Thyroid Gland Flashcards

1
Q

anatomy of the thyroid gland
why does it have a deep red colour

A

located on the anterior surface of the trachea, below the larynx
two lobes connected by isthmus
red from extensive blood supply

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2
Q

what is the functional unit of the thyroid for hormone production

A

thyroid follicle made of a colloid and the surrounding follicle cells

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3
Q

what is the colloid in the thyroid

A

extracellular space where thyroglobulin with attached iodine atoms are stored

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4
Q

what is the role of follicle cells in the thyroid

A

synthesize thyroglobulin and secrete it into the colloid of the thyroid follicles

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5
Q

what is the role of parafollicular (C) cells

A

cells in between the follicles that secrete calcitonin

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6
Q

how is iodine obtained

A

from salt in the diet must be reduced to iodide prior to absorption

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7
Q

what are the basic ingredients T3 and T4
what is the difference between them

A

tyrosine and iodine
depends if the iodide is attached at three or all four sites

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8
Q

where is thyroglobulin synthesised

A

ER/Golgi complex of thyroid follicular cells

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9
Q

how is iodide transported into the follicular cell
how is active iodide transported into the colloid
what enzyme converts iodide to active iodide

A

enters the cell via Na+/I- symporter against its concentration gradient
enters the colloid via pendrin channel down its concentration gradient
thyroperoxidase (TPO)

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10
Q

what are the two possible products of TPO attaching iodide within the thyroglobulin molecule

A

mono-iodotyrosine (MIT - one iodine)
di-iodotyrosine (DIT - two)

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11
Q

what happens upon follicular cell stimulation for thyroid hormone secretion

A

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

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12
Q

thyroid hormone is lipophilic/hydrophobic
what does it bind in the colloid and blood for storage

A

blood: plasma proteins
colloid: thyroglobulin

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13
Q

5 key steps of thyroid hormone synthesis

A

iodide trapping
iodination
coupling
colloid resorption
thyroglobulin proteolysis

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14
Q

why does T4 bind thyroxine-binding globulin (TBG) more than albumin even though albumin is more abundant

A

TBG has a higher affinity for T4

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15
Q

metabolism and excretion of thyroid hormone

A

occurs in liver, kidney and pituitary
T4 can be metabolised to active T3
metabolised by conjugation with glucuronic acid then secreted into bile

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16
Q

what is rT3

A

an inactive form of T3 that acts as a form of control

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17
Q

why does/can T4 act as a reserve of T3

A

T3 is 10 times more potent
T4 can be metabolised to T3 to avoid synthesis waiting time

18
Q

what is the negative feedback pathway of thyroid hormone in the HPT axis

A

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

19
Q

TSH receptor location and action

A

plasma membrane
initiates signalling cascade leading to T3/4 synthesis and release

20
Q

explain how T3/4 control the rate of metabolism

A

control basal metabolic rate/heat production
by controlling the size and number of mitochondria and enzymes involved in oxphos

21
Q

what is the sympathomimetic effect of T3/4

A

TH increases the proliferation catecholamine target-cell receptors
makes cells more responsive to catecholamines
(adrenaline/noradrenaline)

22
Q

what is the cardiovascular effect of T3/4

A

increased HR and force of contraction -> increased CO
due to sympathomimetic effect

23
Q

why is TH essential for normal bone growth and maturation

A

stimulates growth hormone secretion and IGF-1 production
increases their effects
(promotes structural proteins and skeletal growth)

24
Q

what is the effect of thyroid deficiency in children
how is it treated

A

stunted growth
thyroid replacement therapy (excessive TH does not mean excessive growth)

25
Q

role of TH in nervous system

A

crucial role in normal development and maintenance of CNS in adults

26
Q

effect of TH on metabolism

A

increased

27
Q

what can cause hypothyroidism

A

primary failure of thyroid gland
secondary deficiency of TRH/TSH
inadequate dietary supply of iodine

28
Q

key symptoms of hypothyroidism

A

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

29
Q

what is cretinism
what are the results
how are they prevented

A

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

30
Q

what is myxedema
what are the results
how is it treated

A

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

31
Q

what can cause hyperthyroidism

A

production of thyroid stimulating immunoglobulin (TSI)
secondary excess of TRH/TSH
hypersecreting thyroid tumour

32
Q

key symptoms of hyperthyroidism

A

increases metabolic rate
intolerance to heat
weight loss
increases systolic BP
muscle wasting
enlarged thyroid
bulging eyes
tremors
diarrhoea

33
Q

what causes Graves disease

A

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

34
Q

why does thyroid growth and secretion continue unchecked in Graves disease

A

unlike TSH, TSI is not subject to -ve feedback by TH

35
Q

treatments of hyperthyroidism

A

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

36
Q

explain administration of radioactive iodine to treat hyperthyroidism

A

given orally on a one time basis
iodine is only picked up by the thyroid cells so destruction is local
kills hyperactive regions

37
Q

what is goiter
what causes it

A

enlarged thyroid gland
develops when thyroid gland is overstimulated by TSH or TSI
low iodine

38
Q

explain how hyperthyroidism results in goiter

A

excessive activation of TSH receptor by TSI

39
Q

explain how hypothyroidism/low iodine results in goiter

A

increased TSH production by pituitary in response to low TH
lack of iodine -> low TH -> high TSH -> thyroid growth

40
Q

why does taking potassium iodide protect from thyroid cancer

A

stable form of iodine
protects the thyroid from absorbing radioactive iodine if present