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Endocrine Physiology > Thyroid/Parathyroid/Ca2+ Regulation > Flashcards

Thyroid/Parathyroid/Ca2+ Regulation Flashcards

1
Q

What is the embryologic origin of the thyroid?

A

Oral endoderm. More specifically, from the thyroid diverticulum that develops in the foregut at week 3-4. The thyroglossal duct progenitor migrates towards the head and the thyroid reaches its final resting point below the larynx. The duct eventually closes and becomes the foramen cecum.

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2
Q

What is a thyrocyte

A

Follicular epithelium that lines the follicles of the thyroid

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3
Q

How does the thyroid store its hormone?

A

Extracellularly, in an inactive form (FUN FACT: It’s the only endocrine gland that does this)

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4
Q

The thyroid is made of follicular cells. What does the basal side of the cell face? What does the apical side face?

A

Basal side: BLOOD that supplies the iodide you need to make thyroid hormone
Apical side: lumen filled with colloid. Colloid is mainly made of thyroglobulin

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5
Q

Where do you find parafollicular C cells and why do you care about them?

A

You find them within the walls of the thyroid follicles and you care because they make and secrete calcitonin

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6
Q

Okkkkk heres the big one. Describe thyroid hormone synthesis

A
  1. Na-I symporter brings in iodide from blood into follicular cell (aka iodide trapping)
  2. Iodide then diffuses across apical side to the colloid lumen which contains thyroglobulin (TSH helps with this transport)
  3. Oxidation rxn: Thyroid peroxidase, an apical membrane enzyme, brings together iodide and a tyrosine residue on thyroglobulin. This makes free radical versions of iodide and tyrosine
  4. Organification: the free radicals undergo another rxn to make MIT (monoiodotyrosine). Note you’re still on the thryoglobulin at this point.
  5. 2nd organification rxn makes DIT (diiodotyrosine)
  6. MIT and DIT couple together to make T3. Coupling is done by thyroid peroxidase.
  7. 2 DITs couple to make T4
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7
Q

What is thyroglobulin

A

It is a glycoprotein that is made by thyroid follicular cells and transported across the apical membrane to the colloid lumen. The tyrosine residues on this glycoprotein are what become iodide-ized to make thyroid hormones

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8
Q

How is thyroid hormone released? Another big one, mah bee.

A
  1. TSH binds to surface receptors on thyroid epithelial cells
  2. This causes luminal colloid to be pinocytosed into the follicular cell (this vesicle contains thyroglobulin, which remember has T3 and T4 attached to it)
  3. In the follicular cell, the vesicle fuses to a lysosome and protein breakdown occurs, freeing up T3 and T4 from the thyroglobulin
  4. T3 and T4 transported across basal side to circulation
  5. Some of the protein breakdown products include MIT and DIT. The iodine from these molecules are removed by deiodinase and recycled for more thyroid hormone synthesis
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9
Q

Now an easy one: is T3 or T4 the major thyroid hormone secreted from the thyroid.

A

T4. Good job. BUT remember that T3 is the physiologically active form. HA TRICKED YA

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10
Q

What’s T4/T3’s travel buddy in circulation?

A

Thyroxine-binding globulin (TBG). Made in the liver, and helps increase t1/2 and prevent pee-ing out of T4/T3

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11
Q

How is T4 activated?

A

5’-Deiodinase removes an iodine atom from T4 to make T3. This enzyme is found in the liver, kidneys, thyroid and target organs

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12
Q

How is T4 inactivated?

