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PMCOL 200 > Thyroid Gland and Calcium/Phosphate Deck > Flashcards

Thyroid Gland and Calcium/Phosphate Deck Flashcards

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1
Q

Thyroid Gland

A

Butterfly shaped gland at the base of the neck

Releases two main classes of hormones:
- T3 (triiodothryoxine - most active and T4(thyroxine) thyroid hormones)
- Calcitonin

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2
Q

What hormones control the thyroid gland?

Hint: HPA axis

A

TRH – thyroid releasing hormone (secreted from the hypothalamus) stimulates the pituitary
TSH – thyroid stimulating hormone (released from the pituitary) stimulates the thyroid gland
T3 and T4 – they exert negative feedback on both upstream glands

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3
Q

What are the physiological effects of thyroid hormone

A
  1. Increased basal metabolic rate – people are usually lean (they can metabolize sugars and other substances fast/makes the enzymes work faster)
  2. Sensitization of catecholamines
    - increased heart rate, breathing rate, and cardiac output
  3. it plays an important role in growth and development
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4
Q

How does the thyroid gland concentrate Iodine from the bloodstream?

A

Na+/I- co-transporter is modulated by the sodium-potassium pump

sodium goes down its concentration gradient by actively pumping Iodine into the cell, both go inside the cell simultaneously.

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5
Q

What is the main objective of the Iodine in the cell?

A

Iodine is transported into the follicle lumen, and eventually added to thyroglobulin (precursor for the thyroid hormones) tyrosines during the Iodination step

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6
Q

What is the apical side of the follicle lumen?

A

This is the site of Iodination and coupling of thyroglobulin

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7
Q

What happens inside the thyroid cells?

A

Processing of thyroglobulin – precursor for thyroid hormones – after it has been iodinated and coupled

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8
Q

Which side are the T3 and T4 released?

A

Basolateral side – towards the bloodstream and are released here

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9
Q

Thyroglobulin

A

Precursor protein for thyroid hormone production

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10
Q

Thyroglobulin Peroxidase

A

The enzyme that iodinates the tyrosine molecule, and the enzyme that couples tyrosine chains

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11
Q

What does TSH do?

A

It causes the precursor protein to be endocytose into the follicle, and processed into T3 and T4.

It than also promotes the release of T3 and T4 into the blood stream from basal lateral side

***T4 is more predominantly released

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12
Q

What type of receptor is a thyroid hormone receptor?

A

Thyroid hormone receptor is an intracellular type receptor – acts as a transcription factor after binding of thyroid hormone

However, T3 and t4 are not very lipid soluble and need to be taken up into cells by a transporter protein – many different types – in order to reach their receptors

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13
Q

What is the mechanism of the thyroid hormone?

A

At rest:
- The thyroid hormone response element (DNA transcription start site) is bonded to TR-DBD (DNA binding domain)
- The TR-DBD is bound to TR-LBD (Ligand-binding domain)
- The TR-LBD is bound to a corepressor

When active:
- The T3 hormone and T4 hormone enter the cells through a transmembrane receptor
- T4 is deiodinated to T3 by 5’DI (deiodinase)
- The T3 binds to one of the TR-LBD (ligand binding domain) and takes a co-activator
- The other TR-LBD is swapped with RXR retinoid acid receptor to form a heterodimer with the thyroid hormone receptor
- This RXR allows the co-repressor to leave by changing the substrate specificity
- The co-activator recruited on the other TR-LBD allows the transcription of genes of interest

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14
Q

What are the common causes of hypothyroidism?

A
  • Iodine deficiency (lack in the diet)
  • autoimmune disease (Hashmito’s thyroiditis)
    It occurs when your body makes antibodies that attack the cells in your thyroid.
  • congenital defect (birth)
  • inappropriate hormonal regulation (too less TSH/TRH/T3/T4)
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15
Q

What are the symptoms of hypothyroidism?

A
  • fatigue
  • weight gain
  • goiter
  • hypersensitivity to cold
  • bradycardia (low heart beat)
  • brittle hair and nails
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16
Q

What is primary hypothyroidism?

A

Defect in the functioning of Thyroid Gland
- low T3/T4
- High TSH

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17
Q

What is secondary hypothyroidism?

A

Central defect – poor function of the anterior pituitary or hypothalamus
- low T3/T4
- low TSH/TRH

Generally problems with pituitary lower the levels of TSH and TRH, respectively

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18
Q

What are the treatments for hypothyroidism?

A

Hormone Replacement Therapy
- Give individuals synthetic thyroxine – T4
- Extremely commonly prescribed

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19
Q

Levothyroxine

A

Synthetic T4 hormone given during hormone replacement therapy

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20
Q

What is the cause of hyperthyroidism?

A
  • Graves Disease
  • Hyperplasia (tumour to the thyroid gland/goiter/thyroid adenoma)
21
Q

What is graves disease?

A
  • Auto-immune disease
  • Creates anti-bodies against TSH receptors
  • These antibodies activate the receptor (leading to excess thyroid hormone released)
22
Q

What are the features of thyroid hyperplasia?

A
  • High T3 and T4
  • Low TSH (negative feedback mechanism)
  • weight loss
  • feeling warm/generating excessive heat
  • irregular heart beat/rapid heart beat
23
Q

What are the features of secondary hyperthyroidism?

A
  • High T3 and T4
  • High TSH/TRH

Caused by: Defects in the production of TSH by anterior pituitary ==> produces too much TSH

24
Q

What is the Similarities/Difference between Grave’s disease and Hashimoto’s thyroiditis?

