thyroid gland metabolism Flashcards

1
Q

what is the HPA axis

A

hypothalamus anterior pituitary adrenal gland axis

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2
Q

feedback control of the HPA axid

A

negative feedback control

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3
Q

where are serum binding proteins produced

A

primarily in the liver

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4
Q

what are serum binding proteins made for

A

lipophilic homrone distribution

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5
Q

what do lipophilic steroids bind to

A

reversibly to serum albumin which is a large plasma protein present in high concentration

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6
Q

what binds to serum albumin to deliver and extend half life of secreted lipophilic hormones

A

specific binding proteins

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7
Q

exmaple of a specific binding protein that binds to albumin

A

CBG- corticosteroid binding globulin of SHBG sex hormone binding globulin

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8
Q

what has a longer molecule life than peptide hormones

A

lipophilic hormones

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9
Q

TRH

A

thyrotropin releasing hormone

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10
Q

what secretes thyroid hormone

A

follicular cells

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11
Q

what is colloid

A

a glycoprotein

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12
Q

what secretes calcitonin

A

c cells

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13
Q

what are the two hormones of the thyroid hormone

A

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

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14
Q

facts about iodine

A

it is a halogen meaning it readily forms negative ions

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15
Q

synthesis of thyroid hormones

A
  1. follicular cell synthesizes enzymes and thyroglobulin for colloid
  2. I- is transported into the cell with Na+ and transported into colloid
  3. 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
  4. intracellular enzymes separate T3 and T4 from the protein
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16
Q

what oxidizes peroxidase iodide ions and why

A

thyroid peroxidase so they are incorporated into tyrosine mmoities of thyroglobulin. then MITS and DITS couple to make T3 and T4

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17
Q

what happnes once T3 and T4 are cleaved

A

they diffuse out o fthe follicular cells bc they are lipophilic.

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18
Q

what do T3 and T4 have to bind to in the blood

A

TBG- thyroxine binding globulin

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19
Q

how do thyroid hormones bind with proteins

A

reversibly mostly with TBG

the bound form is in equilibrium with the free form

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20
Q

what are the bioactive forms of T3 and T4

A

the free form

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21
Q

what causes nuclear translocation and gene expression changes

A

thyroid hormones bindning to thyroid hormone receptors (T3)

22
Q

how does widespread activity in the body occur when thyroid hormones bind reversibly to proteins

A

though THR

23
Q

matabolism of thyroid hormones

A

T4 convertisng to T3

24
Q

how is T4 converted to T3

A

deiodination n the liver and kidney reuting in 80% of the circulating T3

25
bioactivity of T3 and T4
3 is four times more bioactive than 4so it is the principal thyroid hormone
26
how is reverse T3 created
through conversion of some T4
27
How is the ratio of rT3/T3 regulated
increaed during fasted state or carb constriction to concserve energy since T3 stimulates metabolism
28
regulation of thyroid hormone synthesi and secretion
every step controlled by TSH from anteroir pituitary TSH production controlled by hypothalamic TRH
29
TRH
thyrotropin releasing hormone
30
excess TSH
produces hypertrophy and pyperplasia of folliuclar cells- more cells being formed
31
excess TSH
produces hypertrophy and pyperplasia of folliuclar cells- more cells being formed
32
goiter
enlarged thyroid
33
what tissues are affected by thyroid hormone
virtually every tissue
34
bioactivity of thyroid hormones
1. metabolism- BMR 2. growth and development 3. nervous system development and function
35
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
36
normal amounts of thyroid hormone production effect on intermediate metabolism
anabolic
37
pathalogically high amounts of thyroid homrone production effect on intermediate metabolism
catabolic as it causes a futile cycle of metabolism
38
what is permissive to GH activity
thyroid hormones
39
thyroid hormone deficient children
show growth retardation such as dwarfism due to cretinism
40
what can we do when there is a congenital deficienty in thyroid hormone
replacement therapy for cretinism or neonatal hypothyroidism
41
what is essential for normal CNS function in adults including mentation
thyroid hormone
42
tyroid hormone effect on NS
enhances sympathetic NS activity has sympathomimetic effect by increasing catecholamine receptor expression and increasing speed of nervous reflexes
43
hypothyroidism
low secretion of thyroid hormones
44
hyperthyroidism
excess secretion of thyroid hormone
45
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
46
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
47
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
48
LATS
long acting thyroid stimulator
49
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
50
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
51
goiter in hypo
due to lack of iodine
52
goiter in hyper
due to exess TRH or TSH in graves due to autoimmune antibodies that stimulate TSH receptors