A

A separate deiodinase enzyme targets a different iodide atom, forming reverse T3 (rT3). Inactivation occurs mostly in the liver and kidneys

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13
Q

Tell me again, how is thyroid hormone regulated? I don’t remember

A

Low T3/T4: increased TRH from the hypothalamus and TSH from the pituitary
High T3/T4: decrease TRH and TSH

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14
Q

Name 5 main roles of thyroid hormone

A

Think 4 B’s: (I know I said 5, look at the rest of the card)
Brain Maturation, Bone growth, Beta-adrenergic effects, basal metabolic rate increases

More detail:

  1. Bone growth: increase GH gene expression in somatotrophs and stimulate calcification/closure of growth plates
  2. CNS development: promotes differentiation of neurons (important for babies)
  3. Adrenergic effect: Make B1-adrenergic receptors in the heart more responsive to signaling molecules, increasing CO.
  4. BMR: Increased synthesis of cytochromes, cytochrome oxidase and Na+/K+ ATPase and increases # of mitochondria.
  5. Intermediary metabolism: Gluconeogenesis, lipolysis and glycogenolysis to support the increased BMR.
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15
Q

Where and how does Ca2+ regulation take place?

A
  1. Bone: PTH and vitamin D increase bone resorption. Calcitonin does the opposite.
  2. Intestine: Vitamin D directly increases Ca2+ reabsorption. PTH indirectly helps Vitamin D.
  3. Kidney: 99% of filtered Ca2+ is unaffected by hormones but the other 1% is controlled by PTH
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16
Q

What is secreted by the parathyroid gland

A

PTH: acts on kidney and bone. increases serum Ca2+ and decreases serum phosphate

17
Q

What’s the blood supply/drainage situation of the parathyroid gland?

A

Supply: inferior thyroid artery
Drainage: thyroid venous plexus

18
Q

What’s the blood supply/drainage situation of the thyroid gland (you thought I wouldn’t ask didn’t you)

A

Supply of top ½: superior thyroid artery
Supply of bottom ½: inferior thyroid artery
Drainage: superior, middle and inferior thyroid veins. Superior and middle veins drain into the IJV and the inferior vein drains into the brachiocephalic veins

19
Q

An embryological gem: what pharyngeal arch(es) does the parathyroid gland come from

A
  1. Superior lobes: 4th pouch
  2. Inferior lobes: 3rd pouch
    The lobes migrate inferiorly and medially to their final resting place behind the thyroid
20
Q

What kind of cells do you find in the parathyroid gland. Do you know what they do? I bet you don’t. Just kidding. You got it.

A
  1. Chief cells: most common cells. Contain secretory granules containing PTH.
  2. Oxyphil cells: unknown function. Contain acidophilic mitochondria
21
Q

Where is all the calcium in your body???? What is the plasma concentration of Ca2+ (just cuz they put this in the lecture notes a milli times)

A
  1. 99% stored in bone
  2. 0.9% is intracellular
  3. 0.1% found in ECF
    Of the Ca2+ in the ECF:
    A. 40% is bound to plasma proteins
    B. 10% is complexed with anions like phosphate and citrate
    C. 50% is free and ionized (biologically active component)

Plasmsa concentration: 10mg% (10mg/100ml)

22
Q

How is PTH made?

A

It’s made as a big preprohormone that is cut into its active form and stored in chief cells

23
Q

How is PTH regulated?

A
  1. Low serum calcium increases PTH release
  2. Mildly low serum magnesium stimulates PTH secretion.
  3. Extreme decreases in magnesium inhibits PTH secretion.
24
Q

What are 4 things that PTH is responsible for doing?

A
  1. Stimulates osteoclasts (more than osteoblasts), which increases serum Ca2+ and phosphate (rapid effect)
  2. Stimulates distal renal tubule to reabsorb Ca2+ (rapid effect)
  3. Inhibits phosphate reabsorption in the proximal renal tubule. Less serum phosphate means less serum Ca2+ that’s complexed to it.
  4. Increases 1a-hydroxylase in the kidney, which increases 1,25-(OH)2 vitamin D (aka calcitriol), which increases intestinal absorption of Ca2+ and bone resorption (slowww effect)
25
Q

What are the two forms of vitamin D?

A
  1. Ergocalciferol (vitamin D2)

2. Cholecalciferol (vitamin D3)

26
Q

Where do you get the two types of vitamin D from (D2 and D3?)

