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CLINICAL PATHOLOGY > Calcium and Phosphate Metabolism > Flashcards

Calcium and Phosphate Metabolism Flashcards

1
Q

Why is bone turnover important?

A

For homeostasis of serum calcium and phosphate

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2
Q

What affects the homeostasis of serum calcium and phosphate?

A
  • Parathyroid Hormone (PTH) = increases Ca2+
  • Vitamin D = Increases Ca2+
  • Calcitonin = Decreases Ca2+
  • FGF-23
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3
Q

What is the distribution of body calcium?

A

99% in the bone

1% intracellular

<0.1 extracellular (this maintains Ca2+ balance)

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4
Q

What maintains Ca balance?

A

Hormonal control of small extracellular fraction (<0.1%) of calcium

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5
Q

What is the composition of calcium in extracellular fluid?

A

Half is free (Ca2+) and physiologically active

Other half is protein bound (mainly albumin)

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6
Q

What is the distribution of phosphate?

A

85% of phosphate is in bone

Remainder is intracellular

Extracellular = H2PO4-, HPO4-

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7
Q

What are the clinical features of hypercalcaemia?

A

PAINFUL BONES, RENAL STONES, ABDOMINAL GROANS, PSYCHIC MOANS

  • Depression, fatigue, anorexia, nausea, vomiting
  • Abdominal pain, constipation
  • Renal calcification (kidney stones)
  • Bone pain
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8
Q

What are clinical features of severe hypercalcaemia?

A
  • Cardiac arrthymias
  • Cardiac arrest
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9
Q

What are the common causes of hypercalcaemia in ambulatory patients?

A

Primary hyperparathyroidism

  • e.g tumour within the thyroid gland
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10
Q

What is the most common cause of hypercalcaemia in hospitalised patients?

A

Hypercalcaemia of malignancy

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11
Q

What are less common causes of malignancy?

A

Hyperthyroidism/ excessive intake of vitamin D

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12
Q

What would the serum biochemistry look like in someone with hypercalcaemia?

A
  • Serum calcium = modest to marked increase
  • Serum phosphate = low to low normal
  • Serum alkaline phosphatase = 20% of cases due to increased bone turnover
  • Serum creatinine = May be elevated in long standing disease
  • Serum PTH = interpreted in relation to calcium
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13
Q

What does high alkaline phosphatase indicate?

A

Increase in bone remodelling

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14
Q

What is the function of PTH?

A

Secreted when blood calcium levels drop to prevent hypocalcaemi

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15
Q

What are the main actions of PTH?

A
  • Promote release of Ca and Pi from bone
  • Increases renal Ca reabsorption from DCT
  • Decreases renal Pi reabsorption fromo DCT (increases excretion)
  • Upregulates 1 alpha hydroxylase activity activating vitamin D
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16
Q

What are the main actions of PTH on bone?

A
  • Will promote bone remodelling
  • PTH receptors are present on osteoblasts and pre-osteclasts
  • PTH will bind to osteoblast receptors activating pre-osteoblasts via RANKL and OPG inhibition (normally inhibits RANK)
  • Osteoclasts will absorb bone and release more calcium and phosphate
17
Q

How does PTH regulate itself?

A

As free Ca2+ levels are low serum PTH levels rise, as free Ca2+ levels are high serum PTH levels decrease.

18
Q

What is hypercalcaemia of malignancy?

A

Most common cause of hypercalcaemia in HOSPITALISED PATIENTS

  • humoural e.g lung carcinoma secreting PTHrP (PTH related peptide)
  • Metastatic
  • Haematological (e.g myeloma)
19
Q

What is the most common cause of hypocalcaemia?

A
  • Vitamin D deficiency
  • Renal failure
20
Q

What is a less common cause of hypocalcaemia?

A

Hypoparathyroidism

21
Q

What can vitamin D deficiency result in?

A

Rickets (in children)

  • failure in bone mineralisation and disordered cartilage formation

Osteomalacia (in adults)

  • Impaired bone mineralisation (soft bones)
22
Q

What are features of osteomalacia?

A
  • Bone pain
  • Waddling gait, muscle weakness
  • On X-ray, stress fractures
23
Q

What is the serum biochemistry of osteomalacia?

A
  • Low/normal calcium
  • Hypophosphataemia
  • Raised alkaline phosphatase
  • Secondary hyperparathyroidism (the low calcium would stimulate PTH release)
24
Q

What is osteoporosis?

A

Loss of bone mass/density due to the thinning of both cortical bone and trabecular mesh

25
Q

What are some causes of osteoporosis?

A
  • Endocrine
  • Malignancy
  • Drug-induced
  • Renal disease
  • Nutritional
  • Age
26
Q

What is the difference between osteoporosis and osteomalacia?

A

Osteoporosis

  • Loss of bone mass/ density

Osteomalacia

  • Loss of bone mineralisation
27
Q

First sign of osteoporosis

A

Sustaining a fracture, usually:

  • Wrist
  • Neck of the femur
  • Intervertebral
28
Q

How do we diagnose osteoporosis?

A

Dual Energy X-Ray Absorptiometry Scan (DEXA)

  • Measures bone mass density
29
Q

How does DEXA work?

A
  • Bone mineral density is at its peak in a young adult (25 years old)
    • after it will slowly decline
  • With DEXA we will achieve a T score by taking the average bone density for a young adult and then interpreting your bone mineral density score in relation
    • T score = Number of standard deviations below average bone mineral density for a young adult at peak bone density (- 25yo)
30
Q

Endocrine causes of osteoporosis

A
  • Hypogonadism = notably any cause oestrogen deficiency
  • Excess gluocorticoids - endogenous or exogenous
  • Hyperparathyroidism
  • Hyperthyroidism
31
Q

What are the treatments of osteoporosis treatments?

A
  • · Hormone Replacement Therapy- effects well established but safety of long-term treatment has been questioned
  • Bisphosphonates
    • · Inhibit function of osteoclasts (e.g. risedronate, alendronate)
  • PTH Analogues
    • · Intermittent doses of PTH promote good bone remodelling- not an excess of osteoclast over osteoblast activity (whereas raised prolonged doses of PTH tend to favour osteoclast activity for bone reabsorption)
  • Denosumab
    • · Antibody against RANK ligand
  • Romosozumab
    • · Antibody against sclerostin protein (which usually inhibits osteoblast differentiation)
    • Ensure adequate calcium and vitamin D intake, appropriate exercise

CLINICAL PATHOLOGY (52 decks)

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