thyroid gland physiology Flashcards

1
Q

what 2 molecules does the thyroid gland produce?

A
  • thyroxine -T4 (as it contains 4 iodines)
  • Triiodothyronine - T3 (three iodines) - most T4 is converted to T3 so this is the major thryoid hormone
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2
Q

where is the thyroid gland situated?

A

situated in the midline of the anterior neck

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3
Q

what structure seperates the right and left lobe of thyroid gland?

A

the isthmus

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4
Q

what does the thyroid gland contain?

A
  • there are numerois follicles within the thyroid gland
  • each of the follicles are composed of a sphere of epithelial cells (follicular cells)
  • these cells surround a core containing a protein rich material called a colloid
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5
Q

what is the function of these follicular cells?

A

they **synthesise and secrete thyroid hormones **in response to the anterior pituitary thyroid stimulating hormone (TSH)

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6
Q

other than follicular cells, what is the second type of endocrine cell found in the thyroid gland?

A
  • parafollicular cells
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7
Q

what is the** function of parafollicular cells**?

A
  • they secrete a peptide hormone called calcitonin which plays a role in Ca2+ homeostasis
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8
Q

what does the synthesis of the thyroid hormones require?

A

iodine

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9
Q

Describe the steps synthesis of the thyroid hormones

A
  • Thyroid hormone synthesis requires iodine ( supplied from blood)
  • iodide uptake from blood is performed by follicular cells in thyroid through secondary active transport - coupled to Na+ - iodide trapping
  • oxidation of I- to I+ (iodide - iodine) & reacts with tyrosine residues of thyroglobulin to form monoiodotyrosine and diiodotyrosine
  • formation of T3 & T4 from MIT/DIT
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10
Q

where are the thyroid hormones stored?

A

in the colloid

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11
Q

what is T3 and T4’s mechanism of action in target cells?

A
  • T3 & T4 enter target cells where T4 is deionated to T3
  • T3 is transported into nucleus and binds to thyroid hormone receptor ( TR)
  • the hormone receptor complex binds to the hormone response element HRE and **alters the rate of gene transcription **
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12
Q

what hormone is responsible for oxidising iodides and attaching them to tyrosines on thryglobulin ?

A

thyroid peroxidase

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13
Q

what are the physiological functions of T3/T4?

A
  • regulate basal metabolic rate (the rate at which the body uses energy while at rest to maintain vital functions)
  • important for CNS development
  • important for growth
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14
Q

how are T3/T4 carried/transported in the plasma?

A

bound to plasma proteins

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15
Q

what are the 3 major plasma proteins that carry T3 or T4?

A
  • thyroxine binding protein (TBG)
  • transthyretin
  • albumin
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16
Q

what enzyme converts T4 into T3?

A
  • 5’ monodeiodinase
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17
Q

what enzyme inactivates T3 in liver ?

A

5 monodeiodinase

note no ‘

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18
Q

what does the basal metabolic rate depend on?

A
  • sex
  • body surface area
  • activity level
  • body composition
19
Q

what are the** effects** of the thyroid hormones on cellular respiration and metabolism ?

A

thyroid hormones increase the
* size and No. of mitochondria
* oxygen consumption
* ATP production
* protein and lipid turnover
* **increases basal metabolic rate **

20
Q

why is thyroid hormone essential for normal growth?

A
  • protein synthesis
  • increases energy production and substrate availability
21
Q

why is thyroid hormone essential for CNS development?

A
  • promotes nerve growth
  • growth of dendrite cells
  • myelin formation
22
Q

what is cretinism?

A

*** untreated congential hypothyroidism **(at birth) - ie partial or complete loss of thyroid gland function
* causes impaired CNS development & intellectual/ developmental disability

23
Q

How does thyroid hormone affect the heart? (ie HR and cardiac output)

A
  • thyroid hormone stimulates the release of metabolic endproducts
  • this causes local vasodilatation which reduces systemic resistance
  • then the blood pressure also decreases
  • TH causes increase in HR and cardiac output & contractility of the heart
24
Q

what is the hypothalamus-pituitary-thyroid axis?

