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PHYSIOLOGY IV > LECTURE 3 (Thyroid) > Flashcards

LECTURE 3 (Thyroid) Flashcards

1
Q

Thyroid secretion is controlled by which hormone?

A

Thyroid-stimulating hormone (TSH)

[secreted by the anterior pituitary gland]

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2
Q

What is the difference between Triiodothyronine and Thyroxine?

A
  • T3 is more potent than T4
  • T3 is present in the blood in much smaller quantities
  • T3 persists for a much shorter time
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3
Q

Describe the physiologic anatomy of the Thyroid gland

A
  • Large number of follicles filled with “colloid”
  • Follicles lined with cuboidal epithelial cells that secrete into the interior of the follicles
  • Thyroglobulin found in colloid
  • Large blood supply
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4
Q

Describe the process of Iodide tapping

A

Iodide is pumped actively into the cell by a SODIUM-IODIDE SYMPORTER (NIS) which co-transports one iodide ion along with 2 Na2+ ions across the plasma membrane
[energy comes from sodium-potassium ATPase pump which generates a gradient for facilitated diffusion of Na2+ into the cell]

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5
Q

What is the difference between TSH and Hypophysectomy?

A

TSH = stimulates iodide pump

Hypophysectomy (surgical removal of pituitary gland) = greatly diminishes activity of iodide pump in thyroid cells

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6
Q

How is iodide transported out of the thyroid cells?

A

Iodide is transported out of the thyroid cells across the apical membrane into the follicle by a chloride-iodide ion counter-transporter called PENDRIN

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7
Q

What are Thyroid hormones synthesised from?

A

Tyrosine & Iodine

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8
Q

What is Thyroglobulin?

A
  • Large protein produced by thyroid follicular cells
  • “backbone” containing numerous tyrosine molecules
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9
Q

What must happen to iodide in our diet for thyroid hormone synthesis?

A

1) Taken up by follicular cells
2) Oxidised to I2 “OXIDATION”
3) Added to organic/carbon structures “ORGANIFICATION”

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10
Q

Where is Thyroid peroxidase usually located?

A

In the apical membrane or attached to it

Explanation: Provides oxidised iodine the point in the cell where the thyroglobulin molecule issues forth from the Golgi apparatus and through the cell membrane into the stored thyroid gland colloid

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11
Q

What happens when the peroxidase system is blocked or when it is hereditarily absent from cells?

A

The rate of formation of thyroid hormones falls to zero

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12
Q

Describe Thyroid hormone synthesis

A

1) Iodide enters the follicular cell via NA-IODINE SYMPORTER with Sodium
2) “OXIDATION” Iodide is oxidised to I2 via THYROID PEROXIDASE
3) “ORGANIFICATION” Tyrosine + Iodine (I2) is converted to either MONOIODOTYROSINE (MIT) [1 iodine] or DIIODOTYROSINE (DIT) [2 iodine] via THYROID PEROXIDASE
4) “COUPLING REACTIONS” MIT + DIT = TRIIODOTHYRONING (T3) or DIT + DIT = THYROXINE (T4)

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13
Q

Describe how T3 and T4 is released from Thyroglobulin

A

1) Apical surface of thyroid cells sends out PSEUDOPOD EXTENSIONS that close around small portions of the colloid to form PINOCYTIC VESICLES that enter the apex of the thyroid cell
2) Lysosomes in cell cytoplasm fuse with vesicles to form digestive vesicles containing digestive enzymes from the lysosomes mixed with the colloid
3) Multiple proteases digest thyroglobulin molecules and release thyroxine and triiodothyronine in free form
4) T3 and T4 diffuse through the base of the thyroid cell into the surrounding capillaries

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14
Q

What happens to the freed T3 and T4 not secreted into the blood?

A

Iodine is cleaved from them by DEIODINASE ENZYME that makes the iodine available for recycling

ADDITIONAL INFO: In people with absence of the enzyme, they can become iodine deficient because of failure to recycle

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15
Q

What is the function of Thyroid Peroxidase (TPO)?

A

It catalyses
- Oxidation of iodide
- Organification into MIT/DIT
- Coupling of MIT/DIT into T3/T4

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16
Q

What is produced more, T3 or T4?

A

T4 (>90% of thyroid hormone produced is T4)

Explanation: More T4 is produced initially but more T3 is needed since it is a more POTENT hormone, thus T4 must be converted to T3 via 5’-DEIODINASE

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17
Q

How are T3 and T4 transported in the blood?

