thyroid gland metabolism Flashcards
what is the HPA axis
hypothalamus anterior pituitary adrenal gland axis
feedback control of the HPA axid
negative feedback control
where are serum binding proteins produced
primarily in the liver
what are serum binding proteins made for
lipophilic homrone distribution
what do lipophilic steroids bind to
reversibly to serum albumin which is a large plasma protein present in high concentration
what binds to serum albumin to deliver and extend half life of secreted lipophilic hormones
specific binding proteins
exmaple of a specific binding protein that binds to albumin
CBG- corticosteroid binding globulin of SHBG sex hormone binding globulin
what has a longer molecule life than peptide hormones
lipophilic hormones
TRH
thyrotropin releasing hormone
what secretes thyroid hormone
follicular cells
what is colloid
a glycoprotein
what secretes calcitonin
c cells
what are the two hormones of the thyroid hormone
T3- triiodothyronine and T4 tetraiofothyronine or thyroxine
they are members of the tyrosine class which is synthesized in the body but iodine must be obtained from the diet
facts about iodine
it is a halogen meaning it readily forms negative ions
synthesis of thyroid hormones
- follicular cell synthesizes enzymes and thyroglobulin for colloid
- I- is transported into the cell with Na+ and transported into colloid
- thyroid peroxidase oxidizes iodide ions so they are incorporated into tyrosine moities of thyroglobulin. then MITS and DITS couple to make T3 and T4
4.thyroglobulin with attached T3 and t4 is pinched off is taken back into the follicular cell by endocytosis - intracellular enzymes separate T3 and T4 from the protein
what oxidizes peroxidase iodide ions and why
thyroid peroxidase so they are incorporated into tyrosine mmoities of thyroglobulin. then MITS and DITS couple to make T3 and T4
what happnes once T3 and T4 are cleaved
they diffuse out o fthe follicular cells bc they are lipophilic.
what do T3 and T4 have to bind to in the blood
TBG- thyroxine binding globulin
how do thyroid hormones bind with proteins
reversibly mostly with TBG
the bound form is in equilibrium with the free form
what are the bioactive forms of T3 and T4
the free form
what causes nuclear translocation and gene expression changes
thyroid hormones bindning to thyroid hormone receptors (T3)
how does widespread activity in the body occur when thyroid hormones bind reversibly to proteins
though THR
matabolism of thyroid hormones
T4 convertisng to T3
how is T4 converted to T3
deiodination n the liver and kidney reuting in 80% of the circulating T3
bioactivity of T3 and T4
3 is four times more bioactive than 4so it is the principal thyroid hormone
how is reverse T3 created
through conversion of some T4
How is the ratio of rT3/T3 regulated
increaed during fasted state or carb constriction to concserve energy since T3 stimulates metabolism
regulation of thyroid hormone synthesi and secretion
every step controlled by TSH from anteroir pituitary
TSH production controlled by hypothalamic TRH
TRH
thyrotropin releasing hormone
excess TSH
produces hypertrophy and pyperplasia of folliuclar cells- more cells being formed
excess TSH
produces hypertrophy and pyperplasia of folliuclar cells- more cells being formed
goiter
enlarged thyroid
what tissues are affected by thyroid hormone
virtually every tissue
bioactivity of thyroid hormones
- metabolism- BMR
- growth and development
- nervous system development and function
BMR
estimate of individual basal or lowest energy expenditre required to maintain vital functions ususally measured after a 12 hour fast in a resting state
normal amounts of thyroid hormone production effect on intermediate metabolism
anabolic
pathalogically high amounts of thyroid homrone production effect on intermediate metabolism
catabolic as it causes a futile cycle of metabolism
what is permissive to GH activity
thyroid hormones
thyroid hormone deficient children
show growth retardation such as dwarfism due to cretinism
what can we do when there is a congenital deficienty in thyroid hormone
replacement therapy for cretinism or neonatal hypothyroidism
what is essential for normal CNS function in adults including mentation
thyroid hormone
tyroid hormone effect on NS
enhances sympathetic NS activity
has sympathomimetic effect by increasing catecholamine receptor expression and increasing speed of nervous reflexes
hypothyroidism
low secretion of thyroid hormones
hyperthyroidism
excess secretion of thyroid hormone
what cuases hypothyroidism
failure of thyroid gland due to autoimune inflamation - thyroiditis- andsubsequent fibrosis
failure of hypothalamus or pituitary to secrete TRH or TSH
lack of iodine in diet
signs of hypothyroidism
depressed NS activity
-slow weak pulse
-slow reflexes, mentation and speech
-lack of alertness
-poor memory
low metabolic rate
-intolerance to cold
-elevated blood cholesterol
-weight gain
-fatigue
-puffy, foughy appearance, myxedema
what can cause hyperthyroidism
autoimune disease such as graves disease or thyrotoxicosis when TSI (thyroid stimulating immunoglobulin) stirumlates TSH receptors LATS
thyroid tumor secreting thyroid hormones
excess secretion of TRH or TSH by hypothalamus or anteroir pituitary
LATS
long acting thyroid stimulator
simptoms of hyperthyroidism
high metabolic weight
-intoleracne of heat, exessicve sweating
-weight loss
-muscle wasting and weakness due to catabolasis
increasing NS activtiy
-high heart rate and palpitations
-irritability, anxiety, inappropriate emotionally
bulging eyes
bulgign eyes name
exopthalmos due to abnormal fluid and swelling behind eyes
cant close lid and reduce range of motion and pain and tearing and sensitivity to light and disrupted vision
goiter in hypo
due to lack of iodine
goiter in hyper
due to exess TRH or TSH
in graves due to autoimmune antibodies that stimulate TSH receptors
