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Endo/Repro I Exam 1 > Lecture 4: Thyroid Gland > Flashcards

Lecture 4: Thyroid Gland Flashcards

1
Q

What are the 3 stimulatory factors for the secretion of thyroid hormones?

A

1) TSH
2) Thyroid-stimulating immunoglobulins
3) Increased TBG levels (i.e., pregnancy)

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2
Q

What effect do Perchlorate and Thiocynate have on thyroid hormones?

A

Inhibit the Na+/I- cotransporter

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3
Q

What is the functional unit of the thyroid gland; surrounded by; how can the cells change?

A
  • Thyroid follicle
  • Surrounded by single-layer of epithelial cells
  • Follicular lumen filled w/ colloid
  • Size of epithelial cells and amount of colloid change w/ activity
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4
Q

How does a single dose of thyroxine (T4) affect BMR?

A

Increases BMR after several hours and the effect is long-lasting >6 hrs

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5
Q

What levels of TBG and T3 resin uptake in a patient who is pregnant vs. hepatic failure?

A
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6
Q

What does PTU inhibit and what is it used to treat?

A
  • Effective tx for hyperthyroidism
  • Inhibits peroxidase, so it has multiple layers of inhibition
  • Inhibits production of final thyroid products
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7
Q

What are the actions of thyroid hormones on CHO metabolism?

A
  • Increased gluconeogenesis and glycogenolysis to generate free glucose
  • Enhancement of insulin-dependent entry of glucose = increased glucose absorption
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8
Q

How are thyroid hormones transported in the blood stream?

A

Either bound to plasma proteins (99%) or free (1%)

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9
Q

What proteins are synthezised under the direction of thyroid hormones specific to the cardiac muscle cells?

A
  • Myosin
  • B1-adrenergic receptors
  • Ca+ ATPase
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10
Q

What is the second messenger for TSH?

A

cAMP

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11
Q

Most circulating thyroid hormons are found in what form; what is the half-life of T4 vs. T3?

A
  • Most found as T4
  • T4 half-life is 6 days
  • T3 half-life is 1 day
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12
Q

Enough hormone is stored as iodinated TG in the follicular colloid to last the body for how long?

A

2-3 months!

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13
Q

What levels of T4 and T3 resin uptake in a patient w/ high TBG vs. low TBG?

A
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14
Q

Explain the T3 resin uptake test

A
  • Standard amount of radioactive T3 is added to a sample that contains a pt’s serum + the T3-binding resin
  • Rationale is radioactive T3 will first bind to unoccupied sites on the patients TBG and any “leftover” radioactive T3 will bind to the resin
  • T3 resin uptake is increased when circulating levels of TBG are decreased (i.e hepatic failure) or when endogenous T3 levels are increased
  • T3 resin uptake is decreased when circulating levels of TBG are increased (i.e., pregnancy) or when endogenous T3 levels are decreased
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15
Q

A deficiency of intrathyroidal deiodinase mimics?

A

Dietary I- deficiency

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16
Q

What function do thyroid hormone play a role in CNS development; what can a deficiency lead to in a newborn/neonate?

A
  • Important for CNS maturation
  • Deficiency during perinatal period leads to:
  • Abnormal development of synapses
  • Decreased dendritic branching and myelination
  • Neural changes induced by thyroid hormone deficiency during the perinatal period are irreversible and lead to Cretinism unless replacemet therapy is started soon after birth
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17
Q

How does hyperthyroidism vs hypothyroidism affect BMR?

A

Hyperthyroidism: leads to a high BMR

Hypothyroidism: leads to a low BMR

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18
Q

Thyroid hormones contain a large amount of which mineral; where does synthesis of thyroid hormones occur; what is the major secretory product?

A
  • Large amount of iodine
  • Synthesis occurs part intracellulary and part extracellularly
  • T4 is the major secretory product
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19
Q

What occurs once iodine is in the lumen to join up with thyroglobulin?

