Endocrine 8: parathormone Flashcards

1
Q

other names for Parathyroid hormone

A
  • Parathormone
  • PTH
  • Parathrin
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2
Q

Nature of Parathromone

A

polypeptide hormone –> 84aa

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3
Q

Mechanism of action of Parathormone

A

membranous receptors for Gs & Gq:
* Gs: adenyl cyclase —> increase cAMP
* Gq: Phospolypase C —> intracellular calcium —> Protein Kinase C

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4
Q

Describe effect of PTH on bone tissue

A

Rapid phase=Osteolysis= within minutes:
* binds to receptors of osteocyte of osteocytic membrane —> increase permiability to Ca2+
* Calcium pumps pump Ca2+ into ECM under the effect of Vit. D3 (1,25 DHCC)

Slow Phase= days/ weeks:
1. stimulates Osteblasts to release RANKL & IL-6
2. RANKL & IL-6 stimulates Osteoclast prolifertion
3. Osteoclast break down bone matrix, releasing Ca2+ & PO4- & hydroxyproline
4. they are then released into ECM

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5
Q

Describe effect of PTH on the Kidney:

A

Decrease phosphate reabsorption in PCT:
* Phosphaturic action
* Hypophosphatemia

PTH & decreased phosphate activate 1 alpha hydroxylase —> activated vitamin D3 (1,25 DHCC)

PTH + 1,25 DHCC:
* Increase Ca+ reabsorption in DCT
* Hypocalcinuria
* Hypercalcenemia

Increase magnesium reabsorption

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6
Q

Describe effect of PTH on intestines

A

along with 1,25 DHCC, they increase reabsorption of Phosphate & Calcium

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7
Q

state what happens to urine calcium in chronic excessive PTH

A

Hypocalciuria turns into Hypercalciuria

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8
Q

Describe regulation of PTH

A
  • Not under control of pituitary gland, instead by feedback mechanism of plasma Ca2+ concentration
  • when Phosphate level rises (the body need to increases Ca2+):
    1.increase PTH
    2.increased Phosphate –> Increase in FGF23 –> bind to FGF receptor of kindet —> decrease phosphate reabsorption in PCT & binds to FGF receptor of Parathyroid gland –> increase PTH secretion
  • Beta adrenergic stimulation –> increase cAMP in parathyroid gland cells –> increase PTH secretion
  • 1,25 DHCC inhibits PTH synthesis & secretion
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9
Q

Cause of primary hyperparathyroidism

A

Parathyroid tumor

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10
Q

Charactaristics of primary hyperparathyroidism

A
  • Hypercalemia
  • decreased Neuromuscular excitability
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11
Q

Causes of secondary hyperparathyroidism

A

Decreased calcium reabsorption:
* Vit. D diffeciency
* Malabsorption syndromes
* Decreased calcium intake
* Bariatric surgeories (GIT bypass)

Renal infufficiency:
causing phosphate retention (secondary decrase in calcium)

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12
Q

charactars of secondary hyperparathyroidism

A

Elevated PTH with normal to low serum Calcium

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13
Q

cause of tertiary hyperparathyroidism

A

long period of secondary hyperparathyroidism –>nodules independent and do not comply with feedback mechanism

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14
Q

lab results show:
* Low/ non changes plasma calcium
* High plasma PTH
* High phosphate

Diagnosis ?

A

secondary hyperparathyroidism

High Phosphate caused by phosphate retention in renal insufficinecy

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15
Q

lab results show:
* normal/high calcium
* High plasma PTH
* High phosphate

Diagnosis ?

A

teritary hyperparathyroism; despite high calcium nodules are independent and not complying with feedback

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16
Q

lab results show:
* High plasma calcium
* High plasma PTH
* Low phosphate

Diagnosis ?

A

primary hyperparathyroidism caused by parathyroid tumour

17
Q

Cause of hypoparathyroidism

A

Thyroidectomy error

18
Q

Manifestations of hypoparathyroidism

A

Tetany

19
Q

Site of calciumSR

A
  • Parathyroid glands
  • calcitonin secreting cells
  • kidneys
20
Q

CalciumSR acts as a:

A

Calciostat