week 3-L2-thyroid gland Flashcards
thyroid gland labels top to bottom
thyroid cartilage, thyroid gland, isthmus and pyramid
thyroid gland interior structures
follicles, follicular cells and colloid + parafollicular cells
dangers of thyroidectomy
presence of parathyroid glands and left recurrent laryngeal nerves that runs close to thyroid
recurrent laryngeal nerve function
supply the vocal cords
parathyroid glands
embedded in thyroid and control calcium levels
thyroid gland embryology
originates base of tongue thyroglossal duct develop divides to 2 lobes duct disappear leaving foramen caecum final position by week 7 thyroid glands develop
problems with thyroid glands development
may not develop at all or may not completely descend
thyroid gland mechanism to TSH
binding of TSH to TSH-R
I- and Na+ transportation into follicular cell and colloid
oxidation aka iodination of I- to I
binding to TSH-R cause enzyme activation TPO and TG
TPO catalyse peroxide breakdown
peroxides cause TG and binding of tyrosine residue forming MIT and DIT
coupling reaction to form T3 and T4
secretion into the blood
T3 formation
coupling between DIT and MIT
presence of 3,5,3 iodine
T4 formation
coupling between 2 DIT molecule
presence of 3,5,3,5 iodine
T4 aka
thyroxine
which is the main hormone product in the thyroid gland
thyroxine or T4
why is T4 the main hormone product?
can be deiodinated to T3, its bioactive form
deiodination of T4/ thyroxine
produce 2 different products- T3 active and reverse T3
NB: reverse T3 is not active, 2 iodine on the 2nd side chain
enzyme- deiodinase
circulating T3
80% from T4 deiodination and 20% from direct thyroidal secretion
plasma protein bound to T3 and T4
thyroid-binding globulin
albumin
prealbumin
are plasma bound T3 and T4 active
no oney unbound components are active
where is TG found
only in the thyroid
where is TGB found
in the circulation
% T3 and T4 unbound and what does it show?
0.05 T4 and 0.5 T3, most thyroid hormone are inactive
T3 and T4 mechasnim of action
T4 conversion to T3 and T3 alter gene expression
cretinism
untreated congenital hypothyroidism due to foetal growth and development impaired as thyroxine not produced by own body
how is TSH measure in newborn
heel prick test, if high=> not producing own thyroid hormone
thyroid hormone actions
increase basal metabolic rate
protein, fat and carbohydrate metabolism
potentiate action of catecholamines
effects on the GI, CNS and reproductive system
T4 half life
7-9 days
T3 half life
2 days
are thyroid disorders most common in mean or women or same?
women with 4:1 ration due to autoimmune system and pregnancy
overreactive thyroid or under reactive thyroid more common?
same
primary hypothyrodism
autoimmune damage to the thyroid
thyroxine levels drops and TSH levels increase
suppose the thyroid is chopped off- decr in T3 and T4- -ve feedback to hypothalamus to produce more TSH- side effects due to other hormone produced along with TSH
common forms of autoimmune thyroid disease
Hashimoto thyroiditis and Graves’s disease
what does presence of 1 autoimmune disease imply
may increase the risks of other autoimmune diseases
signs and symptoms of hypothyrosidm
cold intolerance, depression and tiredness, weight gain with reduced appetite, constipation, Bradycardia, deepening of voice, eventual myxoedema coma
drugs for primary hyperthyrodism
levothyroxine
mechanism of action of levothyroxine
production of T4 as alternative to be deiodinated
dosing of levothyroxine
common dose is 100mg administered orally but adjusted according to normal range of TSH
potential complication of to levothyroxine
minor-weight loss or headache
major-heart attack and rapid heart rate
why no use Liothyroxine
T3 supplement are not needed due to deiodinase action and can be dangerous intake due to increase toxicity
hyperthyroidism aka secondary hypothyroidism
over production of thyroxine-thyroxine level increase -TSH level drops
causes of over production of thyroxine
Graves disease aka autoimmune- toxic multi nodular goitre- solitary toxic nodule
combined therapy of T3 and T4
complication of toxicity due to overload of T3 and T4 hormones leading to palpitations, tremor and anxiety
Graves disease
autoimmune condition where antibodies bind and stimulate TSH receptor leadings to smooth goitre
Or antibodies bind to muscles behind eyes- exophthalmos
Or stimulate the growth of soft tissues of shins- pretibial myxoedema
signs and symptoms of hyperthyroidism
heat intolerance, weight loss and increase appetite, diarrhoea, tremors and palpitations, myopathy, sore eyes and goitre, mood swings.