A
  • Iodine goes through the process of organification mediated by peroxidase and is joined w/ thyroglobulin
  • Thyroglobulin binds to T4, T3, and intermediates MIT/DIT which has now formed the storage molecule within the colloid
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20
Q

How can circulating levels of TBG be indirectly assessed?

A

T3 resin uptake test

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21
Q

How do we get the thyroglobulin necessary for organification of iodine in the follicular lumen?

A
  • Thyroglobulins are synthesized in the ribosome from the pre-cursor tyrosine, intracellularly. They are processed in the rough ER and golgi before being secreted into the lumen.
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22
Q

What is the main role of TBG?

A

Provide a large reservoir of circulating thyroid hormones, which can be released and added to the pool of free hormone

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23
Q

What are the actions of thyroid hormones on lipid metabolism; specifically fat mobilization, oxidation of FA, cholesterol/TAG concentration, and fat-soluble vitamins?

A
  • Stimulate fat mobilization –> increases concentration of FA in plasma
  • Enhance oxidation of FA
  • Plasma concentration of cholesterol and TAGs are inversely correlated w/ thyroid hormones (i.e., hypothyroidism = increased blood cholesterol)
  • Required for the conversion of carotene to vitamin A (hypothyroid patients can suffer from blindness and yellowing of skin)
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24
Q

How do high thyroid hormone levels play a role in β1-adrenergic receptors and sympathetic stimulation?

A

When thryoid levels are high, the myocardium has an increased number of β1 receptors and is more sensitive to stimulation by the sympathetic nervous system

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25
Q

T3 (active form) is needed to provide neg. feedback to the pituitary and hypothalamus for the release of TRH and TSH, but how is this possible if most of the circulating thyroid hormone is T4?

A

We have a particular deiodinase (type 2) in the brain that can convert T4 to T3

26
Q

Hypothyroidism due to iodine deficiency affects thyroid hormones and TSH levels how?

A
  • Transient decrease in the synthesis of thyroid hormones
  • TSH levels are elevated
  • Goiter
  • If gland maintain normal blood levels of thyroid hormones, patient is euthyroid and asymptomatic
  • If gland cannot maintain normal blood levels, pt exhibits hypothyroid
27
Q

In general hypothyroidism leads to changes in body function?

A
  • Slowing down of body’s functions
  • Fatigue
  • Weight gain
  • Cold intolerance
28
Q

What are some of the indirect effects of thyroid hormones on cardiac muscle?

A
  • Increased heat production and CO2 in tissues
  • Decreased peripheral vascular resistance
  • Decreased diastolic BP
  • Reflex increases adrenergic stimulation
29
Q

What are some of the direct cardiovascular effects of thyroid hormones?

A
  • Increases cardiac muscle
  • Myosin hevavy chain α/β ratio
  • Na+-K+ ATPase
  • β-adrenergic signaling
  • G-protein stimulatory/inhibitory ratio
  • Increases ventricular contractility and function
  • Decreases peripheral vascular resistance
30
Q

What is primary vs. secondary hyperthyroidism; how are TSH levels affected?

A

Primary: Graves disease (most common cause of thyrotoxicosis)

Secondary: TSH-secreting pituitary

TSH levels:

  • Decreased due to neg. feedback of T3 on the anterior lobe of the pituitary
  • If defect is in the anterior pituitary TSH level are increased
31
Q

What are the binding proteins for the transport of thyroid hormones in circulation; which is the most abundant; where is it made; what does it have the highest affinity for?

A

1) Thyroxine binding protein (TBG) = MAIN
- Synthesized in the liver
- Binds 1 molecule of T3 or T4
- Has higher affinity for T4
2) Transthyretin (TTR)
3) Albumin

32
Q

What are the causes of Cretinism?

A
  • Iodine deficiency
  • Maternal intake of ant-thyroid medication
  • Impaired development of thyroid gland
  • Inherent deficit in the synthesis of thyroid hormones

*Untreated postnatal hypothyroidism results in cretinism*

33
Q

Causes of Primary Hypothyroidism?