A
  • **thyroid function is controlled by the hypothalamus and pituitary gland **
  • hypothalamus - TRH regulates TSH secretion in anterior lobe
  • anterior pituitary lobe -secretes **TSH **which increases the production of T3 and T4
25
Q

what effect does T3 and T4 have on TSH & TRH production?

A

negative feedback

26
Q

other than increasing the production of T3 and T4, what other effects does TSH have?

A
  • increases protein synthesis in follicular epithelial cells
  • maintenance and growth of gland
27
Q

what can happen if the thyroid gland cells are exposed to greater TSH concentrations & what condition can this occur in?

A
  • they will undergo** hypertrophy **- ie they will **increase in size **
  • goiter (enlarged thyroid gland)
  • this can occur in hypothyroidism - a low amount of T3/T4 results in increases in TSH - goitre
28
Q

what is** hypothyroidism**?

A
  • a condition in which the plasma conc of thryoid hormones is below normal
  • most are due to damage or loss of function of thyroid tissue or inadequate iodine consumption
29
Q

Describe hypothyroidism

what is it? what occurs the the HPT axis as a result?

A
  • the synthesis of thyroid hormone is compromised
  • this releases the hypothalamus and the pituitary gland from the negative feedback inhibition
  • this leads to an increase in TRH conc and also TSH conc
  • TSH will cause goitre of thyroid gland
30
Q

what are the common symptoms of hypothyroidism?

A
  • goitre (in adults)
  • decrease in appetite - decrease in BMR
  • decrease in heart rate and cardiac output - as less TH will stimulate increases in HR and CO
  • tiredness - low BMR
  • weight gain - low BMR
  • cretinsim in children
31
Q

what is primary hypothyroidism?

A
  • abnormality of thyroid itself
  • may be due to** iodine deficiency,genetic causes, autoimmune (antibodies against TSH receptor)
32
Q

what is secondary hypothyroidism?

A

a problem with the hypothalamus or pituitary gland

33
Q

How is **primary hypothyroidism diagnosed **? - also include what might be present if caused by autoimmune disease

NB - exam?

A
  • decreased T3 & T4
  • increased TSH
  • if autoimmune - presence anti-thyroid antibody
34
Q

what is the autoimmune disorder associated with primary hypothyroidism called & what does it involve?

A
  • Hashimoto’s Thyroiditis
  • antibodies against TSH receptor which act as TSH antagonists
35
Q

how is primary hypothyroidism treated?

A
  • replacement therapy with levothyroxine
  • or dietary iodine supplement
36
Q

what is myxedema?

A

puffiness in the face - increased water retention within the connective tissue

37
Q

what is hyperthyroidism?

A

when there is an excess of thyroid hormone in the plasma

38
Q

what are some of the** causes of primary hyperthyroidism**? (prob with thyroid itself)

A
  • autoimmune disorder - Graves disease
  • thyroid tumour
39
Q

what is graves disease?

A
  • autoimmune disorder
  • production of antibodies that bind to and activate the TSH receptors on thyroid gland cells - which leads to chronic overstimulation of the growth and activity of the thyroid gland - may lead to goitre
40
Q

what are the symptoms of hyperthyroidism?

A
  • nervousness
  • increase in heart rate - may cause arrythmias - TH increases HR etc
  • goitre - due to overstimulation of gland - hypertrophy
  • myxedema - bulging eyes
  • increase in BMR- therefore increase in body temp
  • weight loss - high BMR
41
Q

How ia hyperthyroidism diagnosed?

A
  • increased T3/T4 production
  • decreased TSH( in primary and elevated in secondary)
  • if autoimmune - presence of antibodies to TSH
42
Q

how can hyperthyroidism be treated?

A
  • with agents that interfere with the production of T3 or T4
  • destruction of thyroid gland eg thryoidectomy - surgical removal of some of gland
43
Q

what is** thyrotosis crisis**?

A
  • a life threatening complication associated with untreated or undertreated hyperthyroidism
  • symptoms include tachycardia, arrhythmias, dehydration etc
44
Q

what medication can be used to** treat thyrotoxic crisis**?

A
  • beta blockers to reduce sympathetic activation
  • glucocorticoids - to reduce T4 to T3 conversion