A
  1. vitamin D2: plant and fungal sources (not made in the body)
  2. vitamin D3: animal sources. This can also be made from 7-dehydrocholesterol in the skin after exposure to the sun.
27
Q

How is vitamin D3 (cholecalciferol) activated?

A

In all these steps, vitamin D has a travel buddy through circulation known as the globulin carrier protein.
1. Cholecalciferol (D3) goes to the liver, where it is hydroxylated to become 25-hydroxycholecalciferol
(this is what you measure in vit D lab tests, and is also the vit D storage form)
2. 25-hydroxycholecalciferol goes to the kidney and undergoes another hydroxylation by 1a-hydroxlase, making 1,25-dihydroxycholecalciferol (1,25-(OH)2 vitamin D)=active form=calcitriol
*Note: 1a-hydroxylase is only present in the kidney.
3. Goes to the intestine and bone to do its job

28
Q

What does vitamin D do? Other than give you an excuse to tan.

A

Generally: increase serum Ca2+ and phosphate by:

  1. increase Ca2+ and phosphate absorption from the stomach.
  2. increase bone resorption of Ca2+ and phosphate
  3. increase renal reabsorption of Ca2+ and phosphate (minor)
29
Q

What’s the deal with calcitonin. On a scale of important to not-important, how important is it in Ca2+ regulation?

A

It is secreted by the parafollicular/C cells of the thyroid gland. It reduces extracellular Ca2+ by decreasing bone resorption by osteoclasts but IS NOT necessary for Ca2+ homeostasis (peeps without thyroids do just fiiiiiine)

30
Q

RANK/RANKL/OPG…what’s goin on

A
  1. Receptor activator of nuclear factor kappa-beta (RANK) present on osteoclasts
  2. RANK ligand (RANKL), released from osteoblast, binds RANK, activating osteoclast
  3. Osteoprotegerin (OPG) binds RANKL, preventing it from binding RANK, and preventing osteoclast activation (tx for osteoporosis anyone?)
31
Q

What is the effect of PTH and estrogen on RANKL and OPG

A

Estrogen: increases OPG, decreases RANKL (less Ca2+ release)
PTH: increases RANKL, decreases OPG (more Ca2+ release)

32
Q

To beat this in: 3 hormones that you think of when you think Ca2+ regulation:

A

PTH, Vitamin D, Calcitonin

33
Q

How does plasma pH affect serum Ca2+ levels

A

Increases in pH causes albumin to hold onto Ca2+ more strongly

34
Q

What is 24-hydroxylase and when does it do it’s job?

A

Forms an inactive form of vitamin D (24,25-(OH)2D3), by adding an OH to the 24, not 1, position. This happens when there is an excess of vitamin D (too much tan time ruh roh)

35
Q

How is phosphate regulated in the body?

A
  1. Bone and intestine: tags along with Ca2+ in and out of bone and in the intestine
  2. Kidney: PTH causes increased excretion of phosphate as more Ca2+ is reabsorbed.
36
Q

What are calmodulins?

A

Cytosolic Ca2+ receptors. Can bind up to 4 Ca2+ at a time and are used in tons of different processes (inflammation, metabolism, memory etc). They have a high affinity for Ca2+ and can bring Ca2+ to target proteins that can’t bind Ca2+ by themselves.

37
Q

How does PO4 enter the body

A

Enters: Intestinal absorption and bone resorption
Exits: intestinal excretion, pee, bone deposition

38
Q

Osteoporosis. What’s the basic idea here.

A
  1. Decreased bone mineral density.
  2. Thought to occur due to decreased activity of 1a-hydroxylase–> less activated vitamin D–>less Ca2+ absorbed from the intestine–>must get Ca2+ from bone resorption
  3. Often see this in post-menopausal females due to decreased estrogen (and estrogen is a stimulator of 1a-hydroxylase sooo this makes sense)

Endocrine Physiology (9 decks)

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