Thyroid gland Flashcards

1
Q

What are the thyroid hormones?

A

T3 triiodothyronine
T4 thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the output % of T3 and T4?

A

T4 (thyroxine) - 90% of output
T3 (triiodothyronine) - 10% of output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which is more biologically active: T3 or T4, and why?

A

T3 is far more active because of higher affinity to thyroid hormone receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the main precursor in all vertebrates to thyroid hormones?

A

Thyroglobulin

It’s produced from iodine in thyroid epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the hypothalamic-pituitary-thyroid (HPT) axis?

A
  1. Neurons of the hypothalamus secrete TRH
  2. Anterior lobe synthesizes and releases TSH
  3. T4 and T3 are released in thyroid gland
  4. T4 and T3 have negative feedback loops both in thyrotrophs and in hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How are T4 and T3 circulating?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Factors that affect thyroid hormone concentrations

A

-Many diseases
-Pharmacological agents (i.e. glucocorticoids)
-Breed differences (i.e. small breeds have more TT4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Metabolism of thyroid hormones

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How quickly does thyroid hormone act?

A

There is a lag time of hours or days before full physiological effects take place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Physiological effects of thyroid hormones

A

Help maintain normal:
-Energy levels
-Weight
-Thermoregulation
-Heart rate
-Bowel movement
-Mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

4 types of hypothyroidism in young animals:

A

-Acquired juvenile hypothyroidism
-Thyroid dysgenesis
-Defective thyroid hormone synthesis
-Central (secondary) hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Prominent sign of juvenile hypothyroidism

A

Dwarfism (+ also all the “normal” signs)

Thyroid hormones are crucial for growth and development of all body tissues, particularly the skeleton.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes acquired juvenile hypothyroidism?

A

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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is thyroid dysgenesis?

A

Thyroid gland does not develop or function properly; is absent, reduced in size or abnormally located.

Common in dogs, also seen in cats.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is defective thyroid hormone synthesis?

A

Congenital enzyme deficiency that prevents synthesis of thyroid hormones

Quite rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is central (secondary) hypothyroidism?

A

Due to TSH deficiency
Can be pituitary or hypothalamic

Usually accompanied by decreased secretion of other pituitary hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Two types of hypothyroidism in adult animals:

A

Primary hypothyroidism -95% of cases
Central hypothyroidism -5% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the pathogenesis of primary hypothyroidism?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathogenesis of primary hypothyroidism in cats?

A

Iatrogenic hypothyroidism from radioiodine therapy or surgical thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical manifestations of primary hypothyroidism in adult dogs:

A

-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

21
Q

Hematological and biochemical findings in hypothyreosis

A

-Nonregenerative anemia
-Hypercholesterolemia
-Hypertriglyceridemia
-Mild hyperglycemia

22
Q

Treatment of primary hypothyroidism

A

Lifelong thyroid hormone replacement therapy

T4 therapy will correct T3 also

23
Q

Prognosis of primary hypothyroidism

A

Usually excellent with appropriate treatment and follow-up examinations

24
Q

Cause and what happens in central hypothyroidims

A

-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

25
Q

SUMMARY of hypothyroidism in dogs:

A
  1. Primary hypothyroidism (95%):
    -Autoimmune (lymphocytic) thyroiditis
    -Destruction of thyroid tissue
    -Idiopathic atrophy
    -Thyroid tumor
  2. Secondary (central) hypothyroidism:
    -Inadequate TSH secretion
    -Head trauma, cysts/nodules, tumors
  3. Tertiary hypothyroidism:
    -Deficiency of TRH (extremely rare in dogs)
26
Q

What is and what causes hypoerthyroidism in cats?

A

-Relatively common disease in middle-aged and elderly cats
-Thyroid adenomatous hyperplasia in one or both thyroid lobes

27
Q

Classic presentation of hyperthyroid cat

A

Skinny, restless, elderly cat with polyphagia and polyuria

28
Q

Clinical manifestations of hyperthyroidism in cats

A

-Weight loss
-Polyphagia

-Panting
-Tachycardia
-Arrhythmias
-Left ventricular hypertrophy

-Restlessness (irritability)
-Polyuria
-Increased fecal volume

29
Q

Hematological and biochemical findings in hyperthyroid cats

A

-Neutrophilic leukocytosis with eosinopenia and lymphopenia (a bit like stress leukogram)
-Elevated plasma ALT, AP, LDH
-Hypokalemia
-Urinary corticoid:creatinine ratio elevated

30
Q

What is “apathetic hyperthyroidism”?

A

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

31
Q

Three treatment options for feline hyperthyroidism:

A

1) Radioiodine ablation of the thyroid
2) Surgical thyroidectomy
3) Antithyroid drugs (methimazole, carbimazole)

32
Q

How does radioiodine therapy work?

A

Radioiodine selectively destroys hyperfunctioning thyroid cells while sparing the normal thyroid tissue and parathyroid glands.

33
Q

Prognosis of hyperthyroidism in cats

A

Without severe cardiac or kidney disease, the prognosis is good

34
Q

What are calciotropic hormones?

A

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

35
Q

Major cell type in parathyroid glands

A

chief cells

36
Q

What stimulates PTH synthesis and release?

A

-Hypocalcemia
-Increase in phosphorus concentration
-Low levels of calcitriol (vitamin D3)

37
Q

How many parathyroid glands are there?

A

Four

38
Q

What inhibits PTH secretion?

A

-Increase in extracellular Ca2+

39
Q

How PTH circulates and half-life

A

Circulates free in plasma
Half life 4 minutes

40
Q

Hypoparathyroidism?

A

Rare
Results in decreased Ca2+-levels in plasma –> neuromuscular manifestations

41
Q

How is hypoparathyroidism diagnosed?

A

If there is hypocalcemia and hyperphosphatemia in the absence of renal failure

Low plasma PTH concentration will confirm diagnosis

42
Q

Treatment of hypoparathyroidism

A

If there is hypocalcemic tetany, treat that first with slow IV injection of calcium

Oral maintenance therapy comprises of vitamin D + calcium supplementation

43
Q

Prognosis of hypoparathyroidism

A

Needs adequate monitoring of plasma calcium concentration but prognosis is excellent

44
Q

Hyperparathyroidism, two types

A

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)

45
Q

Where is calcitonin produced?

A

In thyroid gland, by C cells

46
Q

What stimulates calcitonin secretion?

A

High serum Ca2+

47
Q

What inhibits calcitonin secretion?

A

Low serum Ca2+

48
Q

What does calcitonin do?

A

Main role is to inhibit bone resorption
Lowers serum Ca2+ levels
Protects bone mass
I kidneys, increases excretion of Ca2+ and some other substances