A

Similarities
- auto-immune disease effecting the thyroid gland

Differences

Hashimoto
- causes a decrease in the production of T3 and T4
- more TSH in the blood
- antibodies are generated to destroy the thyroid proteins – lead to damage of thyroid gland overall

Graves
- excessive T3 and T4 hormones
- less TSH in the blood
- antibodies cause the stimulation of the TSH receptor

25
Q

Why do people with Graves get exophthalmos?

A

immune cells damage
muscle/fibroblasts in the eyes

26
Q

Fibroblasts

A

Cells that build connective tissues in the body, these cells are effected by immune cells in Graves

27
Q

Goitre

A

Swelling of the throat due to over activation of the thyroid tissues by stimulatory antibodies

28
Q

How to treat hyperthyroidism?

A

A) Surgery

B) Radioactive Iodine Treatment

C) Anti-thyroid drugs

D) Sympathomimetic treatment

29
Q

Methimazole

A

Anti-thyroid drug

Prevents steps in the formation of T3/T4 hormones

Specifically – prevents iodination and coupling steps mediated by thyroperoxidase enzyme

Diverse side effects

30
Q

Iodine - 131 isotope

A

Treat hyperthyroidism

Concentrate radioactive Iodine-131 in the thyroid gland

Radiation destructs the thyroid

Should NOT be used in women who are pregnant or nursing – Breast feeding – it can defect the thyroid gland irreversibly in the baby child

31
Q

Symptomatic treatment

A

Used to treat symptoms of hyperthyroidism

Ex. Beta blockers for fast heart rate (tachycardia)

Does not influence/treat the underlying cause of the disease

Better to give it with a treatment plan that treats the disease

32
Q

What are the drawbacks to surgery of the thyroid gland?

A

The thyroid gland is also home to the parathyroid glands, which is responsible for regulating/balancing Ca2+ concentrations…. so someone whose thyroid has removed may in danger of hypothyroidism and hyperthyroidism…so they are prescribed hormones – like levothyroxine

33
Q

What does bone hold?

A
  • 98% calcium
  • 85% phosphate
34
Q

Why do we need calcium and phosphate?

A
  • we need bone strength – osteoporosis/osteopenia (less bone density)
  • too dense (osteropertosis) – breaks/fractures are also common
  • electrical excitability of the cells
  • basically, calcium can bind to glycosilated proteins on the cells
  • big impact on the electrical excitability of the cells
  • muscle contraction
  • activation of calcineurin
35
Q

How do glucocorticoids promote bone resorption?

A

“Glucocorticoids increase bone resorption by stimulating osteoclastogenesis by increasing the expression of RANK-L ligand and decreasing the expression of its decoy receptor, osteoprotegerin” (Canalis and Delany)

They are steroid hormones – they work intracellularly

36
Q

What can you treat hypocalcemia?

A

Short Term Management
- pills for Calcium
- pills for active D3 metabolites

37
Q

Teriparatide

A

Counterintuitive treatment

Fully active PTH fragment from 1-34 amino acids

PTH acts primarily at stimulating osteoblasts in promoting bone formation

PTH acts indirectly on promoting the growth and maturation of osteoclasts via RANK-L

The overall effect mostly allows promoting osteoblast activity – such as bone formation

Often this drug is given through proper timing – dosage could be once daily – to ‘tip the balance’ towards osteoblast activity

38
Q

Osteoporosis or Osteopenia

A

Abnormal bone loss –> susceptible to fractures

Long-term gradual disorder, loss of balance between formation and resorption of the bone –> too much resorption than formation

Most common in aging females due to symptoms of menopause

Other common causes
- Long term use of glucocorticoids
- Hyperparathyroidism

39
Q

How is osteoporosis treated in post-menopausal women?

A

Commonly treated by hormone replacement therapy – serious adverse effects such as cancer, etc.

For example….they are given estrogen mimics like SERMs (eg. Raloxifene)

40
Q

Bisphosphonates

A

Inhibits osteoclast activity – such as bone resorption – by inhibiting their attachment to the bone (stops the cells from attaching to the bone)

Side effects – cancer, abnormal fractures

Inhibits glucocorticoids

All drugs share similar features – two phosphonate group

High affinity for Ca2+, so easily accumulate in the bone

They target osteoclasts and have a variety of toxic effects on them

41
Q

Alendronate

A

Most commonly prescribed bisphosphanate

42
Q

Osteoprotegerin

A

Endogenous inhibitor of RANKL ligand system

Naturally occurring in the body

“Inhibits bone resorption and binds with strong affinity to its ligand RANKL, thereby preventing RANKL from binding to its receptor RANK” (https://doi.org/10.1016/s1297-319x(03)00131-3)

RANKL ligand is responsible for binding to RANK receptors on premature osteoclasts, and promoting their maturation so that they can bind to the bone and allow the resorption of the bone

43
Q

Denosumab

A

Monoclonal antibody (made in the mouse) direct against RANK-Ligand

44
Q

What can cause hypocalcemia?

A

Secondary effects
- kidney failure (stops resorbing calcium in the blood)
- kidney failure causes secondary hyperparathyroidism

Long term effects
- breakdown and weakening of the bones

45
Q

What are the symptoms of hypercalcemia?

A

Effects related to loss of cellular excitability, lethargy, coma, also pain in bones if due to excessive PTH

46
Q

Trousseau’s sign

A

causes hyper excitability in nerve cells due to a lack of calcium

unresolved, can lead to seizures, muscles, tetany/spasms

46
Q

Trousseau’s sign

A

causes hyper excitability in nerve cells due to a lack of calcium

unresolved, can lead to seizures, muscles, tetany/spasms

46
Q

Trousseau’s sign

A

causes hyper excitability in nerve cells due to a lack of calcium

unresolved, can lead to seizures, muscles, tetany/spasms

PMCOL 200 (3 decks)

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