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ER Week 1 > Thyroid Physiology > Flashcards

Thyroid Physiology Flashcards

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1
Q

What comprises a thyroid follicle?

A

a capsule-enclosed layer of cuboidal epithelium (follicular cells) that surrounds colloid

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2
Q

What is the hypothalamus hormone here?

A

thyrotropin releasing hormone

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3
Q

What is the pituitary hormone here?

A

thyroid stimulating hormone

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4
Q

What are the two end product hormones?

A

T3 and T4 (thyroxine)

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5
Q

What are other negative regulators of this system?

A

somatostatin, dopamine and high levels of glucocorticoids

all will decreased TSH release to suppress this axis

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6
Q

How is thyrotropin releasin ghormone translated?

A

as a preprohormone,

the mature protein is a tripeptide

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7
Q

What is the important role for the thyroid axis?

A

regulation of energy homeostasis, feeding behavior, thermogenesis, and autonomic regulation

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8
Q

How does TRH work?

A

binds to transmembrane TRH receptor on the thyrotrophs of the anterior pituitary gland

promotes release and synthesis of thyroid stimulating hormone TSH

(signals invved are G protein, PLC, IP3, etc)

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9
Q

Describe the structure of TSH

A

it’s a glcoprotein consisting of alpha and beta chains (the alpha is similar to those used in other pit hormones, but beta is specific)

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10
Q

Where is the receptor for TSH?

A

the plasmamembrane of thyroid follicular cells

it’s a GPCR

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11
Q

How does T3 and T4 get out of the follicular cell?

A

ther ear especific transporters for them

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12
Q

What does the 3 and 4 mean?

A

how many iodines are on the tyrosine

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13
Q

What is the first step in thyroid hormone synthesis?

A

dietary iodide is required and active transport of I- into the thyroid follicular cell occurs

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14
Q

What is the second step?

A

oxidize the iodide to iodine (organification)

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15
Q

third?

A

iodination of tyrosines attached to thyroglobuli protein backbone to make monoiodothyronin (MIT) and diiodothyronine (DIT)

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16
Q

WHat is the fourth step?

A

conjugation of MIT and DIT to make T3 and T3

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17
Q

What enzyme does that conjugation?

A

thyroid peroxidase

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18
Q

What then happends to the conjugates?

A

endocytosed into the follicular cell

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19
Q

What happens to the conjugate in the follicular cell?

A

Proteolysis into mature T3 and T4

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20
Q

THen what happens?

A

movement of T3 and T4 out of the cell

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21
Q

How does iodide get into the cell?

A

it’s an iodide/Na symporter - active transport

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22
Q

What’s the main drug target in this system?

A

the thyroid peroxidase

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23
Q

How are T3 and T4 related

A

T3 is more active than T4

T4 will be converted to T3 intracellularly so T3 has the action

T3 has a shorter circulating half life

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24
Q

So which one binds to thyroid hormone receptors?

A

trick question - both do

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25
Q

What binds up 75% of T4 and T3?

A

thyroxin binding globulin

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26
Q

What binds 20% of T4 and 5% of T3?

A

transthyrten

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27
Q

What binds the rest?

A

Albumin

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28
Q

Which ones has 1 bindin site? 2 binding site? multiple binding sites?

A

Thyroxine binding globulin has 1 binding site

Transthyretin has 2 binding sites

Albumin has several binding sites

MAJORITY OF T4 and T3 are bound

29
Q

WHen will these carrier proteins icnrease?

A

pregnancy, estrogen/androgen treatment

30
Q

When will these carrier proteins decrease?

A

hyperhtyroidism
malnutrition and nephritis syndrome (diseases that cause protein loss)

so focus on free hormone when measuring the axis

31
Q

T4 to T3 activation in the cell requires activity of what enzyme?

A

deiodinase I and II

these can also convert to inactive state, but don’t woryr about it

32
Q

Where is DI most prevalent?

A

Liver and kidney

33
Q

What does Deiodinase I do?

A

converts the less active T4 to the more active T3 so increases T3 within the cells and in circulation

34
Q

What will DI convert T4 into for disposal?

A

rT3

35
Q

DI is the target for what drug?

A

prophylthiouracil

36
Q

Where is deiodinase II?

A

brain, pituitary, skeletal and cardiac muscle

37
Q

Where is deiodinase III?

A

brain, skin and placenta

but mainly only involved in deactivation of the hormones, not activation

38
Q

What are the three ways TSH will promote production of new thyroid hormone?

A
  1. increases thyroid peroxidase synthesis
  2. increases thyroglobulin transcription
  3. increases the Na+/I- transport activity to get more iodide into the follicular cell
39
Q

The thyroid hormone transporters make sure that intracellualr levels of thyroid hormone are ____ than in the ECF or plasma.