A
  • Agenesis
  • Gland destruction (i.e, surgical removal, autoimmune disease, idiopathic atrophy)
  • Inhibition of thyroid hormones synthesis and release (i.e., iodine deficiency, inherited enzyme defects, drugs that interfere w/ thyroid homeostasis)
  • Transient (i.e., after surgery or therapeutic radioiodine, postpartum, thyroditis)
  • Hypothalamic disease (damage to 3rd tier)
  • Pituitary disease (i.e., Sheehan’s syndrome)
  • Resistance to thyroid hormones
34
Q

Goiter can develop for a number of reasons affecting what axis; imbalances include?

A
  • HPT axis
  • Hyperthyroidism: Graves and TSH-producing tumor (2° hyperthyroidism)
  • Primary Hypothyroidism: lack of adequate iodine in the diet, sporadic hypothyroidism of unknown etiology, chronic thyroditis (Hashimotos; autoimmune-induced deficiency in thyroid function)
35
Q

What is the Wolff-Chaikoff effect?

A

High levels of I- inhibit organification and synthesis of thyroid hormones (neg. feedback)

36
Q

What are the major clinical signs of Graves disease; diagnosed by; how is this disease distinguishable from other pathologies?

A
  • Exopthalmos (abnormal protrusion of the eyeball) and periorbital edema (due to recognition by the anti-TSH receptor Ab’s of a similar epitope within the orbital cells)
  • Dx by: elevated serum free and total T4 or T3 level and clinical signs of goiter and opthalmopathy
  • Presence of circulating TSI, helps distinguish Graves from adenoma of pituitary thyrotrophs
37
Q

Which transporters are located on the basolateral membrane/blood side of the follicular epithelial cell?

A
  • Na+/K+ ATPase
  • Na+/I- symporter (NIS, 2/1 ratio)
  • The iodide trap
38
Q

Major control of the synthesis and secretion of thyroid hormones occurs via which axis?

A

HPT axis

39
Q

Overall what do the direct and indirect effects of thyroid hormones lead to in regards to cardiovascular function and blood volume?

A
  • Increased cardiac rate and output
  • Decreased TPR/systemic resistance
  • Increased inotropic effects
  • Increased blood volume/preload
40
Q

Grave’s disease, thyroditis (hyperthyroidism), and thyroid nodules (hot, or toxic) all have common thyroid function test results (TSH, T3/T4, and TSI), what are they?

A
  • Decreased TSH
  • Increased T3/T4
  • Graves’ disease will have positive TSI test, others won’t.
41
Q

What is the role of TSH and what is it regulated by; how does the secretion of TSH differ from GH

A

TSH: regulates the growth of the thyroid gland (trophic effect) and secretion of thyroid hormones

  • TSH is regulated by TRH and free T3 (feedback)
  • TSH secretion, in contrast to the secretion of GH (pulsatile) occurs at a steady state
42
Q

What levels of T4 and T3 resin uptake in a patient w/ hyperthyroidism vs. hypothyroidism?

A
43
Q

How does hepatic failure alter the fraction of free thyroid hormones?

A
  • Decreased blood levels of TBG
  • Transient increase in the level of frere T3, T4
  • Followed by inhibition of synthesis of T3, T4 (neg. feedback)
44
Q

How does pregnancy alter the fraction of free thyroid hormones?

A
  • Increased TBG levels
  • Increased bound T3, T4, decreased free T3, T4
  • The transient decrease in free T3, T4 causes an increase in synthesis and secretion of T3, T4
  • Increased total levels of T3 and T4, but levels of free, physiologically active, thyroid hormones are normal (person is said to be clinically euthyroid)
45
Q

How do we treat hypothyroidism; why do we take age into account, what can overprescribing to post-menopausal women lead to?

A
  • Replacement doses of T4
  • Metabolism of T4 decreases and the plasma half-life increases w/ age, higher doses are required in younger patients
  • In women beyond menopause, overprescribing T4 can contribute to development of osteoporosis
46
Q

How do thyroid hormones affect BMR; what accounts for most of this change; how does this affect O2 and heat production?

