ENDO-thyroid and parathyroid Flashcards

1
Q

describe steps 1-4 of thyroid hormone synthesis

A
  1. Iodine Trapping
    - >Iodine (I-) is actively transported (as iodide) into the cytosol of follicular cells in response to TSH.
  2. Synthesis of thyroglobulin (TGB)
    - >TGB is produced in the RER and golgi apparatus and packaged in secretory vesicles. Vesicles are released into lumen of follicle via exocytosis.
    - >N.B. this step happens at the same time as iodine trapping.
  3. Oxidation of iodine
    - >Iodide (I-) is oxidised to form Iodine (I0) when it passes through the membrane into the lumen of the follicle.
  4. Iodination of tyrosine
    - >Iodine reacts with the tyrosine amino acids of TGB.
    - >Binding of a single Iodine forms monoiodotyrosine
    - >Binding of two Iodines forms diiodotyrosine
    - >The region of TGB with attached iodine atoms is called colloid
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2
Q

describe steps 5-9 of thyroid hormone synthesis

A

5-COUPLING OF T1 AND T2

  • > 2 T2 molecules can join to form thyroxine (T4)
  • > 1 T1 molecule and 1 T2 molecule can join to form triiodothyronine (T3)
  1. Pinocytosis and Digestion of Colloid
    - >Parts of colloid re-enter follicular cells via pinocytosis and merge with lysosomes
    - >TGB is broken down via digestive enzymes, and T3 and T4 is cleaved off.
  2. Secretion of Thyroid Hormones
    - >T3 and T4 are lipid soluble (despite being amino acid derivatives) so diffuse out of follicular cell into interstitial fluid via plasma membrane, then into blood.
  3. Transport into blood
    - >T3 and T4 bind to thyroxine binding protein in the blood to be transported to target cells.
  4. Conversion of T4 to T3
    - >T4 is secreted in a greater amounts but T3 is more potent.
    - >T4 is converted to T3 in the liver and kidney.
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3
Q

what are the roles of thyroid hormone?

A
  • > Increase basal metabolic rate (BMR)
  • > increase ATP production
  • > increase heart rate, BP, force of heart beat
  • > increase production of GH and IGFs
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4
Q

what does the increase in production of GH and IGFs result in?

A

increase of formation of ossification centres in bone

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5
Q

how is ATP production increased due to thyroid hormone?

A
  • via additional Na+/K+ ATPase synthesis
  • increasing number of cellular mitochondria
  • increasing the concentration of enzymes involved in respiration.
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6
Q

how are increased heart rate, BP, force of heart beat achieved due to increase in thyroid hormone?

A

via up-regulating β-adrenergic receptors which increases binding of adrenaline and noradrenaline

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7
Q

what is hypothyroidism?

A

underproduction of thyroid hormone

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8
Q

what can thyroid deficiency in infancy cause?

A

can lead to severe mental retardation and stunted bone growth

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9
Q

what are some of the signs of hypothyroidism?

A
  • goitre
  • bradycardia
  • non-pitting oedema
  • delayed relaxation
  • hypertension
  • slow speech/ movement
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10
Q

what are some of the symptoms of hypothyroidism?

A
  • fatigue
  • cold intolerance
  • mental slowness
  • depression
  • dry skin
  • constipation
  • irregular menses
  • muscle cramps
  • infertility
  • weight gain
  • fluid retention
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11
Q

what is primary hypothyroidism caused by?

A
  • > Caused by disease in the thyroid gland itself-TSH production is increased
  • > Most common cause is autoimmune
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12
Q

what is secondary hypothyroidism caused by?

A

->Insufficient production of TSH from anterior pituitary gland

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13
Q

what is tertiary hypothyroidism caused by?

A

Insufficient TRH production from hypothalamus

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14
Q

what are the functions of calcium?

A
  • cell division
  • cell adhesion
  • plasma membrane integrity
  • protein secretion
  • glycogen metabolism
  • muscle contraction (inc. cardiac muscle)
  • neuronal excitability
  • blood coagulation
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15
Q

what are the functions of phosphate?