A

By binding to plasma proteins

PLASMA PROTEINS:
- Thyroxine-binding globulin (main!!)
- Thyroxine-binding pre-albumin
- Albumin

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18
Q

What is the general effect of thyroid hormone?

A
  • Activate nuclear transcription of large number of genes
  • Generalised increase in functional activity throughout the body
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19
Q

How do thyroid hormones work?

A

1) Thyroid hormone receptors are either attached to the DNA genetic strands or located close to them -> thyroid hormone receptor forms a heterodimer with RETINOID X RECEPTOR (RXR) at specific THYROID HORMONE RESPONSE ELEMENTS on the DNA
2) Thyroid hormone binds, receptors become activated and initiate transcription process
3) Large number of mRNAs are formed followed by RNA translation to form new intracellular proteins

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20
Q

What happens to mitochondria when the number of thyroid hormones increases?

A
  • Mitochondria increase in size and number
  • Total membrane surface area increases in proportion to metabolic rate
  • Increase in activity -> increase in ATP for cellular function
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21
Q

What is the effect of thyroid hormones on active transport?

A

Increase in thyroid hormones acts on Sodium-Potassium ATPase which increases the rate of transport of Na2+ and K+ across cell membranes. It also makes some cell membranes “leaky” to Na2+ -> further activates sodium pump -> further increase in heat production

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22
Q

What is the Thyroid hormone’s effect on growth?

A
  • hyperthyroid = excessive growth of children + bones mature rapidly, epiphyses close earlier -> eventual height shortened
  • hypothyroid = growth and maturation of brain are greatly retarded -> no thyroid therapy -> child will remain mentally deficient throughout life
23
Q

What is the Thyroid hormone’s effect on Plasma and liver fats?

A

Increased thyroid hormone decreases the concentrations of cholesterol, phospholipids and triglycerides in the plasma even though it increases the free fatty acids

24
Q

Why do you need more vitamins when you increase thyroid hormones?

A

Thyroid hormone increases the quantities of many bodily enzymes which require vitamins -> vitamin deficiency can occur when excess thyroid hormone is secreted (unless increased quantities of vitamins are made available)

25
Q

What are the different effects of the thyroid hormone on the cardiovascular system?

A
  • Increased blood flow & cardiac output (increased metabolism + oxygen utilisation -> greater release of metabolic end products -> increased vasodilation to get rid of heat)
  • Increased HR (increase excitability of heart -> increased HR)
  • Increased heart strength (thyroid hormone increased a lot -> heart muscle strength depresses due to long-term excessive protein catabolism -> death due to cardiac decompensation)
  • Arterial pressure stays normal
  • Increased respiration
  • Increased GI motility
  • Excitatory effects on the CNS (anxiety, worry, paranoia)
  • Increased muscle strength (overtime muscles become weakened due to protein catabolism)
  • Muscle tremor
  • Sleep (increase = cannot sleep, decrease = sleep too much)
  • Sexual function (decreased = libido and polymenorrhea (frequent menstrual bleeding in women), increased = impotence in men and amenorrhea in women)
26
Q

What is TSH?

A

Also known as “Thyroid Stimulating Hormone” or “Thyrotropin”
- an anterior pituitary gland hormone
- increases thyroid secretion

27
Q

What are the effects of TSH on the Thyroid gland?

A
  • Increased proteolysis of thyroglobulin stored in follicles (increases T3 and T4 release)
  • Increased activity of the iodide pump (increases “iodide tapping”)
  • Increased iodination of tyrosine to form thyroid hormones
  • Increased size and secretory activity of thyroid cells
  • Increased number of thyroid cells (also change from cuboidal to columnar cells + infolding of thyroid epithelium into follicles)
28
Q

Describe how cAMP mediates the stimulatory effect of TSH

A

1) TSH binds with specific TSH receptors on the basal membrane surfaces of the thyroid cell which activates ADENYLYL CYCLASE, increasing formation of cAMP in the cell
2) cAMP acts on a second messenger to activate protein kinase which causes a cascade
3) Causes increased secretion of thyroid hormones and prolonged growth of thyroid glandular tissue

29
Q

Describe how TSH is released from the pituitary gland

A

1) Thyrotropin-releasing hormone (TRH) is secreted by nerve endings in the median eminence of the hypothalamus and is then transported to the ANTERIOR PITUITARY via the HYPOTHALMIC-HYPOPHYSIAL PORTAL BLOOD
2) TRH binds with TRH receptors in the pituitary membrane which activates the PHOSPHOLIPASE SECOND MESSENGER SYSTEM inside the pituitary cells to produce large amounts of PHOSPHOLIPASE C
3) A cascade of second messengers (Ca2+ and diacyl glycerol) follows which leads to TSH release

30
Q

What happens when the blood portal system from the hypothalamus to the anterior pituitary gland becomes blocked?