A
  • Increased activity of Na+-K+ ATPase accounts for most of the increase in metabolic rate (BMR)
  • Leads to increased O2 consumption and heat production
47
Q

What clinical states are associated w/ a reduction in the conversion of T4 to T3?

A
  • Fasting
  • Medical and surgical stress
  • Catabolic diseases
48
Q

We consume iodide and must convert it to iodine to make our prohormone T4 and T3, explain this process.

A
  • Iodide is oxdized to iodine
  • Iodine is joined w/ tyrosine making MIT or 2 iodines w/ tyrosine to make DIT
  • DIT + DIT will give us a thyroxine (T4)
  • DIT + MIT will give us a triiodothyronine (T3)
49
Q

What is Hashimoto’s Thyroiditis?

A
  • Thryoid hormone synthesis is impaired by thyroglobulin or TPO antibodies, which leads to decreased T3, T4 secretion
  • TSH levels are high due to low levels of circulating hormone
  • High TSH has a trophic effect on thyroid = Goiter
50
Q

How do thryoid hormones play a role in the growth and development of the fetus, neonate, and adolescent?

A
  • Fetal development requires proper thyroid hormone levels
  • Synergistically works with GH and somatomedins to promote bone formation
51
Q

In general hyperthyroidism leads to changes in body function?

A
  • Increases the speed of bodily functions = weight loss
  • Sweating and rapid heart rate
  • High BP
52
Q

What is responsible for the synthesis of key metabolic enzymes in the liver and adipose tissue?

A

Thyroid hormones

53
Q

What is occuring in Graves disease; why are TSH levels low, but thyroid levels are still high?

A
  • Thyroid-stimulating immunoglobulins bind to TSH receptor and cause unregulated overproduction of thyroid hormones
  • TSH levels are lower than normal because the high circulating levels of thyroid hormones inhibit TSH secretion
54
Q

Thryoid hormones are responsible for the synthesis of a vast array of proteins, what are they?

A
  • Na+-K+ ATPase
  • Transport proteins
  • B1-adrenergic receptors
  • Lysosomal enzymes
  • Proteolytic enzymes
  • Structural proteins
55
Q

What does the thyroid gland produce and what is the key step to utilize these hormones?

A
  • Produce prohormone tetraiodothyronine (T4) and the active hormone triiodothyronine (T3)
  • Peripheral conversion by deiodinases is key
56
Q

What occurs to the MIT and DIT leftover after the proteolytic cleavage of the thyroid hormones and release into circulation?

A
  • MIT and DIT are deiodinated inside the follicular cell by the enzyme intrathyroidal deiodinase
  • The I- generated by this step is recycled into the intracellular pool and added to the I- transported by the pump
  • The tyrosine molecules are incorporated into the synthesis of new TG to begin another cycle
  • Both I- and tyrosine are “salvaged”
57
Q

What is colloid composed of; what is the blood supply like to the thyroid?

A
  • Composed of newly synthesized thyroid hormones attached to thyroglobulin
  • Rich blood supply
58
Q

How can the activity of the thyroid gland be assessed?

A

Radioactive iodine uptake

59
Q

What is located on the apical membrane/follicular lumen of the follicular epithelial cell and their function?

A
  • Pendrin: Cl/I- counter-transporter
  • Peroxidase: oxidizes iodide for combination with thyroglobulin
60
Q

How do we get release of the thyroid hormones from the colloid?

A
  • Stimulation by TSH causes the colloid to be taken up via pinocytosis into the follicular epithelial cell where it is engulfed by lysosomes
  • In the lysosome proteases cleave T4 & T3 from thyroglobulin for release into circulation
61
Q

When the availability of iodide is restricted, the formation of what is favored?

A

T3

62
Q

Once we have T4, which is inactive, how do we get it to the active form T3; where do we get active T3 from?

A
  • Outer ring deiodination by deiodinase type 1 (periphery) and type 2 (brain)
  • Give us active T3 and reverse T3 (inactive)
  • Most T3 from peripheral conversion (90%)
  • Some T3 from direct secretion from thyroid gland (10%)

Endo/Repro I Exam 1 (12 decks)

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