A

higher

40
Q

Again, what type of receptor pattern is the thyroid hormone receptor?

A

an RXR - heterodimerizes

41
Q

What does thyroid hormone do for oxygen consumption?

A

promotes it

42
Q

What does thyroid hormone do for heat produciton?

A

increases it

43
Q

What does thyroid hormone do for free radical formation?

A

promotes it

44
Q

What does thyroid hormone do in terms of glucose?

A

increased glucose utilization, uptake and synthesis

45
Q

What does thyroid hormone do to the sympathetic nervous system?

A

it’s permissive - allows for increased heart rate and increased contractility

46
Q

Why do most states mandate newborn testing ot thyroid function?

A

because you need to initiate thyroid hormone replacement if necessary within the first few days of life, otherwise they’ll fall behind in both growth and neurological development (cretinism)

47
Q

In infants, what are the effects of hypothyroid?

A 
profound mental retardation
short
delayed motor dev
coarse hair
protruberant abdomens
respiratory difficulty
cyanosis
poor feeding
jaunduce
hoarse cry
umbilical hernia
48
Q

What is the maternal hypothyroidism etiologies?

A
  1. lack of iodine in maternal diet
  2. Hashimoto’s thyroiditis
  3. exposure to radioactive iodine or antithyroid drugs during pregnancy (makes it tricky to treat someone with hyperT in pregnancy)
49
Q

What are the natural sources for iodine?

A

sea life - kelp, certain seafood, and platns grown on iodine-rich soil

50
Q

How do we get most of our iodine now?

A

iodized salt

51
Q

If you catch a congenital hypothyroidism later on, which will catch up with supplementation - grwoth or brains?

A

growth only. can’t get back the lost brain development unfortunately

52
Q

What does excess thyroid hormone do to catecholamien post-receptor action?

A

amplifies it - the issue with thyroid storm

53
Q

What does excess thyroid hormone do in terms of erythropoietin release and erythropoiesis?

A

the increased O2 demand from all the increased metabolism leads to increased production of erythropoietin and increases erythropoiesis

54
Q

What does excess thryoid hormone do to the GI tract?

A

promtoes hyperdefacation

55
Q

What does excess thyroid hormone do to bone?

A

pomotes bone turnover with net bone loss and hypercalciuria

56
Q

What does excess throid hormone do to muscle?

A

increases protein turnover and net loss in skeletal muscle with myopathy

so muscle weakness, muscle degeneration, muscle fatigue, and heat intolerance

57
Q

What does thyroid hormone do in terms of muscle contraction?

A

increases the speed of muscle contraction and relaxation (this is why they have increased deep tendon reflexes and clonus in severe cases)

58
Q

What are the ways in which thyroid hormone increases glucose levels in the blood?

A
  1. increases hepatic gluconeogenesis
  2. increases hepatic glycogenolysis
  3. increases intestinal glucose absorption
59
Q

What does TH do to cholesterol?

A

increasees the LDL receptor # and thus increases LDL clearance (so total LDL cholesterol levels are typically elevated with hypothyroidism)

60
Q

What does hyperthyroidism cause in terms of puberty?

A

precocious puberty

61
Q

Why can hyperthyroidism cause gynecomastia in men?

A

it promotes aromatization of androgens to estrogens and increased sex hormone binding globulins

62
Q

Why can hyperthyroidism cause fertility issues?

A

impairs gonadotropin releasing hormone

63
Q

What does thyrotoxicosis refer to?

A

thyroid hormone toxicity in the body (any cause of excessive thyroid hormone)

64
Q

What are the drugs we use to avoid thyroid storm?

A

beta adrenergic blockers
thioamines (antithyroid)
corticosteroids - to cover for functional hypoadrenalism incuced by thyrotoxicosis

65
Q

What is the incidence for thyroid storm?

A

10% of people hospitalized for thyrotoxicosis

66
Q

What is the mortality rate for thyroid storm?

A

20-30%!

hard to control 0 better to prevetn

67
Q

Where is the problem in primary hypothyroidism?

A

the thyroid gland isn’t making enough?

68
Q

Why does goiter develop in the case of iodine deficiency?

A

if you have decreased iodine, you have low T3 and T4 being made.

this signals the hypothalmus to produce TRH, which signals the pituitary to make TSH

the TSH signals the thyroid gland to produce the T3 and T4 (but it can’t!), but also to GROW - it just keeps snowballing until you get a goiter

69
Q

Why does goiter develop in Graves?

A

the thyroid-stimulating immunoglobulins act like TSH, which triggers the thalamus to make T3 and T4, but you also get the grwoth signal from the immunoglobulins

ER Week 1 (11 decks)

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