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ENDO > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Describe the structure of the thyroid gland?

A

It is a bi-lobed endocrine gland in the neck.

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2
Q

What are the primary and secondary roles of the thyroid gland?

A

Primary: Secretion of thyroid hormones

  • Which have effects on a wide variety of cells in the body
  • Thyroid hormones help control the rate of metabolism

Secondary: Secretion of calcitonin

  • Which plays a part in the regulation of calcim concentration in the blood
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3
Q

When and how does the thyroid gland develop in utero?

A

The thyroid is the first endocrine gland to develop in utero.

On day 24 of gestation, the thyroid gland arises from the floor of the embryonic pharynx

Develops as an evagination from the floor od the embryonic pharynx (explains teh occasional presence of thyroif tissue in atyoical locations, such as the base of the tongue)

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4
Q

Describe the histological make-up of the thyroid gland?

A

Gland is made up of numeroud sperical follicles, lined by a single layer of cubical, secretory epithelial cells, filled with colloid (highly vascularised gland)

Around and between the follicles clear cells or C cells or parafollicular cells are found.

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5
Q

How would you describe the location of the thyroid gland?

A

Below the larynx and anterior, wrapping round the trachea

Extends from the level od the 5th cervical vertebra down to teh 1st thoracic vertebra

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6
Q

What do C cells secrete?

A

Calcitonin

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7
Q

Label the following parts of the thyroid gland and surrounds.

A
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8
Q

What is the artery that suppies the thyroid gland, found in only 3-10% of people. And what issues can it cause?

A

3-10% of people ahve an artery that runs off anteriorly over the trachea from aorta to thryoif and supplies the thyroid gland.

Name = Thyroid Ima Artery

Important to be known if presen in sugeries such as Trachiostamy and Thyroidetomy etc. as if accidentally cut and cause prefuse bleedins as it has high pressure of blood coming straight off of the aorta.

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9
Q

What are thyroid follicles and what are they made up of?

A

The functional unit of the thyroid gland is the thyroid follicle.

Thyroid follicles are the portion of the thyroid concerned witht eh production of thyroid hromone.

Each follicle is surrounded by a single layer of eptihelial cells and filled with pink-staining protein rich fluid - colloid

Colloid consists predominantly of the glycoprotein, thyroglobuiln.

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10
Q

What histological differences would be seen between an active and inactive gland?

A

Inactive Gland = the colloid is abundant, the follicles are large, and the cells lining them are flat

Active Gland = the follicles are small, the cells are cuboid or columnar, and areas where the colloid is being actively reabsorbed into the thyrocytes are visible as reabsorption lacunae.

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11
Q

What are the two major hormones secreted by the thyroid gland?

A

Thyroixine (tetraiodothyronin/T4)

Triiodothyronin (T3)

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12
Q

What is the major component of the hormones secreted by the thyroid galnd?

A

Iodine

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13
Q

What is teh basic make up of T3 and T4 and what is their funciton?

A

Dervied from modificaition of an amino acid (tyrosine)

Act on most cells of teh body to promote cabohydrate, protein and liid metbaolism

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14
Q

What does the secretion of calcitonin by C cell do?

A

Influences calcium metabolism by opposing the action of PTH

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15
Q

What effects does thyroid gland hypofunction have on the body?

A

Causes mental and physical slwoing

Poor resistance to cold

Mental retardation and dwarfism in children

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16
Q

From what are thyroid hormones derived from?

A

Tyrosine

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17
Q

What type of hormones are thyroid hormones and what are some other hormones similar to this type?

A

AMINE GROUP HORMONE

  • METABOLISM HORMONE

Similar metabolism horomes

  • GH, Cortisol, Adrenalin, Noadrenalin, Insulin, GLucagon etc
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18
Q

What is thyroglobulin and waht role does it play in hormone biosynthesis?

A
  • A large glycoprotein
  • Thyroglobulin is syntehsised in the follicualr cells and secreted into the colloid by exocytosis of granules
  • Thyroglobulin is packaged in secretory vesicles and extruded into the follicular lumen
  • Numerous tyrosine amino acids are attaches to each thyroglobulin molecule
  • These amino acids are iodinated in the production of thyroid hormones
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19
Q

What is the role of the iodide pump, how does it work and what is exchanged?

