Thyroid Endocrine Flashcards
Hormones produced in the thyroid
T3 -triiodothyronine
T4 -thyroxine
Calcitonin – peptide hormone from C-cells
How is Iodine transported into the follicle
Iodide in the blood
–> Na+/I- symporter –> apicial surface Pendrin channel (allows I- into colloid) –> oxidized to Iodine and iodinates Thyroglobulin (tyrosyl residues)
Thyroid cysts
Follicular or thyroglossal duct
4 causes of thyroid atrophy
- decreased TSH stimulation
1. 2ndary to lack of trophic hormone
2. Immune-mediated destruction
3. Compression/invasion by neoplasm
4. Colloid goiter
Causes of Thyroid hyperplasia
- Iodine deficiency goiter
2. Feline hyperthyroidism
2 types of thyroid neoplasms
- Follicular cell adenoma/carcinoma
2. C-cell adenoma/carcinoma
Causes of HYPOthryoidism
- 2ndary
- Goiter
- Iodine-deficient goiter
- Iodine-excess or goitrogens
- Gongenital dyshormonogenetic goiter
- Follicular atrophy
- Iatrogenic
- Idiopathic (autoimmune)
- Lymphoplasmacytic thryoiditis
Microscopic features of Thyroid atrophy
- cuboidal epithelial cells
- dense colloid
- distended follicles
Congenital dyshormonogenetic goiter
Symmetrical hyperplastic goiter
- Hypothyroidism
- decreased growth rate = stillborn
- abnormal coat = hairless when born
- Autosomal recessive -ruminants, dog/cat
- defective Tgb synth or iodination
Microscopic features of hyperplasic goiter
- follicular epithelium
- tall columnar
- forms a papillary projection /endocytic vacuoles - follicular lumen
- Pale colloid
- narrow follicular lumen
Feline Hyperthyroidism
Thyroid lesions
- Follicular adenomas
2. Adenomatous hyperplasia
Non-thyroid lesions associated with Feline Hyperthyroidism
- Increased Phos –> Reciprocal decrease in Ca
- Increased PTH (due to low Ca) –> hyperparathyroidism
- Hypertrophic cardiomyopathy
Thyroid tumors
(adenoma vs carcinoma?)
in Dog vs Cat vs Horse vs cattle
Dog = carcinoma Cat = adenoma Horse = C-cell adenoma --w/o clinical signs Cattle = C-cell Carcinoma --Dairy bulls
What cell secretes PTH
Chief cell
Main target organs of PTH
- Bone
- Renal tubules
- -Blocks Phos reabsorption
- -Enhances Ca reabsorption - Intestines
-mobilizes Ca
Stimulating release of PTH
Recently synthesized PTH:
- released directly without entering the storage pool
- stimulated only by a decreased calcium ion concentration
PTH from the storage pool:
- mobilized by
- cAMP and β-agonists
- epi
- norepi
- isoproterenol
- lowered blood calcium ion
- cAMP and β-agonists
Parathyroid gland disorders
- Parathryoid (Kursteiner’s) cysts
- Hyperparathryoidism –Most common
- Hypoparathyroidism –Immune-mediated parathyroiditis
Causes of Hyperparathryoidism
- Primary
1. Chief cell adenoma
2. Chief cell carcinoma - Secondary
1. Nutritional
2. Renal
Causes of Pseudohyperparathyroidism
aka Humoral hypercalcemia of malignancy
- Lymphoma
- Anal sac apocrine carcinoma
- does not have a true elevation of PTH
- persistant hypercalcemia
- should cause atrophy of Parathyroid gland
Secondary lesion due to Parathyroid adenoma
Severe thinning of cortical bone and large resorptive cavities
Lesion seen with Iodine deficiency
Early stage or fetus
-Hyperplastic goiter (enlarged, firm, dark red-brown)
After correction of iodine deficiency or maturation of the animal
-progresses to a colloid goiter (involutional stage)
Pathogenesis of Feline Hyperparathyroidism
IgG acts on TSH receptors –> proliferation of thyroid follicular cells –> multiple hyperplastic nodules or follicular adenomas
Common thyroid tumor in Dairy bull
Cell cell carcinomas
-Ca-rich diet
Pathogenesis: Renal Dz –> Hyperparathyroidism
- Decrease Phos excretion –> hyperphosphatemia –> decreased Ca:P –> stimulates PTH release
- Decreases Vitamin D3 production –> decrease intestinal absorption of Ca
Nutritional imbalances leading to Hyperparathyroid
- Insufficient Ca
- Excess Phos
- Cholecalciferol deficiency
