Path 1 - Endocrine 4

pbhati17's version from 2017-03-01 23:14

Endocrinology 6.4: Thyroid Gland

Thyroid (read over how thyroid hormone is made to make all of this clear)

Question Answer
Lymphocytic (immune-mediated) thyroiditis → Who does this usually affect?Seen in dogs
Obese strains of chickens
Nonhuman primates
Buffalo rats
What exactly is happening in Lymphocytic thyroiditis? What is the result of this?Autoantibodies to thyroglobulin & other colloid antigens. Affected dogs may or may not develop clinical hypothyroidism.
What do the microscopic lesions look like in lymphocytic thyroiditis?Multifocal to diffuse infiltrates of lymphocytes, plasma cells & macrophages (lots of WBCs), replacement fibrosis, colloid is vacuolated → cellular debris mixed w/ inflammatory cells


Question Answer
What IS a goiter?Nonneoplastic, noninflammatory enlargement of thyroid gland due to hyperplasia of thyroid follicular cells: (inadequate Thyroxine synthesis → ↓ blood lvls of T3 & T4 → ↑ TSH secretion → hyperplasia of thyroid follicular cells)
**What are the 4 Pathogenic mechanisms for developing a goiter?(1) Iodine deficient diet
(2) Excess dietary
iodide (NOT iodine)
(3) Goitrogenic compounds interfering w/ thyroxinogenesis
(e.g., Brassica & Cruciferae plants)
(4) Genetic enzyme defects in hormone synthesis
Explain how an iodine deficient diet leads to a goiterPrevents production of both T4 & T3 but does not stop the formation of thyroglobulin (stuff that binds w/ other stuff to start to make T4 & T3). Thus, no hormone is available to inhibit production of TSH by the pituitary → excessive TSH secretion → thyrocytes secrete colloid into the follicles & the gland enlarges (colloid= fluid that contains the prohormone thyroglobulin)
Explain how excess dietary iodide leads to a goiter (4 things)(1) Too much ioDIDE inhibits uptake of ioDINE by the thyroid. (This ↓ the rate of ioDIDE trapping (from blood, the first step in thyroid hormone production), which ↓ the rate of iodination of tyrosine to form T4/T3, which means endocytosis of colloid from the follicles by thyrocytes is "paralyzed”)
(2) Blocks peroxidation of iodide to iodine
(3) Interferes w/ conversion of MIT to DIT
(4) Blocks the release of hormone from the follicle
What are 4 goitrogenic compounds which lead to formation of a goiter? (Just name, how they work in other cards)(1) Brassica & Cruciferae plants
(2) Sulfonamides
(3) Anions
(4) Thionamides
Explain how Brassica & Cruciferae plants are goitrogenicThey interfere w/ steps in thyroxinogenesis(making thyroxine, which is T4)
Explain how sulfonamides are goitrogenicInhibit thyroperoxidase & interfere w/ iodination of tyrosine (sulfur & iodine, yum)
Explain how anions are goitrogenicInhibit iodide transport by "salting out"
Explain how thionamides are goitrogenicinhibit organification of thyroglobulin (thigh organs)
Explain which genetic enzyme defects in hormone synthesis result in a goiterGenetic impairment of thyroglobulin synthesis
What are the 4 TYPES of goiters?(1) Diffuse hyperplastic
(2) Colloid goiter
(3) Multifocal nodular hyperplasia
(4) Congenital dyshormonogenetic goiter


Question Answer
Diffuse hyperplastic → Who does this goiter usually happen to & how?More common in young animals born to dams in which the DAMS had: iodine deficient diet, excess iodide (e.g., dry seaweed often fed to mares), or if they consumed goitrogenic substances (thiouracil, sulfonamides, anions of the Hofmeister series, plants of the family Brassicacceae)
What are the lesions associated w/ a diffuse hyperplastic goiter?Marked enlargement of glands, w/ the follicles being irregular, colloid is lightly eosinophilic & vacuolated (diffuse foamy huge irregular follicles)
Colloid goiter → HOW does this happen & who does this usually happen in?Involutionary phase of diffuse hyperplastic goiter (following correction of the problem in diffuse hyperplastic goiter) (←the first type covered, where the baby got the prob bc of the dam). Bc of this, it is usually seen in young adult & adult animals. The "correction" which results in the involution to create this goiter is either after sufficient amounts of iodide have been added to the diet or after requirements for thyroid hormones have diminished in an older animal
Explain what happens in correction of the problem in diffuse hyperplastic goiter to result in colloid goiterHyperplastic thyrocytes continue to produce colloid → return of blood [T4 & T3] to normal → ↓ conc of TSH → ↓ ENDOCYTOSIS of colloid from the lumen
**What are the lesions associated w/ a colloid goiter?Follicles are larger (Macrofollicles) & have densely eosinophilic colloid & less vascularized (colloid likes color, but not blood red)
Multifocal nodular hyperplasia → Who do you see this type of goiter in? (2)(1) Incidental lesion in old animals
(2) Functional (hyperthyroidism) in cats
Multifocal nodular hyperplasia → Hyperthyroidism in cats → What can be risk factors for developing this condition?Canned food
Cat litter
Genetic mutation in TSH receptors
↓ (-)ve inhibition of cAMP cascade
C-ras oncogene mutations → hyperplasia
Multifocal nodular hyperplasia → What do lesions look like for this type of goiter?Moderate enlargement of thyroids, multiple, irregular, non-encapsulated nodules (resulting from alternating periods of hyperplasia & colloid involution)
Congenital dyshormonogenetic goiter → Who gets this?Autosomal recessive disorder in some breeds of sheep (Corriedale, Dorset Horn, Merino & Romney breeds)
Afrikander cattle
Saanen dwarf goats
Congenital dyshormonogenetic goiter → What is going on/how does this happen?It czs genetic impairment of thyroglobulin synthesis! (T4 & T3 lvls are ↓ even though iodine uptake & turnover are ↑)
Congenital dyshormonogenetic goiter → What are the lesions associated w/ this type of goiter? (Gross body & thyroid)Subnormal growth rate, sparse hair coat, myxedema, weakness & sluggish behavior (most die shortly after birth). Thyroid lobes are symmetrically enlarged at birth bc of an intense diffuse hyperplasia of follicular cells
Which goiter often results in death soon after birth?Congenital dyshormonogenetic goiter