A
  • The iodide pump or sodium-iodide cotransporter is present in the follicular epithelial cells
  • Actively transports (pumps) iodine, in the form of the iodide ion (I-) into the follicular cells
    • Symporter that transports two Na+ ions and one I- ion into the cell
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20
Q

What is oxidised during synthesis and how does this occur?

A

Iodide is oxidised to iodine.

This reaction is catalysed by peroxisade (Thryoid peroxidase) in the folicular cell membrane

This occurs because I2 is teh reactive form

I2 is organified by combination with tyrosine on thyroglobulin

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21
Q

What is organification and what is happens?

A

Organification = It is the incorporation of iodine into thyroglobulin for the production of thyroid hormone, a step done after the oxidation of iodide by the enzyme thyroid peroxidase (TPO).

Oxidised iodine binds with typosine amino acids to form MIT (monoiodotyrosine) and DIT (diiodotyrosine)

  • Iodine binds to the 3’ and 5’ sites of the benzene ring of tyrosine residues on thyroglobulin molecules
  • Iodination with one or two iodine molecules produces the hormone precursors monoiodotyrosine and diiodotyrosine

High levels of iodide inhibit organification

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22
Q

What does the coupling of DIT + DIT produce?

A

Thyroxine (T4)

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23
Q

What does the coupling of one molecule of MIT and DIT form?

A

Triiodothyronin (T3) is formed

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24
Q

Is iodinated thyroglobulin stored, if yes where?

A

Iodinated thyroglobulin is sotred in the follicule lumen until gland is stimualted to secrete

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25
Q

How are iodinated tyrosines deiodinated?

A

Iodinated tyrosines are deiodinated by a microsomal iodotyrosine deiodinase

  • Recovers iodine and bound tyrosines and recycle them for additional rounds of hormone synthesis
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26
Q

Are thyroid hormones lipophilic or lipophobic? And what does this mean for their mechanism of action?

A

Thyroid hormones are lipophilic, so they diffuse easily a=through the follicular cell membrane into the blood.

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27
Q

What does the pendrin do?

A

PENDRIN = exchanges I- to CL-

Pushing I- into colloid and Cl in

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28
Q

What is the brief process of thyroid hormone biosynthesis? (Including Event, Enzymes and site of action)

A
  1. Synthesis of TG; extursion into follicular lument
    * Site: Rough ER, Golgi Apparatus
  2. Iodide pump
  • Site: Basal Membrane
  • A Na+-I- symporter brings I- into the cell. THe pendrine transporter moves I- into the colloid
  1. Oxidation fo I- –> I2 membrane
  • Site: Apical (luminal)
  • Enzyme: Peroxidase
  1. Organification fo I2 into MIT and DIT
  • Site: Apical Membrane
  • Enxyme: Peroxidase
  1. Coupling reaction of MIT and DIT into T3 and T4
  • Site: Apical Membrane
  • Enzyme: Peroxidase
  1. Endocytosis of TG
    * Site: Apical Membrane
  2. Hydrolysis of T4, T3,RT3,MIT,DIT; T4,T3 and RT3 enter circulation
  • Site: Lysosomes
  • Enzyme: Proteases
  1. Deiodination of residual MIT and DIT. Recycling of I-
  • Site: intracellular
  • Enzyme: Deiodinase Tyrosine
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29
Q

What mineral is adequately required in the diet for normal thyroid function? And waht is the normal dietary intake?

A

Adequate IODINE intake is required for normal thyroid function

The normal dietary intake of iodine is 150ug/day, of which 125ug is used by the thyroid gland for hormone synthesis

Ingested iodine is taken up and concentrated in the thyroid

30
Q

What can insufficient dietary intake of iodine cause in the body?

A

Insufficient dietary iodine can cause an increase in the size of the thyroid gland in a condition called endemic goitre

31
Q

What happens to left over MIT and DIT?

A

Left over MIT and DIT are deiodinated by thyroid deiodinase

The I2 that is released is utilised to synthesise more thyroid hormones

32
Q

What does TSH cause to occur in the body?

A

TSH increases all knwon secretory activities of the thyroid glandular cells

33
Q

What is rT3?

