Parathyroid And Thyroid Gland Flashcards

1
Q

What is a parathyroid adenoma

A

Mass of chief cells distrusting Ca metabolism

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2
Q

What do chief and oxyphil cells:
- do and how
- look like

A
  • Chief cells secrete PTH allowed by tons of Golgi apparatus and ER
    They look smaller but more abundant with a paler stain
  • oxyphil cells increase with age- cause unknown
    They are larger but less abundant with a darker stain
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3
Q

Where does PTH synthesis begin
How much aa does it start out with
Where does it go and what happens to it
What element is a co factor

A
  • starts RER where pre- pro- PTH is produced which is 115 aa long (biologically active sequence, signal and pro sequence)
  • the signal is cleaned within ER lumen leaving pro- PTH
  • transferred to Golgi appertains where pro sequenced is cleaned to make PTH
  • Mg is a co factor
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4
Q

Explain the humural synthesis that allows PTH to increase Ca

A

Increases RANKL production on osteoblasts which induce cytokines to act on osteoclasts which increase bone reabsorption and increase Ca resorption in the loop of henle and DCT and increase phosphate excretion in the PCT which prevents kidney stones

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5
Q

What does PTH do when it stimulates 1- alpha- hydroxylase

A
  • increases calcitriol which induces calbindin D- 28K (Ca binding protein) in the intestine which is vital D depended and is how 1, 25- dihydroxycholecalcifiol increases Ca and phosphate absorption
  • Vit increases mineralisation of bone as well as
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6
Q

How is vit d (25 hydroxycholecalcifiol) formed and what is it bound to in plasma and how does it become 1,25 dihydroxycholecalcifiol

A
  • formed from cholecalciferol (D3)n in the liver
  • bound to alpha globulin in plasma
  • 1 alpha hydroxylase hydroxylases it
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7
Q

What is the negative feedback of Ca via chief cells and vit D

A

Chief cells have unique G protein CaR on surface which Ca binds ot when in excess which leads to phosphinositide production which prevents PTH secretion
- vit D/ calcitriol acts on parathyroid gland to decrease PTH gene transcription so less PTH synthesised

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8
Q

What is the action of calcitonin and is it short or long term

A
  • only long term
  • inhibits osteoclast bone resorption
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9
Q

What is the thyroid gland supplied and drained by

A
  • supplied by superior thyroid aa from ECA and inferior thyroid aa from SCA and thyrocervical aa
  • drained via superior and middle vv from IJV and inferior thyroid vv from brachiocephalic trunk
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10
Q

Where is calcitonin that decreases blood Ca secreted and where are they

A

Spaces between colloid filled follicles have parafollicular cells which secrete calcitonin which inhibits osteoclasts

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11
Q

What does follicle cells look like in hyper/ hypothyroidism

A
  • hyper look columnar with little colloid
  • hypo look flattened with large lumen of colloid
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12
Q

What is the function of thyroid gland with examples
Via what hormones acting on what receptors on target tissues
How is the desired effect achieved

A
  • metabolic regulators, gluconeogenesis, protein synthesis, lipogenesis
  • via T3 and T4 acting on nuclear receptors
  • achieved by increasing size and number of mitochondria within cells, increasing Na-K pump activity and presence on beta receptors in cardiac muscle
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13
Q

How does iodide get into follicular cells and then to colloid and what can act as competitive inhibitors

A
  • active transport via Na-I symportot thats more active with lower Iodide levels and is maintained via Na-KATPase
  • then to colloid via pendrin
  • comp inhibit is thiocyanase and penchorase
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14
Q

What os thyroglobulin, where is it formed and where does it go and what is it stored as

A
  • large protein rich in tyrosine and formed in follicular ribosomes and placed in secretory vesicles
  • exocytosis of thyroglobulin into follicle lumen where it is stored as colloid which acts as the scaffold of hormone synthesis
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15
Q

What happens to thyroglobulin as colloid and what enzyme helps and what happens to the products
What inhibits

A
  • Iodination and oxidation, making it reaction by TPO or thyroid peroxide into MIT (I at position 3) and DIT (I at position 3 and 5) mono/ dityrosine
  • MIT and DIT make T3 and DIT and DIT make T4
  • inhibited by I- (wolff chaikoff)
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16
Q

How does iodinated thyroglobulin get back into follicular cells and what happens to it

A

Endocytosis and proteolysis cleaves iodinated tyrosine residues releasing T3 and T4

17
Q

What are the potent y and half life of T3 and T4 and what are their solubility and what do they attach to in plasma
Where is T4 deiodinatied and what by

A
  • T3 is more potent but has a shorter half life
  • fat soluble and carried by albumin (and globulin)
  • deidinated by 5 prime- deiodinase in kidneys and liver
18
Q

How are thyroid hormones released

A

Hypothalamus releases TRH (thyrotropin releasing hormone) into hypopheaseal portal system to ant pit; binding to thyrotrophic cells which releases TSH to thyroid gland which realises T3 and T4

19
Q

When is thyroxine binding globlin inhibited from breaking down and due to what
When is it measured and why

A
  • pregnancy stops breakdown due to oestrogen increases thyroid synthesis stoping negative feedback
  • its measured as a T3 resins uptake test to access its circulating levels in case of decrease due to hepatic failure/ hyperthyroidism because of increased free thyroid hormones and decreased thyroid binding globulin as no new hormones are being synthesed