A

The rate of secretion of TSH by the anterior pituitary decreases greatly but is not reduced to zero

31
Q

What are the effects of cold on TRH and TSH secretion?

A

Decrease in temperature -> Excitation of hypothalamic centers for body temp control -> Increase in TRH and TSH secretion -> Increase in metabolism

32
Q

What are the effects Anxiety and Excitement on TRH and TSH secretion?

A

Excitement and anxiety greatly stimulate the sympathetic nervous system -> increase metabolic rate and body heat -> decrease in secretion of TRH and TSH to counteract effect

33
Q

What is the feedback effect of thyroid hormone?

A

Increased thyroid hormone in the body fluid decreases secretion of TSH by the anterior pituitary

34
Q

What are the different Antithyroid drugs?

A
  • Thiocyanate
  • Propylthiouracil
  • Inorganic iodides
35
Q

What is the MOA of Thiocyanate?

A

The same active pump that transports iodide ions into the thyroid cells pump thiocyanate ions -> high concentration cause COMPETITIVE INHIBITION of iodide transport into the cell, inhibiting “iodide trapping” -> prevents thyroglobulin from being iodinated forming thyroid hormones -> increased secretion of TSH by anterior pituitary gland -> overgrowth of thyroid gland “goitre”

[DOES NOT PREVENT FORMATION OF THYROGLOBULIN]

36
Q

What is the MOA of Propylthiouracil?

A
  • Inhibits TPO (Thyroid peroxidase) -> decreases T3/T4 from thyroid gland
  • Inhibits 5’deiodinase -> decreased T4 into T3 conversion in peripheral tissues
  • Overstimulation of TSH causes goitre
37
Q

What is the MOA of Iodides in high concentrations?

A
  • It reduces the rate of Iodide trapping -> rate of iodination of tyrosine to form thyroid hormones I decreased
  • Normal endocytosis of colloid from follicles by thyroid glandular cells is paralysed -> immediate shutdown of thyroid hormone secretion
  • Decrease all phases of thyroid activity -> slight decrease in size of thyroid gland + blood supply

CLINICAL CORRELATION:
frequently administered to patients for 2 to 3 weeks before surgical removal of thyroid gland to decrease necessary amount of surgery and bleeding

38
Q

What happens in Hyperthyroidism?

A

The thyroid gland is increased to two to three times the normal size, with tremendous hyperplasia and infolding of the follicular cell lining into the follicles

39
Q

What is Graves’ disease?

A

An autoimmune disease in which antibodies called “Thyroid-stimulating immunoglobulins (TSIs)” form against the TSH receptor in the thyroid gland

CAUSE:
Antibodies bind with the same membrane receptors that bind TSH and induce continual activation of the cAMP system of cells, resulting in hyperthyroidism.

LAB FINDINGS:
High level of hormone secretion cause by TSI suppress anterior pituitary formation of TSH -> TSH concentrations are less than normal rather than enhanced

Antibodies were formed due to autoimmunity against Thyroid

40
Q

What is Thyroid Adenoma?

A

A localised adenoma (tumour) that develops in the thyroid tissue and secretes large quantities of thyroid hormone causing hyperthyroidism

[It depresses the production of TSH by the pituitary gland]

41
Q

What are the symptoms of Hyperthyroidism?

A
  • High state of excitability
  • Intolerance to heat
  • Increased sweating
  • Mild to extreme weight loss
  • Varying degrees of diarrhoea
  • Muscle weakness
  • Nervousness/other psychic disorders
  • Extreme fatigue/inability to sleep
  • Tremor of the hands
42
Q

What is Exophthalmos?

A

Protrusion of the eyeballs that is caused by oedematous swelling of the retro-orbital tissues and degenerative changes in the extraocular muscles

COMPLICATIONS:
- Eyeball protrusion stretches the optic nerve enough to damage vision
- Eyelids do not close completely when the person blinks or is asleep -> epithelial surfaces of the eyes become dry and irritated and often infected, resulting in ulceration of the cornea

43
Q

What diagnostic tests are used for Hyperthyroidism and Hypothyroidism?

