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GERR > Lecture 20: Thyroid Hormones > Flashcards

Lecture 20: Thyroid Hormones Flashcards

1
Q

what joins the two lobes of the thyroid gland

A

section of tissue called isthmus

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2
Q

what is the thyroid gland comprised of

A

lobules of spherical follicles filled with colloid

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3
Q

what type of cells make up the follicles present in thyroid lobules

A

follicular cells –> cuboidal epithelial cells

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4
Q

what is the primary constituent of colloid

A

thyroglobulin

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5
Q

what is incorporated into a thyroglobulin molecule

A

residues of amino acid tyrosine

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6
Q

what is the function of the C (parafollicular) cell

A

produces hormone calcitonin

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7
Q

where does thyroid hormone synthesis take place

A

in colloid

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8
Q

what molecule acts as a scaffold for thyroid hormone synthesis

A

thyroglobulin

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9
Q

what are the basic ingredients for thyroid hormone synthesis

A

tyrosine and iodine

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10
Q

which ingredient of thyroid hormone synthesis needs to be consumed in the diet

A

iodine

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11
Q

give examples of food that contains iodine

A
  • sea vegetables
  • iodised salt
  • eggs
  • cranberries
  • seafood
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12
Q

consequence of low iodine in diet

A

hypothyroidism

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13
Q

outline how thyroxine (T4) and triiodothyronine (T3) are formed

A
  • I + tyrosine = MIT
  • MIT + I = DIT
  • DIT + DIT = T4
  • DIT + MIT = T3
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14
Q

explain how iodine gets into the follicle cell and then colloid in thyroid

A
  • iodine reduced by digestion in stomach to iodide
  • co-transported with Na+
  • secondary active transport using energy from Na+/K+ ATPase pump
  • 2 Na+ ions transported with 1 I-
  • move through follicle cell by diffusion
  • I- transported across apical membrane via I-/Cl- transporter into lumen (colloid)
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15
Q

how is T3/ T4 formed in the colloid

A
  • iodide is oxidised back to iodine by hydrogen peroxide
  • thyroid peroxidase (TPO) attaches iodines to tyrosine in thyroglobulin
  • coupling of DIT/MIT to give T3 or T4
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16
Q

what is the use of radioactive iodine

A
  • diagnostic, tracer, and therapeutic (causes cells to die in hyperthyroidism
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17
Q

which thyroid hormone is produced most in thyroid gland

A

T4 (80-90%)

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18
Q

which thyroid hormone is more biologically active

A

T3 - binds with greater affinity to nuclear receptors

19
Q

how is T4 converted to T3

A

T4 needs to be deionised by deiodinase

20
Q

what are the types of deiodinase and where do they come from

A

type 1 –> liver, kidney, thyroid, pituitary, heart

type 2 –> pituitary, brain, skeletal muscle, brown adipose

type 3 –> placenta, uterus, brain, kidney, liver, thyroid, fatal tissues

21
Q

where does most systemic T3 come from

A

liver and kidney by type 1 deiodinase

22
Q

which molecule is responsible inactivation of T3

A

type 3 deiodinase

23
Q

how are thyroid hormones transported in plasma

A 
- thyroid hormones are lipophilic 
transported by:
--> thyroid binding globulin (TBG) 
--> thyroid binding pre albumin (TBPA) 
--> thyroid binding albumin (TBA)
  • tiny % of thyroid hormone unbound in blood
24
Q

which thyroid hormone being transported is biologically active

A

free unbound thyroid hormone

25
Q

where are majority of thyroid receptors located

A

in nuclei of cells

26
Q

how does thyroid hormone cause suppression or activation of genes in a cell

A
  • binds to receptors in nucleus of a cell causing genomic effect
  • translocation to hormone response element on DNA
  • proteins produced after suppression/activation of genes
27
Q

function of proteins after suppression/activation of genes by thyroid hormone

A

increase metabolism within cell therefore thyroid hormones increase basal metabolic rate

