Thyroid gland Flashcards
What are the thyroid hormones?
T3 triiodothyronine
T4 thyroxine
What are the output % of T3 and T4?
T4 (thyroxine) - 90% of output
T3 (triiodothyronine) - 10% of output
Which is more biologically active: T3 or T4, and why?
T3 is far more active because of higher affinity to thyroid hormone receptors
What is the main precursor in all vertebrates to thyroid hormones?
Thyroglobulin
It’s produced from iodine in thyroid epithelium
What is the hypothalamic-pituitary-thyroid (HPT) axis?
- Neurons of the hypothalamus secrete TRH
- Anterior lobe synthesizes and releases TSH
- T4 and T3 are released in thyroid gland
- T4 and T3 have negative feedback loops both in thyrotrophs and in hypothalamus
How are T4 and T3 circulating?
More than 99% bound to proteins
Primary binder in dogs - Thyroid-binding globulin (cats don’t really have)
Primary binder in cats - Prealbumin
Hormones bound to proteins are not active, serve as reserve (equilibrium baby)
Factors that affect thyroid hormone concentrations
-Many diseases
-Pharmacological agents (i.e. glucocorticoids)
-Breed differences (i.e. small breeds have more TT4)
Metabolism of thyroid hormones
Deionation is most important thing!
-Liver and kidney deionates T4 into T3 (increases biological activity)
Stuff that affects deionation:
-tissue specific deiodinases
-fasting
-nonthyroidal illness
How quickly does thyroid hormone act?
There is a lag time of hours or days before full physiological effects take place
Physiological effects of thyroid hormones
Help maintain normal:
-Energy levels
-Weight
-Thermoregulation
-Heart rate
-Bowel movement
-Mood
4 types of hypothyroidism in young animals:
-Acquired juvenile hypothyroidism
-Thyroid dysgenesis
-Defective thyroid hormone synthesis
-Central (secondary) hypothyroidism
Prominent sign of juvenile hypothyroidism
Dwarfism (+ also all the “normal” signs)
Thyroid hormones are crucial for growth and development of all body tissues, particularly the skeleton.
What causes acquired juvenile hypothyroidism?
Iodine deficiency
i.e. diet with only meat without additives is deficient in iodine
In severe cases: lack of iodine –> TSH-induced thyroid hyperplasia, “goiter”
What is thyroid dysgenesis?
Thyroid gland does not develop or function properly; is absent, reduced in size or abnormally located.
Common in dogs, also seen in cats.
What is defective thyroid hormone synthesis?
Congenital enzyme deficiency that prevents synthesis of thyroid hormones
Quite rare
What is central (secondary) hypothyroidism?
Due to TSH deficiency
Can be pituitary or hypothalamic
Usually accompanied by decreased secretion of other pituitary hormones
Two types of hypothyroidism in adult animals:
Primary hypothyroidism -95% of cases
Central hypothyroidism -5% of cases
What is the pathogenesis of primary hypothyroidism?
Progressive autoimmune process which leads to lymphocytic infiltration and disappearance of thyroid follicles. (thyroid follicles are replaced by fibrous and adipose tissue)
The immune-mediated destruction is slow, clinical manifestations become evident after 75% of thyroid has been destroyed.
Sometimes the immunologic damage might involve other endocrine glands –> polyglandular failure syndrome
Pathogenesis of primary hypothyroidism in cats?
