of islets |
| What is the treatment for this condition | Require insulin from the time of diagnosis (insulin dependent DM) |
| How would you characterize Dm Type II | Insulin resistance (genetic) and/or dysfunction of beta cells (gradual loss of insulin secretion as beta cells are destroyed slowly), other, constitutional factors like obesity, exercise and diet are important |
| Insulin levels may be high, low or normal but cannot overcome what situation in peripheral tissues | Insulin resistance |
| How is this condition treated | If diagnosed early, animals may have a slight hyperglycemia and can be treated with small doses of insulin (insulin independent DM) |
| Secondary DM reflects antagonism between what | In peripheral tissues between insulin and other hormones |
| The hormones produce a sustained hyperglycemia which have what effect on the insulin producing Beta cells | Exhaustion |
| What effect does progesterone have in regards to insulin | Stimulates release of growth factors which inhibit insulin-receptor activity and intracellular response to insulin |
| Glucagon antagonizes insulin, produced from what | Glucagonomas |
| What other hormones antagonize insulin | Growth hormone, glucocorticoids (endogenous, Cushings, or exogenous, iatrogenic) |
| In dogs, are males or females more often affected by DM | Females |
| Are dogs typically affected with Type I or Type II DM | Type I |
| In the dog, destruction of the pancreatic islets happens concurrently with what conditions | pancreatic necrosis syndrome/acute recurrent pancreatitis, infiltrating tumor |
| Islet cells can also be affected by hypoplasia and by what other condition | Immune mediated |
| In cats, which type of DM is usually seen | Type II |
| What effect does amyloidosis have on the islets | Accumulation of amyloid eventually interferes with insulin secretion and function |
| Prolonged insulin resistance in peripheral tissues can cause an exhauation of the islet, resulting in what kind of appearance | Vacuolation |
| In Dm, hyperglycemia and glucosuria are caused by what conditions | Decreased insulin or insulin resistance |
| Osmotic dieresis causes what clinical signs | PU/PD |
| In DM, there is increased food consumption due to the affects on the satiety center,Why is there weight loss | Glucosuria and catabolism |
| What is the pathogenesis of lilateral cataracts in DM | Increased glucose metabolized by the sorbitol pathway, increased sugar alcohols lead to lens degeneration |
| Hepatic lipidosis and cirrhosis can lead to what condition of the liver | Hepatomegaly |
| Recurrent infections in DM are a result of what condition | Impaired leukocyte kinetics |
| What type of microangiopathies can occur as a result of DM | Glomerulosclerosis, retinopathy, gangrene |
| What is another name for the chemoreceptor organs | Nonchromaffin paraganglia |
| Give some locations of these chemorecepor organs | Carotid body, aortic body, nodose of the ganglion of vagus nevre, cirliary ganglion in orbit, pancreas, internal jugular below middle ear, recurrent branch of glossopharyngeal nerve |
| These receptors are sensitive to what | Changes in the blood Co2, pH and oxygen tension |
| The carotid and aortic bodies can have effects on the respiratory system by which nerves | Parasympathetic, and affect the heart rate and bp by sympathetic |
| Neoplasms or tumors of the chemoreceptor organs are called what | Chemdectomas or non-chromaffin paragangliomas |
| Which type of these tumors is more common in animals | Aortic body adenoma/carcinoma |
| What effect do these tumors usually have | Cause heart failure due to space occupying nature in the pericardium (pressure on aorta and vena cava) |
| Aortic body adenoma/carcinoma is a common cause of heart base tumor and should be differentiated from what other type of tumor | Tumor of ectopic thyroid |
| Which hormone do these tumors usually secrete | Do not usually secrete hormones |
| Where do carotid body adenomas/carcinomas tend to arise | At the bifurcation of the common carotid artery |
| Are they typically unilateral or bilateral | Unilateral, bilateral is rare |
| How would you distinguish an carotid body adenoma from a carcinoma | Adenoma is 1-4cm, well encapsulated and smooth,Carcinoma are large, multinodular, invade the capsule and penetrate into walls of adjacent blood and lymph vessels |
| What effect might these tumors have | May interfere with swallowing and blood flow |
| Heart base neoplasms in dogs can also have their origin where | Ectopic thyroid gland (5-10%) |
| What effect do these tumors tend to have | Compress or invade structures in the cranial mediastinum near the base of the heart |
| How would you distinguish a heart base tumor of ectopic thyroid tissue from other neoplasms | Cells are smaller, more hyperchromatic nuclei, eosiniphilic cytoplasm. |
| What type of cells are not seen in a tumor from ectopic thyroid tissue | Giant cells (and stroma is not prominent) |
| What structures are seen in ectopic thyroid gland neoplasms that cannot be seen in aortic body neoplasms | Primitive follicular structures or colloid-containing follicles |
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