Thyroid Gland Flashcards
anatomy of the thyroid gland
why does it have a deep red colour
located on the anterior surface of the trachea, below the larynx
two lobes connected by isthmus
red from extensive blood supply
what is the functional unit of the thyroid for hormone production
thyroid follicle made of a colloid and the surrounding follicle cells
what is the colloid in the thyroid
extracellular space where thyroglobulin with attached iodine atoms are stored
what is the role of follicle cells in the thyroid
synthesize thyroglobulin and secrete it into the colloid of the thyroid follicles
what is the role of parafollicular (C) cells
cells in between the follicles that secrete calcitonin
how is iodine obtained
from salt in the diet must be reduced to iodide prior to absorption
what are the basic ingredients T3 and T4
what is the difference between them
tyrosine and iodine
depends if the iodide is attached at three or all four sites
where is thyroglobulin synthesised
ER/Golgi complex of thyroid follicular cells
how is iodide transported into the follicular cell
how is active iodide transported into the colloid
what enzyme converts iodide to active iodide
enters the cell via Na+/I- symporter against its concentration gradient
enters the colloid via pendrin channel down its concentration gradient
thyroperoxidase (TPO)
what are the two possible products of TPO attaching iodide within the thyroglobulin molecule
mono-iodotyrosine (MIT - one iodine)
di-iodotyrosine (DIT - two)
what happens upon follicular cell stimulation for thyroid hormone secretion
they internalise Tg-hormone complexes by phagocytosis
lysosomes attack the vesicle formed and split the iodinated products from Tg
T3/T4 diffuse into blood
MITs and DITs are removed by iodinase
thyroid hormone is lipophilic/hydrophobic
what does it bind in the colloid and blood for storage
blood: plasma proteins
colloid: thyroglobulin
5 key steps of thyroid hormone synthesis
iodide trapping
iodination
coupling
colloid resorption
thyroglobulin proteolysis
why does T4 bind thyroxine-binding globulin (TBG) more than albumin even though albumin is more abundant
TBG has a higher affinity for T4
metabolism and excretion of thyroid hormone
occurs in liver, kidney and pituitary
T4 can be metabolised to active T3
metabolised by conjugation with glucuronic acid then secreted into bile
what is rT3
an inactive form of T3 that acts as a form of control
why does/can T4 act as a reserve of T3
T3 is 10 times more potent
T4 can be metabolised to T3 to avoid synthesis waiting time
what is the negative feedback pathway of thyroid hormone in the HPT axis
hypothalamus releases thyrotropin releasing hormone
TRH stimulates anterior pituitary to release thyroid stimulating hormone
TSH stimulates the thyroid to release T3/4
T3 acts on both higher centres to inhibit this pathway
TSH receptor location and action
plasma membrane
initiates signalling cascade leading to T3/4 synthesis and release
explain how T3/4 control the rate of metabolism
control basal metabolic rate/heat production
by controlling the size and number of mitochondria and enzymes involved in oxphos
what is the sympathomimetic effect of T3/4
TH increases the proliferation catecholamine target-cell receptors
makes cells more responsive to catecholamines
(adrenaline/noradrenaline)
what is the cardiovascular effect of T3/4
increased HR and force of contraction -> increased CO
due to sympathomimetic effect
why is TH essential for normal bone growth and maturation
stimulates growth hormone secretion and IGF-1 production
increases their effects
(promotes structural proteins and skeletal growth)
what is the effect of thyroid deficiency in children
how is it treated
stunted growth
thyroid replacement therapy (excessive TH does not mean excessive growth)
role of TH in nervous system
crucial role in normal development and maintenance of CNS in adults
effect of TH on metabolism
increased
what can cause hypothyroidism
primary failure of thyroid gland
secondary deficiency of TRH/TSH
inadequate dietary supply of iodine
key symptoms of hypothyroidism
decreased metabolic activity:
intolerance to cold
weight gain
cardiac complication
brittle nails and hair (less protein turnover)
fatigue
dull expression due to low CNA activity
constipation
what is cretinism
what are the results
how are they prevented
infant condition of low TH from birth
inadequate skeletal and nervous development - dwarfism and mental retardation, delayed puberty
preventable with HRT is given before a few months development
what is myxedema
what are the results
how is it treated
adult condition of low TH
lethargic, depression (low CNS activity), dry skin, hair loss, low temperature, weakness, slow reflexes
‘puffy appearance’ - subcutaneous swelling due to proteins accumulation leading to water retention
treated in HRT with T4
what can cause hyperthyroidism
production of thyroid stimulating immunoglobulin (TSI)
secondary excess of TRH/TSH
hypersecreting thyroid tumour
key symptoms of hyperthyroidism
increases metabolic rate
intolerance to heat
weight loss
increases systolic BP
muscle wasting
enlarged thyroid
bulging eyes
tremors
diarrhoea
what causes Graves disease
most common form of hyperthyroidism autoimmune disease caused by body erroneously producing thyroid-stimulating immunoglobulin
TSI binds TSH receptor and leads to secretion and growth of thyroid
why does thyroid growth and secretion continue unchecked in Graves disease
unlike TSH, TSI is not subject to -ve feedback by TH
treatments of hyperthyroidism
anti-thyroid drugs that interfere with TH synthesis
surgical removal of a portion of over-secreting thyroid gland (can lead to hypothyroidism)
administration of radioactive iodine
explain administration of radioactive iodine to treat hyperthyroidism
given orally on a one time basis
iodine is only picked up by the thyroid cells so destruction is local
kills hyperactive regions
what is goiter
what causes it
enlarged thyroid gland
develops when thyroid gland is overstimulated by TSH or TSI
low iodine
explain how hyperthyroidism results in goiter
excessive activation of TSH receptor by TSI
explain how hypothyroidism/low iodine results in goiter
increased TSH production by pituitary in response to low TH
lack of iodine -> low TH -> high TSH -> thyroid growth
why does taking potassium iodide protect from thyroid cancer
stable form of iodine
protects the thyroid from absorbing radioactive iodine if present