A

rT3 is reverse T3 which is formed during thyroid hormone synthesis and is inactive

34
Q

What percentage of Thyroid Hormones are T3 and T4?

A

93% released TH is thyroxine (T4) and only 7% is T3

35
Q

What happens to the thyroglobulin in order to release T4 and T3?

A

Lysosomal enzymes digest thyroglobulin to release T4 and T3 into teh surrounding capillaries

36
Q

How do thyroid hormones travel in the blood?

A

Over 99% of thyroid hormoes are bound with plasma porteins

  • Thyrocine-binding globulin (TBG; 70% of hormones bound)
  • Much less binding with thyroxine binding prealbumin (Transthyretin) and albumin

Thyroid homones are released to the tissue cells slowly by the plasma porteins

37
Q

Does T4 or T3 have more affinity to bind to proteins?

A

T4 has more affinity to bind to protein than T3

38
Q

What are the features of Thyroid hormones? (e.g. onset and duration)

A

Thyroid hormones have slow onset and long duration of action

39
Q

What happens to TBG levels in liver failure?

A

In liver failure TBG levels decrease

40
Q

What happens to TBG levels in pregnancy?

A

TBG levels in pregnancy increase

41
Q

Which thyroid hormone is more biologically active?

A

T3 is more biologically active thant T4

42
Q

Which thyroid hormone ahs a longer plasma half-life?

A

T4 has a longer plasma half-life than T3

43
Q

What happens to T4 in peripheral tissues and why does this occur?

A

In the peripheral tissues, T4 is converted to T3 by deiodinase.

This is because T3 is more biologically active and four times fore potent than t4

44
Q

Which thyroid hormone has a high affinity for intracellular thyroid hormone receptors?

A

T3

45
Q

Are thyroid hormones lipophilic or lipophobic? And waht does this mean for them?

A

Lipophilic nature.

This allows them to diffuse easily into all cells of the body

46
Q

Where is teh receptor for thyroid hormones found?

A

In the cell nuclei

Thyroid hormones bind with receptos located either attaches to DNA genetic strands or located in proximity to them (TH receptors are present in the nuclie most of the cells of the byd, hence the actions are widespread)

47
Q

What happens when TH horomones bind to receptor complex?

A

Horomone receptor complex increases or decreases the expression of a variety of different genes that code for enzymes which regulate cell function

Largen number of differnt mRNA are formed and are translated to form new intracellular proteins

48
Q

What effect does TH hormones have on basal metabolic rate?

A
  • Increases cellular metabolic activity or has calorigenic effect
  • Oxygen consumption and BMR are increases in all tissues (Except brain, donads and spleen)
  • It maintains the level of metabolism in the tissues that is optimal for their normal function or plasma concentration of thyroif hormone is the major factor thqt sets teh body’s BMR
  • BMR can increase to 60% to 100% above normal when large quantities are present (complete lack - falls 40 to 50%)
49
Q

What effects does TH have on calorgenic action?

A
  • Increased heat production by TH underlies the role of TH in the body temperature regulation
  • TH responsible for strong, immediate, and short-lived increase in the rate of cellular metabolism
  • TH increases the synthesis of Na+-K+ ATPase and consequently increase oxygen consumption related to Na+-K+ pump activity
  • Na+-K+ ATPase consumes ATP and produces heat
  • Rate of utilization of food for energy is increased
  • Increases the number and activity of mitochondria – increases formation of ATPs
50
Q

What effect does TH have on protein metabolism?

A
  • Increased protein synthesis at low thyroid hormone levels
  • Increased protein degradation at high thyroid hormone levels
  • In excessive TH -> protein catabolism as metabolic rate is high - weight loss and increased nitrogen excretion
51
Q

What effect does TH have on carbohydrate metabolism?

A
  • Glucose absorption from the GIT is increased
  • Stimulates all aspects of carbohydrate metabolism – increases absorption of carbohydrates, glycogenolysis, gluconeogenesis and glucose oxidation
  • Increases blood glucose level and can worsen diabetes mellitus
52
Q

What effect does TH have on fat metabolism?

