ENDO-Thyroid and Parathyroid Flashcards

1
Q

Describe the anatomy of thyroid

A

Below the thyroid cartilage

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2
Q

Describe the microcopic anatomy of the thyroid

A

composed of large numbers of closed follicles that are filled with colloid (high level of protein called thyroglobulin that bind TH)

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3
Q

What is required for the formation of thyroid hormone?

A

Iodine

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4
Q

What is the Dietary requirement of iodine

A

150 microgram/day

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5
Q

How is iodine ensured in our diet in developed countries?

A

Salt is iodized

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6
Q

Describe Iodide-trapping

A

1] Iodides are transported into the thyroid gland cells by the sodium-iodide symporter,

2] It gets oxidized by peroxidase into I2,

3] then binds to thyroglobulin, a thyroid hormone binding protein (not clear where it actually happens in cell or outside),

4] Iodine is stored and used with tyrosine to form thyroid hormone (T3, T4)

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7
Q

Describe the sodium-iodide symporter

A

co-transports one iodide ion with 2 sodium ions into the cell, requiers ATP

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8
Q

What stimulates the production of thyroid hormone

A

TSH from pituitary, also stimulates the release

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9
Q

Describe the formation of T3

A

MIT (Monoiodotyrosine) + DIT (diodotyrosine)

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10
Q

Describe the formation of T4 (thyroxine)

A

DIT (diodotyrosine) + DIT (diodotyrosine)

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11
Q

Describe the difference between T4 and T3

A

T3 is more active but less abudant,

T4 is more abundunt but less active

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12
Q

Describe reverse T3

A

A mirror image of T3, it is inactive

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13
Q

Describe the MOA of T3,T4

A

Enters the cell and acts on the nuclear receptor to promote transcription as a transcription factor, system acts like a switch (Receptor inhibits transcription unbound and promotes when bound by hormone)

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14
Q

What family are the thyroid hormone receptors in?

A

steroid receptor family

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15
Q

List the effects of thyroid hormone

A
1] Metabolic Activity, 
2] Growth, 
3] Gut motility – metabolism, activity, 
4] Cerebration = thinking, 
5] Muscle (metabolism of muscle/twitch, 
6] Sleep, 
7] Sex
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16
Q

Describe the regulation of thyroid hormone

A

TSH causes release by activacting cAMP

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17
Q

List the effects of TSH on the thyroid gland

A

1] Proteolysis of thyroglobulin (to release the stored thyroid hormone),

2] Iodide pumping,

3] Iodination of tyrosine,

4] Increase size and secretory activity of gland,

5] Reproductive

18
Q

What controls the regulaton of TSH

A

TRH from hypothalamus

19
Q

Describe the negative feedback of TSH and T4,T3

A

Too much T3, T4 will negatively feedbacks on anterior pituitary and hypothalamus to reduce secretion

20
Q

What is the presentation of thyroid disorders

A

1] changes in metabolism,
2] temperature control,
3] gut motility,
4] mentation overactivity or depression

21
Q

Describe the anatomy of the parathyroid glands

A

Within, around, or under thyroid,
small parathyroid glands.
Usually you have 2 superior and 2 inferior parathyroid glands on each side.

22
Q

Why is calcium and phosphate regulated in a narrow range

A

Both ions are found in the bone, high levels of either will pull the other out of the bones.

High or low levels of calcium has dramatic effects on nervous transmission, muscle cell activity, and can cause spastic or flaccid paralysis

23
Q

What is the daily recommendation for calcium?

A

1000mg/day

24
Q

How much of calcium and phosphate is absorbed

A

35% calcium, almost 100% Phosphorus

25
Q

Describe the excretion of calcium and phosphate

A

900 mg (calcium) lost in the GI tract, Phosphate excreted renally as part of buffering system

26
Q

What is our net Calcium per day?

A

100mg

27
Q

Describe the bone matrix

A

extracelluar part of bone made up Ca+ and Phosphate salts and collagen, so it easily able to fall into solution, especially when there is a supersaturation of ions

28
Q

Describe the dynamics of bone metabolism

A

Constantly breaking down with osteoclasts and building with osteoblasts

29
Q

What is the difference between Amorphous salts vs hydroxyapatite crystals

A

hydroxyapatite crystals are formed from calcium and collagen by osteoblasts
grow over a period of days and weeks, the

amorphous compounds are the initial calcium salts that can easily be precipitated into solution when there is a need for it (ie. hypocalcemia)

30
Q

Describe an osteoclast

A

Break down bone by Secreting an acid that breaks down the bony matrix,

breaks down Ca-P salts

Leaving behind pockets where bone has been degraded

31
Q

What converts vitamin D to its active form?

A

hydroxylation by liver and kidney

32
Q

Describe the pathway of vitamin D

A
7-dehydrocholesterol (ingested)-> converted into cholecalciferol (via sunlight) -> 
25 hydroxycalciferol (liver) ->

1, 25-hydroxycalciferol (in the kidney, under control of PTH which increases Vitamin D production)

33
Q

What is the function of Vitamin D?

A

Vitamin D promotes calcium absorption from GI and is regulated by calcium levels

34
Q

What cells secrete PTH?

A

“Chief” cells

35
Q

Describe the formation of PTH

A

Prohormone 110 aa then is cleaved to active hormone 84aa

36
Q

What are the effects of PTH

A

1] Stimulates bone resorption (metabolizes) causing release of calcium into blood

2] increases reabsorption of calcium and decreases phosphate reabsorption by the renal tubules

3] stimulates activation of vitamin D

37
Q

Decrease the effect of the loss of calcium

A

Growth and secretion of glands with loss of calcium (Rickets/pregnancy) decreased activity with excess

38
Q

Describe Calcitonin

A

THYROID product, made by C cells, Peptide hormone

Shifts dynamic toward deposit of calcium
inhibits formation of new osteoclasts,

Primary stimulus is increase in calcium content,

opposes PTH

39
Q

Describe the efficacy of Calcitonin

A

Effects are weak (initial reduction stimulates PTH, rate of absorption is low anyway – effect greater in kids or disease of osteoclast acitivity;

If you have PTH in your system it will dominate over calcitonin

40
Q

Describe Paget’s disease

A

PTH desegulation changes struture of bone

caused by the excessive breakdown and formation of bone-remodeling

followed by disorganized bone remodeling, too much osteoclast activity

Hosptialized PTS