28
Q

how do thyroid hormones increase ATP production

A

bind to receptors directly on mitochondria

29
Q

describe the metabolic actions of thyroid hormones

A
  • increased O2 consumption (required by proteins produced)
  • increased BMR (basal metabolic rate)
  • calorigenic effect –> thermogenic effect
  • carbohydrate metabolism
  • -> ^ absorption of glucose from GIT, ^ glycogenolysis, ^ gluconeogenesis
  • lipid metabolism
  • -> lipolysis…^ circulatiing FFA, ^ FFA oxidation, decrease cholesterol, ^ No. of LDL receptors
  • protein metabolism
  • -> prot. synthesis and breakdown
30
Q

describe systemic effects of thyroid hormones

A

Heart

  • -> ^ HR, CO, SBP and decrease DBP (sympathomimetic effect)
  • -> ^ blood flow to skin

Lungs
–> ^ vent. rate

GIT

  • -> ^ appetite
  • -> ^ secretion digestive juices
  • -> ^ GIT motility

Reproductive
–> essential for normal reproduction and lactation

MSK

  • -> promotes normal body growth and maturation of skeleton
  • -> promotes normal body function and development of muscles

NS

  • -> promotes normal neuronal development in foetus and infant
  • -> promotes normal neuronal function in adult (^ synaptic activity)
  • -> ^ effects of SNS - sympathomimetic; up regulates B1 adrenergic receptors in heart
31
Q

what effect does cold have on production of TRH in hypothalamus

A

+ve

32
Q

what effect does stress have on production of TRH in hypothalamus

A

-ve –> prevents overstimulation of SNS

33
Q

how does TSH act on thyroid gland

A
  • ^ iodide trapping and binding (by ^ gene transcription of Na+/I- symporter)
  • promotes thyroglobulin synthesis and secretion into colloid
  • TPO synthesis
  • stimulates T3 and T4 synthesis
  • promotes colloid endocytosis into follicular cells
  • ^ size and No. of follicular cells
  • ^ blood flow at thyroid level
34
Q

what do primary/secondary/tertiary levels of hypothyroidism refer to

A

1st - problem at thyroid (failure to respond to TSH)

2nd - problem at pituitary (w/ TSH); deficient TSH secretion –> thyroid atrophy (shrinking)

3rd - problem at hypothalamus (w/ TRH) –> deficient TSH secretion due to deficient TRH secretion

35
Q

what is hypothyroidism

A

deficient production of thyroid hormone

36
Q

name some causes of primary hypothyroidism

A
  • thyroiditis e.g. Hashimoto’s disease or chronic lymphocytic thyroiditis (CLT)
  • severe iodine deficiency
  • severe deficiency of one or more synthesis enzymes
  • removal or destruction of thyroid gland
37
Q

name some consequences of primary hypothyroidism

A
  • elevated TSH levels –> reduced -ve feedback

- thyroid enlarges –> goitre formation

38
Q

how is congenital hypothyroidism diagnosed

A

blood test performed on all newborns (ESSENTIAL EARLY DIAGNOSIS)

39
Q

describe developmental consequences of hypothyroidism in baby

A
  • sometimes enlarged tongue
  • unhappy
  • difficulty feeding
  • difficulty w/ GIT
40
Q

describe developmental consequences of hypothyroidism in adult

A
  • short
  • impaired brain, bone and other development
  • poor coordination
41
Q

what happens if you don’t have a functional thyroid gland

A

thyroid hormone is replaced

42
Q

name causes of hyperthyroidism / thyrotoxicosis

A
  • autoimmune disease –> Grave’s disease
  • thyroid adenoma
  • TSH secreting adenoma
43
Q

how does Grave’s disease cause hyperthyroidism

A
  • autoantibodies stimulate thyroid gland
  • bind to same receptors as TSH
  • thyroid gland secrete excess T3 and T4
44
Q

diagnostic factors of Grave’s disease

A
  • very low TSH
  • goitre
  • exophthalmos
  • retraction of upper eyelid

GERR (46 decks)

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