L5 Calcium homeostasis Flashcards
Why is hypocalcaemia dangerous?
Low calcium <2.15, makes neurones a lot more permeable to Na+ (Ca2+ competes with Na+)
Can cause seizures
Clinical Features of Hypocalcaemia
- Carpopedal Spasm (Trousseau’s sign)
- Chvostek’s sign
- Tetany
Consequences of Hypoalcaemia
Acute
- Thirst
- Polyuria
- Abdominal Pain
Chronic
- Constipation
- Musculoskeletal aches / weakness
- Neurobehavioral symptoms
- Renal calculi
- Osteoporosis
How are calcium levels controlled within a tight normal range?
Parathyroid chief cells are cells in the parathyroid glands which produce parathyroid hormone in response to low levels of calcium.
presence of CaSR sensitive to increase in calcium
How does magnesium levels influence PTH release?
low magnesium prevents PTH release
How does calcium release activate osteoclast
PTH>OSTEOBLAST>Rank Ligand>Rank=osteoclast activation
How is Primary Hyperparathyroidism
diagnosed?
- Serum Calcium increased
- Serum Phosphate reduced
- PTH increased
Complications of Hyperparathyroidism
- Osteoporosis
- Bone cysts
- Renal stones
Diagnosis Hypoparathyroidism
- Serum Calcium low
- PTH low / normal (primary or secondary)
Causes of Primary Hypoparathyroidism [4]
Iatrogenic
Autoimmune
Hypomagnesaemia
Genetic mutations
Causes of Secondary Hyperparathyroidism [4]
- Low / normal serum Calcium + HIGH PTH
- Low serum 25 OH vitamin D
- GI problems
- Renal Failure
Consequence of reduced vitamin D concentration
Rickets
Parathyroid Hormone
peptide hormones
Made by chief cells of the parathyroid gland
Secreted in response to low Ca2+ levels
-Chief cell contain receptors that are Ca2+ sensing
PTH release
Ca2+ sensing receptors on chief cells recognise low Ca2+ levels
- changes shape of the receptor
- Chief cells processes modified to release PTH in the presence of Mg2+
3 effects of PTH
- Efflux of calcium from bone
- decreased loss of Ca from urine
- increased absorption of calcium from GI