A
  • Direct measurement of “free” thyroxine in the plasma using appropriate radioimmunoassay procedures
  • Basal metabolic rate is increased
  • Concentration of TSH in plasma is measured
  • Concentration of TSI is measured (high in thyrotoxicosis but low in thyroid adenoma)
44
Q

What is the treatment for Hyperthyroidism?

A
  • Surgical removal of the thyroid gland
    [administer PROPYLTHIOURACIL for several weeks for normal basal metabolic rate then HIGH CONCENTRATIONS OF IODIDES for 1-2 weeks before the operation]
  • Injected iodide (if injected iodide is radioactive, it can destroy most of the secretory cells of the thyroid gland)
45
Q

What is Hypothyroidism and what causes it?

A

It is when your thyroid gland does not produce enough thyroid hormones

CAUSES:
- Autoimmunity against the thyroid gland (Hashimoto disease)
- “thyroiditis” (thyroid inflammation) which causes progressive deterioration and fibrosis of the gland

46
Q

What is Endemic colloid goitre?

A

“goitre” is a greatly enlarged thyroid gland

CAUSE:
Lack of iodine prevents production of both thyroxine and triiodothyronine -> no hormone to inhibit production of TSH by anterior pituitary which causes pituitary to secrete excessively large quantities of TSH -> TSH stimulates thyroid cells to secrete a lot of THYROGLOBULIN colloid into follicles -> gland grows larger and larger
[due to lack of iodine, T3 and T4 production doesn’t occur in thyroglobulin -> doesn’t cause normal suppression of TSH]

47
Q

What is the difference between Idiopathic nontoxic colloid goitre and Endemic colloid goitre?

A

Endemic colloid goitre = caused by iodine deficiency

Idiopathic nontoxic colloid goitre = not caused by iodine deficiency

48
Q

What is Idiopathic nontoxic colloid goitre?

A

An enlarged thyroid gland NOT caused by iodine deficiency

CAUSES:
Slight hypothyroidism -> Increased TSH secretion and progressive growth on the non-inflamed portions of the gland -> Some portions are growing whereas some are being destroyed by thyroiditis

49
Q

Which hormone systems are affected in Colloid goitre?

A
  • Deficient iodide-trapping mechanism (iodine is not pumped adequately into thyroid cells)
  • Deficient peroxidase system ( iodides are not oxidised to the iodine state)
  • Deficient coupling of iodinated tyrosines in thyroglobulin molecules (thyroid hormones cannot be formed)
  • Deficiency of deiodinase enzyme (prevents recycling of iodine -> iodine deficiency)
50
Q

What are the symptoms of Hypothyroidism?

A
  • Extreme fatigue
  • Extreme muscular sluggishness
  • Slowed heart rate
  • Decreased cardiac output
  • Decreased blood volume
  • Increase in body weight
  • Constipation
51
Q

What is Myxedema?

A

Development of an oedematous appearance throughout the body due to hypothyroidism

CAUSE:
Greatly increased quantities of of hyaluronic acid and chondroitin sulphate bound with protein form an excessive tissue gel in the interstitial spaces -> total quantity of interstitial fluid increases -> excess fluid makes it immobile and non-pitting

52
Q

What is the treatment of Hypothyroidism?

A

Daily oral ingestion of Thyroxine

53
Q

What is Cretinism?

A

Failure of body growth and mental retardation due to extreme hypothyroidism during fatal life, infancy or childhood

CAUSES:
- Congential lack of a thyroid gland (Congenital cretinism) from failure of the thyroid gland to produce thyroid hormone because of a genetic defect of the gland
- Iodine deficiency in diet (Endemic cretinism)

EFFECTS:
After birth the baby is normal (since it got thyroid hormones from mother whilst in utero) but after a few weeks the movements become sluggish and both physical and mental growth become retarded -> Adequate iodine or thyroxine usually causes normal return of physical growth -> If given more than a few weeks, mental growth remains permanently retarded (due to retardation of growth, branching, myelination of neuronal cells of CNS) -> Skeletal growth is more inhibited than soft tissue growth so child is obese and short -> Tongue becomes so large that it obstructs swallowing and breathing causing GUTTURAL BREATHING

PHYSIOLOGY IV (14 decks)

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