A
  • All aspects are increased but degradation (lipolysis) exceeds synthesis (lipogenesis)
  • Increases release of fatty acid from adipocytes
  • On cholesterol metabolism
    • Increases LDL receptors in the liver (increases removal of cholesterol) – decreases plasma cholesterol, phospholipids and triglycerides
53
Q

What effect does TH have on CNS development?

A
  • Attainment of adult stature requires thyroid hormone
  • Maturation of central nervous system requires TH
  • TH plays a crucial role in development of CNS during fetal life and for first few years in postnatal life (for development of synapse, myelination)
  • Thyroid hormone deficiency causes irreversible mental retardation
  • Hypothyroid infants are mentally retarded (cretin). Most affected parts are cerebral cortex, basal ganglia and cochlea.
    • Thyroid therapy must be started within days or weeks after birth
    • Screening tests for hypothyroidism are routine in developed countries
54
Q

What effect does TH hormone have on the bone and skeleton?

A
  • THs are essential for normal growth (of bones, tissues) and skeletal maturation
  • TH act synergistically with GH and somatomedins to promote bone formation
  • TH stimulate bone maturation as a result of ossification and fusion of growth plates
  • TH required for tooth development and eruption
  • Accelerates turnover of minerals in bone
  • Required for normal growth and maturation of epidermis and its hair follicles
55
Q

What effect does TH have on catecholamines?

A
  • TH have permissive effects on catecholamines
  • Increases number and affinity of beta adrenergic receptors in the heart and nervous system
  • Hence symptoms of excess TH closely resemble some of the symptoms of excess of catecholamines (like tachycardia)
56
Q

What effect does TH have on respiration?

A
  • Increased respiration rate and depth
  • Increases dissociation of O2 from Hb –increased O2 delivery
  • Stimulates red blood cell formation and thus enhances oxygen delivery
57
Q

What effect does TH have on the cardiovascular system?

A
  • Increases heart rate and stroke volume
  • Increases cardiac output
  • Vasodilation and increased blood flow
58
Q

What affect foes TH ahve on the GI System?

A
  • Increased appetite and food intake, motility and secretion of digestive juices
59
Q

What occurs to skeletal muscle in hyperthyrodism and hypothyrodism?

A

Hyperthyroidism = muscle weakness (thyrotoxicmyopathy); fine muscle tremor is seen

Hypothyroid = stiffness and aching of muscles, slowness of contraction and relaxation

60
Q

How is thyroid hormone secretion regulated?

A
  • Hypothalamus-Pituitary-Thyroid Axis
  • Negative Feedback Mechanism
  • TRH and TSH level increase by exposure to cold; reduced by stress, dopamine, somatostatin and glucocorticoids
  • Measurement of TSH is regarded as one of the best tests of thyroid function (reduced in thyrotoxicosis & high in hypothyroidism due to diseases of thyroid gland)
61
Q

Via what mechanism does TSH act?

A
  • TSH acts via adenylate cyclase - cAMP mechanism
  • Increases iodide transport into follicular cells
  • Increases production and iodination of thyroglobulin
  • Increases endocytosis of colloid from lumen into follicular cells
  • TSH increases both the synthesis and secretion of thyroid hormones
62
Q

What is Hyperthyrodism? Symptoms and causes?

A
  • An overactive thyroid gland, leading to excess thyroid hormones
  • Symptoms
    • Increased metabolic rate, weight loss, increased heat production, increased cardiac output, tremor, weakness, exophthalmos, insomnia
  • Causes
    • Excessive stimulation of the TSH receptor by an autoantibody (Graves disease)
    • Excessive secretion of TSH from a TSH-producing tumor (i.e., secondary hyperthyroidism)
    • Thyroid hormone – producing (toxic) adenoma (nodular) or toxic multinodular goiter
  • Raised T3 and T4 indicate that hyperthyroidism is present
  • Raised TSH suggests the fault lies in or above the pituitary gland
63
Q

What are examples of primary and secondary HYPERTHYRODISM?

A

PRIMARY = Graves diesea, toxic multinodular goiter, toxiz adenoma, fucntionsing thyroid carcinoma metasatases, activating mutation of teh TSh receptor

SECONDARY = TSH-secreting pituitary adenoma, thyroid hormone resistance syndrome, chronic gonadotropin-secreting tumors, gestational thyrotoxicosis

64
Q

What are the SIGNS and SYMPTOMS of hyperthyroidism?