A

-bone and teeth formation
-DNA synthesis
-ATP synthesis
-cell membrane constituent
(phospholipid)

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16
Q

describe how calcium phosphate regulated?

A

low blood calcium detected—->PTH released from chief cells of parathyroid gland—->effect on bone/ kidney/ intestine
—–>high blood calcium detected—->calcitonin released from c cells of thyroid gland

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17
Q

what is the effect of PTH on bone?

A
  • stimulates osteoclast and inhibits osteoblasts (breaks down bone)
  • releases calcium and phosphate into the blood
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18
Q

what is the effect of PTH on kidneys?

A
  • stimulates retention of calcium or loss of phosphate (vice versa)
  • stimulates release of calcitriol (active vit D)
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19
Q

what is the effect of PTH on the intestine?

A

indirect effect-calcitriol from kidneys stimulates intestines to absorb calcium from food

20
Q

what is the role of calciton?

A
  • stimulates osteoblasts
  • inhibits osteoclasts
  • increased bone formation
  • reduces amount of calcium and phosphate circulating in blood
21
Q

where is calcitonin released from?

A

c-cells of thyroid gland

22
Q

where is PTH released from?

A

chief cells in parathyroid gland

23
Q

what is hyperparathyroidism?

A

Over production of parathyroid hormone.

24
Q

what is primary hyperparathyroidism associated with?

A
  • > Abnormality of parathyroid glands themselves

- >Excessive parathyroid hormone production leads to loss of bone tissue

25
Q

what is secondary hyperparathyroidism associated with?

A

Excessive secretion of PTH in response to hypocalcaemia (low calcium)

26
Q

what is tertiary hyperparathyroidism associated with?

A
  • > Excessive secretion of PTH AFTER secondary hyperparathyroidism treatment
  • > Extremely rare
27
Q

what is hypoparathyroidism?

A

Underproduction of parathyroid hormone.

28
Q

what does hypoparathyroidism result in?

A

Results in low PTH and low Ca2+ levels.

29
Q

what is hypoparathyroidism most commonly caused by?

A

autoimmune disorders

30
Q

what is the effect of vitamin D?

A
  • > increases osteoclast activity

- >increases calcium and phosphate uptake from the GI tract.

31
Q

how is vitamin D synthesised?

A

sun—>keratinocytes in skin—> 7-dehydrocholesterol—->vitamin D

or vitamin D through supplements or food—>vitamin D

—->liver, vitamin D—–>calcidiol [25(OH)D] (via 25-hydroxylase enzyme)—–>active calcitriol [1,25(OH)2D] (kidney)– stimulated by PTH

32
Q

what are the pathologies associated with vitamin D deficiencies?

A
  • rickets
  • osteoporosis
  • osteomalacia
33
Q

what inhibits thyroid hormone?

A

high levels of T3/T4

34
Q

what inhibits parathyroid hormone?

A

high Ca2+ levels

35
Q

what inhibits calcitonin?

A

low ca2+ levels

36
Q

where is active vitamin D secreted from?

A

kidney

37
Q

where is thyroid hormone secreted from?

A

follicular cells of thyroid gland

38
Q

what stimulates thyroid hormone (t3/t4) release?

A

TRH release form hypothalamus—>TSH ant. pit.

39
Q

what stimulates parathyroid hormone release?

A

low ca2+

40
Q

what stimulates calcitonin release?

A

high ca2+

41
Q

what stimulates vitamin D release?

A

UV radiation

42
Q

what type of hormone is thyroid hormone? And what receptor type?

A

amino acid derivative

nucelar

43
Q

what type of hormone is parathyroid hormone? And what receptor type?

A

peptide

GPCR

44
Q

what type of hormone is calcitonin? And what receptor type?

A

peptide

GPCR

45
Q

what type of hormone is vitamin D? And what receptor type?

A

steroid

nuclear