Iatrogenic hypothyroidism from radioiodine therapy or surgical thyroidectomy
Clinical manifestations of primary hypothyroidism in adult dogs:
-Weight gain
-Hypothermia, cold intolerance
-Appetite unchanged or reduced
-Coarse coat, alopecia
-Thickening of skin (myxedema)
-Bradycardia, weak peripherial pulse
-Persistent anestrus, loss of libido, testicular atrophy
-Letharhy
Hematological and biochemical findings in hypothyreosis
-Nonregenerative anemia
-Hypercholesterolemia
-Hypertriglyceridemia
-Mild hyperglycemia
Treatment of primary hypothyroidism
Lifelong thyroid hormone replacement therapy
T4 therapy will correct T3 also
Prognosis of primary hypothyroidism
Usually excellent with appropriate treatment and follow-up examinations
Cause and what happens in central hypothyroidims
-Thyroids are normal, but are deprived of stimulation by TSH
-Rare compared to primary
-Causes: tumor of pituitary or adjacent regions, head trauma, surgical removal of pituitary tumor
SUMMARY of hypothyroidism in dogs:
- Primary hypothyroidism (95%):
-Autoimmune (lymphocytic) thyroiditis
-Destruction of thyroid tissue
-Idiopathic atrophy
-Thyroid tumor - Secondary (central) hypothyroidism:
-Inadequate TSH secretion
-Head trauma, cysts/nodules, tumors - Tertiary hypothyroidism:
-Deficiency of TRH (extremely rare in dogs)
What is and what causes hypoerthyroidism in cats?
-Relatively common disease in middle-aged and elderly cats
-Thyroid adenomatous hyperplasia in one or both thyroid lobes
Classic presentation of hyperthyroid cat
Skinny, restless, elderly cat with polyphagia and polyuria
Clinical manifestations of hyperthyroidism in cats
-Weight loss
-Polyphagia
-Panting
-Tachycardia
-Arrhythmias
-Left ventricular hypertrophy
-Restlessness (irritability)
-Polyuria
-Increased fecal volume
Hematological and biochemical findings in hyperthyroid cats
-Neutrophilic leukocytosis with eosinopenia and lymphopenia (a bit like stress leukogram)
-Elevated plasma ALT, AP, LDH
-Hypokalemia
-Urinary corticoid:creatinine ratio elevated
What is “apathetic hyperthyroidism”?
In 10% of cases the clinical picture is different
There is still weight loss, but the cat is lethargic and anorexic
Might represent end-stage disease and be associated with cardiac disorders
Three treatment options for feline hyperthyroidism:
1) Radioiodine ablation of the thyroid
2) Surgical thyroidectomy
3) Antithyroid drugs (methimazole, carbimazole)
How does radioiodine therapy work?
Radioiodine selectively destroys hyperfunctioning thyroid cells while sparing the normal thyroid tissue and parathyroid glands.
Prognosis of hyperthyroidism in cats
Without severe cardiac or kidney disease, the prognosis is good
What are calciotropic hormones?
Regulate calcium metabolism
-Parathyroid hormone (PTH)
-Calcitonin (CT)
-Vitamin D
Synthesis and release of these hormones are mainly triggered by variations in plasma calcium concentration
Major cell type in parathyroid glands
chief cells
What stimulates PTH synthesis and release?
-Hypocalcemia
-Increase in phosphorus concentration
-Low levels of calcitriol (vitamin D3)
How many parathyroid glands are there?
Four
What inhibits PTH secretion?
-Increase in extracellular Ca2+
How PTH circulates and half-life
Circulates free in plasma
Half life 4 minutes
Hypoparathyroidism?
Rare
Results in decreased Ca2+-levels in plasma –> neuromuscular manifestations
How is hypoparathyroidism diagnosed?
If there is hypocalcemia and hyperphosphatemia in the absence of renal failure
Low plasma PTH concentration will confirm diagnosis
Treatment of hypoparathyroidism
If there is hypocalcemic tetany, treat that first with slow IV injection of calcium
Oral maintenance therapy comprises of vitamin D + calcium supplementation
Prognosis of hypoparathyroidism
Needs adequate monitoring of plasma calcium concentration but prognosis is excellent
Hyperparathyroidism, two types
Primary hyperparathyroidism: usually adenoma of chief cells
Secondary hyperparathyroidism: unrelated to intrinsic disease of parathyroids
(i.e. chronic decrease in calcium concentration. Common reasons: chronic renal failure, ca deficiency during growth)
Where is calcitonin produced?
In thyroid gland, by C cells
What stimulates calcitonin secretion?
High serum Ca2+
What inhibits calcitonin secretion?
Low serum Ca2+
What does calcitonin do?
Main role is to inhibit bone resorption
Lowers serum Ca2+ levels
Protects bone mass
I kidneys, increases excretion of Ca2+ and some other substances
