S11 L1 part 2 - Parathyroid disorders Flashcards

1
Q
  • *Chronic hypercalcaemia**
  • Signs and symptoms
  • Does it cause neurones to become faster or suppressed?
  • Will patients die straight away from this?
  • Treatment
  • Some causes
A
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2
Q
  • *PTHrP**
  • What does this stand for?
  • What does it lead to?
  • Common in which condition (be specific)?
  • Why does PTHrp have this affect?
A

What does this stand for and lead to?
PTHrP: Parathyroid hormone related peptide (PTHrP) is a peptide produced by some neoplastic tumours which may lead to hypercalcaemia.
Common in which conditions?
It is commonly produced by patients with breast or prostate cancer, and occasionally in patients with myeloma.
Why does PTHrp have this affect?
It functions similarly to PTH, causing increased calcium release from bone, and reduced renal calcium excretion. The presence of hypercalcaemic symptoms can be a red flag for cancer.

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3
Q
  • *Hyperparathyroidism – Primary**
  • Causes
  • Leads to
A
  • *Causes:** One of the 4 parathyroid glands develop an adenoma and secrete excessive parathyroid hormone
  • *Leads to:** Hypercalcaemia and serum phosphate falls
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4
Q
  • *Hyperparathyroidism – Secondary**
  • Description
  • Cause
A

Description: The parathyroid glands become hyperplastic
Cause: Often, vitamin D deficiency. Vitamin D deficiency means that their calcium absorption is low resulting in low serum calcium levels. Chronic renal failure – due to failure of hydroxylation of 25(OH)D into 1,25(OH)2D (calcitriol) in the kidney
= both of these then causes PTH levels to rise (trying to compensate)

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5
Q
  • *Hypocalcaemia – general**
  • Signs and symptoms
  • Fatal?
  • Causes
A

Signs and symptoms:
Hyper-excitability of NMJ (Hypocalcaemia – leads to ‘excitable’ nerves – tingling, muscle tetany (spasms), even epilepsy)
- Lower serum calcium, causes increase Na+ entry into neurones, leading to depolarisation and increase likelihood of AP
- Pins and needles
- Tingling around mouths and finger
- Muscle spasms
- Paralysis
- Convulsions
DEADLY – FATAL!!
Causes:
- Total thyroidectomy patients and the parathyroid gland is accidentally removed
Symptoms can develop when serum calcium falls below 2.10mmol/L – symptoms can start within 6 hrs of thyroidectomy (must monitor patients after thyroidectomy for 6 hours)

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6
Q
  • *Rickets**
  • Age group
  • Cause
  • Mechanism leading to the rickets
  • Signs and symptoms
A

Age: Mainly affects children
Cause: Vitamin D deficiency
Mechanism leading to the rickets:
• This leads to poor calcium mobilisation (as vitamin D is involved in the movement of calcium from the gut to where it is needed)
Ineffective mineralisation
• Weakened bone development
• Soft bones

Signs and Symptoms:
• Shortened height and stature
• Painful to walk
• Characteristic bowed legs caused by the forces that have been exerted onto the legs when walking

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7
Q
  • *Osteomalacia**
  • Age
  • Cause
  • Mechanism leading to this condition
  • What can lead to vitamin D deficiency?
A

Age:
• ‘Rickets’ in the adult
Causes:
• Vit D deficiency, leading to poor Ca2+ mobilisation and ineffective mineralisation
• Leads to increased calcium resorption as calcium is difficult to get from food due to low vitamin D
All of the situations below can lead to vitamin D deficiency:
- Kidney disease
- Protection from sunlight - sunlight produces vit D (e.g. often see in women who wear a burqa)
- Surgery to Stomach and intestine (may affect absorption of calcium from food)
- Drugs – phenytoin prevents vit D absorption

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8
Q
  • *Osteoporosis**
  • 3 types and state the causes
A

Osteoporosis

  • Primary type 1 osteoporosis - due to increase in osteoclast number (post-menopausal women) -
    occurs in postmenopausal women
    loss of oestrogen after the menopause (oestrogen keeps the osteoclast number correct)
  • Primary type 2 osteoporosis - due to loss of osteoblast function (older people)
    • occurs in (older) men and women
    • due to loss of osteoblast function (senile osteoporosis)
    • loss of both oestrogen and androgen (these hormones are important in maintaining bone density)
  • Secondary osteoporosis (other factors):
    • result of drug therapy (i.e., corticosteroids, these drugs prevent the action of oestrogen and androgen)
    • processes affect bone remodelling malnutrition, prolonged immobilisation, weightlessness (i.e., with space travel)
    • metabolic bone diseases (i.e., hyperparathyroidism – action of PTH e.g. increases osteoclast activity, metastatic cancers as it could lead to the individual not producing enough oestrogen and androgen hormones)
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