Question Answer
Follicular cell adenoma → What is the gross appearance of this type of neoplasia? Is it functional or nonfunctional?White to tan, small, well demarcated solid nodules or cysts (usually single & encapsulated). MAY be functional
***Follicular cell adenoma → Most common in who?More common in CATS than in dogs & horses
Follicular cell carcinoma → Most common in who?More common in dogs, especially beagles, boxers, golden retrievers
Follicular cell carcinoma → What is the gross appearance of this & how does it behave? (Functional or nonfunctional?)Multinodular, invade local tissues & metastasize early to the lungs (via the thyroid vein before regional lymph nodes)... +/- functional
Which thyroid neoplasm may arise from accessory thyroids (i.e., mediastinum or heart base regions)?Follicular cell CARCINOMA ((car goes places, metastasizes)
HYPERTHYROIDISM → WHO does this occur in most often & in what situation?Mostly in aged cats in w/ multinodular hyperplasia/ adenomas or carcinomas of follicular cells
How does a hyperthyroid clinically present? (LAB PARAMETERS)Marked increased in serum [T4 & T3], moderately increased serum enzyme activities (ALT, AST & AP)
How does hyperthryoidism affect the overall behavior? How does it affect the GI? Renal system?The animal (cat) will experience:

Increased activity
Weight loss in spite of voracious appetite (polyphagia)
Polydipsia & Polyuria
How does hyperthyroidism affect the respiratory system? How might it affect the animal's gross appearance? How would it affect their metabolism/body heat?There can be coughing & dyspnea due to the enlarged gland, you can observe cervical swelling (lump on neck from swollen gland) & they will experience hyperthermia/heat intolerance
**How does hyperthyroidism affect the cardiovascular system? How does it affect electrolytes?Hypertrophic Cardiomyopathy in CATS due to increased heart rate. This might be complicated by the fact there can be disturbances in calcium homeostasis


Question Answer
How does hyperthyroidism affect the parathyroid gland? (Micro appearance)Diffuse chief cell hyperplasia in the parathyroid glands (Chief cells produce PTH)
Hyperthyroidism 2º to thyroid neoplasms depends on what 2 factors?(1) Capability of neoplastic cells to synthesize T4/T3
(2) Extent of the ↑in circulating [T4/T3], which depends on a balance b/t:
   ( (a) Rate of secretion of thyroid hormones by the neoplasm
      (b) Rate of degradation of thyroid hormones (dogs are more efficient than cats in enterohepatic excretion of thyroid hormones) )
Hypothyroidism → Who does this occur in most commonly?Occurs in all species but most commonly in horses & dogs
(Golden retriever
Doberman pinscher
Shetland sheep dog
Irish setter
Miniature schnauzer
Cocker spaniel
****What are 5 etiological czs of HYPOthyroidism (KNOW ALL!)?(1) Idiopathic follicular atrophy (“collapse”)
(2) Lymphocytic thyroiditis
(3) Bilateral nonfunctional tumors
(4) Chronic pituitary lesions (compression/destruction)
(5) Severe prolonged iodine def (prevents production of both T4 & T3)
*What's the clinical expression of hypothyroidism he super emphasized w/ colors?Hypercholesterolemiaatherosclerosis
**How does HYPOthyroidism affect body weight? How does it affect energy, growth & metabolismTRAGIC FACE
Can cz a reduction in basal metabolic rate! this leads to:
Weight gain
Muscular weakness & slow reflexes
Cretinism (stunted growth) in young animals
*How does hypothyroidism affect the musculoskeletal system?Due to the ↓ in basal metabolic rate → muscular weakness, slow reflexes, joint pain & effusion
How does hypothyroidism affect the reproductive system?Sexual inactivity & reproductive failure inclding:
Lack of libido
Infertility (reduction in sperm count, abnormal or absent estrus cycles, reduced conception rates)
How does hypothyroidism affect the cardiovascular system/blood?Hypercholesterolemia

Normocytic Normochromic Anemia
*How does hypothyroidism affect the skin?Hyperkaratosis (so see lots of skin flakes)
Bilateral symmetric alopecia (telogen hairs....lack of thyroid hormone keeps hairs in the telogen which is the resting phase where hair is more easily epilated)
Follicular keratosis
(also calcinosis cutis/atropy)
*Hypothyroidism czs HYPERCHOLESTEROLEMIA!!! This results in...(4)Atherosclerosis
Glomerular & corneal lipidosis

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