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2a > Parathyroid and calcium disorders > Flashcards

Parathyroid and calcium disorders Flashcards

1
Q

What is hypocalcaemia?

A

Low calcium in the blood.

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2
Q

How is serum calcium regulated?

A

When serum calcium decreases, PTH secretion from the parathyroid gland increases. This increases calcium by 3 mechanisms: increased bone resorption, increased gut absorption, and increased reabsorption in the kidney.
(lecture 24.4.18)

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3
Q

How is serum phosphate regulated?

A

PTH decreases phosphate reabsorption in the kidney, decreasing serum phosphate.

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4
Q

What can be the result of a small decrease in serum calcium?

A

A big increase in PTH. A small increase in calcium can cause a big decrease in PTH.

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5
Q

Give an example of a disorder in which there is an appropriate increase in PTH.

A

Vitamin D deficiency. This causes malabsorption of calcium, so serum Ca falls, which triggers an increase in PTH.

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6
Q

Give an example of a disorder in which there is an appropriate increase in PTH.

A

Primary hyperparathyroidism. This is where the thyroid gland does not produce enough PTH.

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7
Q

Give an example of a disorder in which there is an appropriate decrease in PTH.

A

Hypercalcaemia of malignancy. Eg in myeloma or leukaemia, there is bone breakdown, releasing calcium into the blood.

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8
Q

Give an example of a disorder in which there is an inappropriate decrease in PTH.

A

Primary hypoparathyroidism.

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9
Q

How does hypocalcaemia cause muscle spasms and cardiac dysfunction?

A

Resting state of neurons is stabilised by Ca, which prevents spontaneous depolarisation. Hypocalcaemia causes Na channel instability, so the cell depolarises more quickly, and the cell is more excitable. This causes muscle spasms and cardiac changes eg prolonged QT interval and arrhythmias.
(Osmosis, lecture)

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10
Q

What is the result of high intracellular ca?

A

Apoptosis.

osmosis

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11
Q

Give a sign of hypocalcaemia.

A

Chvostek’s sign: facial spasm when facial nerve tapped.

Trousseau’s sign: beak shaped hand when blood pressure cuff inflated.

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12
Q

What can cause hypocalcaemia?

A
  1. Hypoparathyroidism. This can be due to Di George immunodeficiency syndrome.
  2. Renal failure, causing decreased reabsorption of calcium
  3. Hyperalbuminaemia - albumin binds to Ca so less free ca.
    (osmosis, lecture)
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13
Q

How is hypocalcaemia diagnosed?

A
  1. Ca2+ <8.5mg/dL

2. ECG changes: prolonged QT interval, arrythmias

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14
Q

What is pseudohypoparathyroidism? Give the pathophysiology and main features.

A

Resistance to PTH. Therefore there is:
decreased Ca absorption and reabsorption in the intestine and kidney
increased bone resorption of Ca
increased renal phosphate reabsorption
PTH continues to increase in a positive feedback loop. Results in a short 4th metacarpal.

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15
Q

What are 3 actions of 1-a, 25-hydroxyl vit D?

A
  1. Increases calcium and phosphate absorption in the intestine.
  2. Increases bone mineralisation
  3. Induces immune and tumour cell differentiation
  4. Inhibits tumour angiogenesis and proliferation.
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16
Q

What can cause secondary hypoparathyroidism?

A

Radiation, surgery, hypomagnesaemia (Mg is required for PTH secretion).

17
Q

Describe the management of hypocalcaemia.

A

Primary hypoparathyroidism: Give Ca2+ supplements and calcitriol or PTH.
(OHCM)

18
Q

What can cause hypercalcaemia?

A
  1. Most commonly: malignancy - tumour releases PTH-related protein, causing increased osteoclast activity and osteoblast death.
  2. Primary hyperparathyroidism - PTH increases osteoclast activity.
  3. Sarcoidosis
19
Q

What else could cause raised calcium in the blood sample other than true hypercalcaemia?

A

Tourniquet left on for too long

Sample left too long and haemolysed

20
Q

Give 3 clinical features of hypercalcaemia and explain briefly why they occur.

A

Polydipsia/thirst, due to polyuria due to leakage of calcium into the blood (hypercalciuria).
High Ca inhibits Na channels so neurone less likely to depolarise - slow muscle contraction -> constipation
Confusion/coma, slow reflexes, short QT interval
Nausea, abdominal pain
Fatigue
Depression
(bones, groans, moans, stones)

21
Q

Give 3 complications of hypercalcaemia and explain why they occur.

A

Renal stones - hypercalciuria and polyuria
Cardiac arrest - High Ca inhibits Na channels so neurone less likely to depolarise - slow muscle contraction
Ectopic calcification (excess ca)
Hypertension

22
Q

Give an iatrogenic cause of hypercalcaemia.

A

Thiazide diuretics - increased renal Ca reabsorption in the distal tubule.
Excess vitamin D supplements

23
Q

What investigations would you do for hypercalcaemia?

A

Determine cause:
Malignancy: low albumin, alkalosis, high phosphate (due to low PTH)
Hyperparathyroidism: high PTH.
FBC, CXR, bone scan.

24
Q

Describe the management of hypercalcaemia.

A

Treat underlying cause. If Ca2+>3.5mmol/L:

  1. Hydrate with IV 0.9% saline
  2. Bisphosphonates to prevent bone resorption. Eg, zolendronic acid.
  3. Chemotherapy for malignancy, steroids for sarcoidosis.
25
Q

What causes primary hyperparathyroidism?

A

80% solitary benign adenoma

20% hyperplasia of all glands, rarely malignant

26
Q

Give 3 clinical features of primary hyperparathyroidism.

A

Polydipsia/thirst, due to polyuria due to leakage of calcium into the blood (hypercalciuria).
High Ca inhibits Na channels so neurone less likely to depolarise - slow muscle contraction -> constipation
Confusion/coma, slow reflexes, short QT interval
Nausea, abdominal pain
Fatigue
Depression
(bones, groans, moans, stones)

27
Q

What investigations would you do for PHPT?

A

Ca, PTH - raised.
Raised ALP from bone activity
Imaging: bone lesions eg pepperpot skull.

28
Q

Describe the management of PHPT.

A
  1. increase fluid intake to prevent stones,
  2. avoid thiazides and excessive Ca/ Vit D
  3. Excision of adenona/ 4 glands (depending on cause) if needed.
29
Q

Give 3 causes of secondary hyperparathyroidism.

A

Chronic kidney disease.
Malabsorption - eg chronic pancreatitis.
Insufficient vitamin D intake.

30
Q

What is the pathophysiology of secondary hyperparathyroidism due to CKD?

A

The kidneys do not convert enough vitamin D to its active form, and do not excrete enough phosphate. This causes insoluble calcium phosphate to form in the body and remove calcium from the circulation.

31
Q

Describe the management of secondary hyperparathyroidism.

A
  1. Correct causes
  2. Phosphate binders (increase absorption of phosphate).
  3. Vitamin D supplements
32
Q

What would calcium levels be like in SHPT and why?

A

Low, because kidney disease causes formation of calcium phosphate, the process of which removes Ca from the blood, which causes hyperparathyroidism.

33
Q

Describe the pathophysiology of tertiary hyperparathyroidism?

A

Prolonged secondary hyperparathyroidism causes glands to undergo hyperplasia and act autonomously, causing very high PTH levels. This causes serum Ca to increase. It is seen in CKD.

2a (75 decks)

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