Calcium Flashcards
What maintains calcium homeostasis
- regulated ion transport by GIT , bone and kidneys
How is calcium in the body , where is it absorbed and where is it excreted
1- intake from diet
2- absorbed in small intestine
3- excreted in kidneys
What is the main site of calcium storage
- bone
What is the purpose of the exchangeable calcium pool on bone surface
- buffers acute changes in calcium load depravation
Does ICF or ECF have a higher calcium concentration
- ECF
- even though there is more calcium in body cells than in ECF , ICF of one cell has a lower calcium concentration
What is free calcium
- metabolically active calcium
- calcium that causes physiological effect
- diffusible
Other than free calcium what are the other forms of calcium
1- diffusible bound to ions
2- non-diffusable bound to albumin or globulin
What are the two important variables to measure with calcium serum levels
1- Albumin concentration : increase = increase of calcium
2- PH : change equilibrium of albumin calcium complex
What happens to calcium when albumin concentration is low
- higher percentage of total serum calcium will be free and metabolically active
- so patient might not show signs of hypocalcaemia
What happens to albumin and calcium when PH decreases
- H ions increase , displacing Ca from albumin molecule
- increased amount of free calcium
What are the physiological functions of calcium ( 9 )
- bone and teeth
- glycogen metabolism
- protein metabolism
- plasma membrane integrity
- coagulation
- nerve and cardiac excitability
- muscle contraction
- gene regulation
- cell differentiation
How is Ca2+ homeostasis controlled
1- vitamin D :
2- parathyroid hormone : parathormone
3- calcitonin
- all acting on bones , gut and kidneys
What are the two names of active vitamin D
- 1,25-dihydroxycholecalciferol
- calcitriol
Are the parathyroids in the thyroid gland
- no they are separated by a capsule tissue
How many functional parathyroid glands are essential
- at least half of one parathyroid gland is needed for body to function
Explain the manufacturing and release of parathyroid hormone
- when calcium levels are low , calcium sensing receptors on chief cells will detect low levels
- stimulate parathyroid hormone secretion
What are the regulators of Parathyroid hormone
1- low Calcium
2- high phosphate
3- low magnesium
Explain the actions of the Parathyroid hormone ( PTH )
Bone :
1- short term rapid exchange from bone pool to ECF
2- long term resorption through osteoclasts
Kidney :
1- reabsorption of calcium
2- excretion of phosphate
3- formation of 1,25-dihydroxycholecalciferol
Intestine :
1- calcium absorption
Describe the relationship between serum calcium concentration ( ionized ) and PTH secretion
- low ionized calcium = high PTH levels
- this will cause ionized calcium levels to increase until a point where PTH becomes reduced due to calcium levels becoming normal
What is the relationship between calcium and phosphate and why
- reciprocal relationship
- as one increases the other decreases
- product of calcium and phosphate is insoluble so to prevent that from happening it’s reciprocal
Sources of vitamin D in diet
- animal derived sources
- ex: eggs, milk , cheese , tuna
How is vitamin D synthesized
- 7-dehydrocholesterol ( precursor molecule ) will interact with UV light to form vitamin D3 in skin
- converted to active 1,25-dihydroxycholecalciferol form in kidneys
- parathyroid hormone activates vitamin D in kidneys in PCT through enzyme 1 alphahydroxylase
What are the actions of Vitamin D activation ( 5 )
1- Works on intestinal epithelium :
- upregulates calcium binding protein channel production
- increases calcium stimulated ATPase production
- increase alkaline intestinal phosphatase levels
2- calcium reabsorption in kidney
3- calcification and mineralization in bone
Overall effect : increases plasma calcium concentration
4- Immune response , reproduction , cell differentiation
What regulates the production of Vitamin D
1- PTH
2- low phosphate levels
What mediates the actions of Vitamin D
- Vitamin D receptor that’s in the nucleus and membrane of cell
Explain Rickets and Osteomalacia and the causes
Deficiency of Vitamin D
1- lack of dietary vitamin D or sunlight
2- malabsorption of fats ( vitamin D is fat soluble )
3- failure to form calcitriol ( chronic renal failure )
4- mutation of 1alpha-hydroxylase
5- mutations in VDR
What is the difference between Rickets and Osteomalacia
- rickets is in children while osteomalacia is in adults
Effects of Rickets disease
1- Bowing outworks bones in legs
- lack of VD = lack of bone calcification and mineralization
-bones will be soft since calcium is what makes bones hard
- bones won’t be able to handle weight of torso
2- Teeth cavities
- due to teeth being soft
What is the difference between osteoporosis and osteomalacia
- in osteoporosis, bone material itself is normal but there is just too little of it
- in osteomalacia, the bone material is abnormal since it hasn’t been mineralized properly so it’s soft
People at risk of Vitamin D deficiency
1- Elderly
2- housebound people ( nursing homes or extended hospital stays )
3- people with darker skin since they require more sun exposure to make Vitamin D
How is calcitonin produced
- produced in thyroid glands by c-cells ( parafolicular cells)
- increase in calcium levels = increase calcitonin secretion = inhibits osteoclastic activity = reducing bone resorption = decrease blood climb levels
What regulates calcitonin levels
- high calcium levels
Is calcitonin important
- not very important in humans
How oestrogen and testosterone influence bone
- decrease bone resorption
- increase synthesis of protective substance preventing osteoclasts
- increase 1alpha-hydroxylase
How GTH influence bone
- stimulate bone synthesis
How TH influence bone
- increase bone turnover
- excess can lead to osteoporosis
How prolactin influence bone
- increase renal Ca reabsorption and 1alpha-hydroxylase
How Glucocorticoids influence bone
- increase bone resorption and decrease bone synthesis
How inflammatory cytokines influence bone
- increase bone resorption
When is peak bone mass attained and when is it lost
- 20s and maintained until 40s
- bone is lost after 50 at 1% per year and even faster in women
What is the abnormal calcium levels
greater than 3.5 or less than 1.9
Explain what Hypocalcaemia is and its causes
- low serum calcium
- causes : hyperparathyroidism, pseudohypoparathyroidism, vitamin D deficiency
What is pseudohypoparathyroidism and hyperparathyroidism
- hyperparathyroidism: usually due to removal while undergoing thyroidectomy
- pseudohypoparathyroidism: receptor problem causes body resistance to PTH
How is Hypocalcaemia diagnosed ( explain two methods in detail )
- Chvostek’s sign to diagnose neuromuscular excitability followed by tetany : low Ca makes it easier for Na to enter cells = easy depolarization
- Trousseau’s sign which is done by inflating sphygmomanometer above SBP which results to muscle contraction and flection of wrist and metacarpal joints
Explain what Hyperparathyroidism is and its causes
- increase in PTH levels
- causes : primary hyperparathyroidism , secondary hyperparathyroidism , tertiary hyperparathyroidism
What causes primary , secondary and tertiary hyperparathyroidism
- primary : problem with parathyroid , cancer
- secondary : low calcium level due to kidney failure
- tertiary : chronic secondary hyperparathyroidism where parathyroid glands keep secreting PTH
What are the clinical signs of Hyperparathyroidism
1- bone pain
2- kidney stones
3- GI disruption
4- CNS disturbances
What is a big diagnostic sign to distinguish between Hypercalcaemia and Hypocalaemia
- Hyper : short QT interval
- Hypo : long QT interval