A

Signs

  • Warm, moist skin
  • Muscle weakness
  • Tremor
  • Tachycardia
  • Goiter

Symptoms

  • Heat intolerance, sweating
  • Palpitations, Irritability
  • Fatigue and weakness
  • Diarrhoea
  • Weight loss
  • Oligomenorrhea
65
Q

What is hypothyroidism? Symptoms and Causes?

A
  • An underactive thyroid gland leading to deficient thyroid hormones
  • Symptoms-
    • Decreased metabolic rate, weight gain, decrease heat production (cold sensitivity), decreased cardiac output, lethargy, myxedema
  • Causes-
    • Lack of adequate iodine in the diet (nontoxic goiter, endemic goiter)
    • Benign nodules or mutation of growth-related gene (nontoxic goiter)
    • Sporadic hypothyroidism of unknown etiology (nontoxic goiter)
    • Surgical removal of gland
    • Congenital (Cretinism –growth and mental retardation)
  • Free T3 and T4 levels are low, whereas TSH levels are usually raised
  • If TSH is low then a lesion of the hypothalamus or pituitary is likely
66
Q

What are examples of Primary, Secondary and Tertiary hypothyroidism?

A

Primary

  • Autoimmune hypothyroidism: Hashimoto’s thyroiditis, atrophic thyroiditis
  • Iatrogenic: 131I treatment, subtotal or total thyroidectomy, external irradiation of neck for lymphoma or cancer
  • Drugs: lithium, antithyroid drugs, interferon-α and other cytokines
  • Congenital hypothyroidism: absent or ectopic thyroid gland, dyshormonogenesis, TSH-R mutation
  • Iodine deficiency

Secondary

  • Hypopituitarism: tumors, pituitary surgery or irradiation, infiltrative disorders, trauma
  • Isolated TSH deficiency or inactivity

Tertiary

  • Hypothalamic disease: tumors, trauma, infiltrative disorders (deposition of abnormal substances within the tissue)
67
Q

What are the SIGNS and SYMPTOMS of hypothyroidism?

A

Signs

  • Dry coarse skin, cool peripheral extremities
  • Puffy face, hands and feet (myxedema)
  • Brady cardia • Peripheral edema
  • Slow/Delayed reflexes

Symptoms

  • Feeling cold
  • Tiredness, weakness
  • Poor memory, difficulty in concentrating
  • Constipation
  • Weight gain
  • Hoarse voice
  • Oligomenorrhea or amenorrhea
68
Q

What is a goiter?

A
  • A goiter is an enlarged thyroid gland
  • Biosynthetic defects, iodine deficiency, autoimmune disease, and nodular diseases can each lead to goiter, though by different mechanisms
  • Readily palpable and usually highly visible
  • Diffuse goiter [endemic goiter] –most common - caused by iodine deficiency and it affects >5% of the population
  • A goiter may accompany hypothyroidism or hyperthyroidism
69
Q

What is cretinism?

A
  • Congenital hypothyroidism
  • Most common preventable causes of mental retardation
  • Thyroid hormones are essential between birth and puberty for the normal development of the CNS
  • Is a condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormones
  • Congenital hypothyroidism due to maternal nutritional deficiency of iodine can cause irreversible mental retardation
  • Results in dwarfism during childhood
70
Q

What is a myxoedema?

A
  • Caused by hypothyroidism in adults
  • Puffy face because of the accumulation of subcutaneous glycosaminoglycans and other matrix molecules (myxedema)
  • Results in physical and mental sluggishness
71
Q

What is Grave’s disease?

A
  • Most common form of hyperthyroidism
  • Diffuse toxic goitre due to autoimmune reactions
  • Autoantibodies are produced against the TSH receptor (thyroid-stimulating immunoglobulins (TSI)
    • Results in increased metabolism, heat intolerance, rapid heartbeat, weight loss, and exophthalmos
  • The primary clinical state found in Graves disease is thyrotoxicosis—the state of excessive thyroid hormone in the blood and tissues

ENDO (10 decks)

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