L14 Control of Calcium Metabolism Flashcards Preview

Physiology > L14 Control of Calcium Metabolism > Flashcards

Flashcards in L14 Control of Calcium Metabolism Deck (17)
Loading flashcards...

Learning Outcomes (for general perusal)

  1. Distinguish between free and total serum Ca2+
  2. In Ca2+ homeostasis, describe the role of: vitamin D, parathyroid hormone, calcitonin, bone, the kidneys, the gut
  3. Show how other hormones affect bone
  4. Relate the pathology of bone to Ca2+ homeostasis
  5. Explain the effects of hypercalcaemia and hypocalcaemia


How is calcium homeostasis maintained?

as a result of tightly regulated ion transport by the GIT, bone & the kidneys


Outline Calcium Balance in the body 

Balance between Bone Intestine and Kidney with ECF Ca2+ at the centre


1. What are normal calcium blood levels?

2. In what form is it?


3. What are two important variables?

1. 2.35-2.55 mmol/l

2. Can be split into two pools


  • Ionised Calcium (50%)
  • Bound to anions (5%)

Non-Diffusible Protein Bound

  • Bound to albumin (35% )
  • Bound to globulin (10%)

3. Albumin concentration eg.dehydration - an artificially high level of albumin is created

     pH - If acidotic (low pH), competition between H+ and calcium for albumin. Will increase free calcium levels in the blood.


What is the importance of Calcium in the body?

  • cell division
  • cell adhesion
  • plasma membrane integrity
  • protein secretion
  • muscle contraction
  • neuronal excitability
  • glycogen metabolism
  • coagulation

eg. Muscle contraction - Cardiac and smooth muscle need a rise in extracellular calcium to take place.

Reduction in ECF level, Cardiac muslce and smooth muscle will have reduced ability to contract


What is body calcium regulated by?

  • Parathyroid Hormone (PTH)
  • Vitamin D
  • Calcitonin (not as much of a role in humans)


Parathyroid Hormone

  1. What causes it's release?
  2. What are it's actions?

1. Low calcium levels - detected by chief cells in parathyroid glands


 Bone: Calcium resorption by osteoclasts

Kidney: reabsorption of Ca

  - excretion of PO4 (Reciprocal relationship between PO4 & Ca to avoid precipitaion of calium phosphate)

  - formation of 1,25-dihydroxycholecalciferol





  1. What is the formula of active vitamin D
  2. What is the name?
  3. What regulates it's active form?
  4. What are it's actions?

  1. 1,25(OH)2D
  2. 1,25-dihydroxycholecalciferol or calcitriol
  3. PTH, Low PO4
  4. Intestine: enhances Ca absorption (increases Ca transport proteins – calbindin-D proteins)

    Kidneys: facilitates Ca absorption

    Bone: increases calcification & mineralisation (essential for normal osteoblast differentiation & function)


  1. What is the inactive type of vitamin D in the skin called?
  2. What is the main storage form of the cholecaliferol?
  3. How does PTH bring about an activation of the storage form of vitamin D?
  4. What is the main site of activation of the storage vitamin D?
  5. What switches of the production of PTH in the negative feedback?
  6. How does the active 1,25-dihydroxycholecalciferol act?

  1. Cholecaliferol (inactive vitamin D3)  
  2. 25-hydroxycholecalciferol
  3. increases expression of regulatory enzyme 1-alpha-hydroxylase, activates to 1,25-dihydroxycholecalciferol
  4. Kidneys
  5. Chief cells in parathyroid gland
  6. At intestinal epithelium to increase calcium-binding protein, calcium-stimulated ATPase, and alkaline phosphatase, all resulting in the intestinal absorption of calcium and an increase in the plasma calcium ion concentration -- negative feedback loop will then act.


What are the causes of Rickets (children) and Osteomalacia (in adults)?

Lack of dietary Vit D &/or sunlight (UV)

Malabsorption of fats

Failure to form calcitriol – can be due to chronic renal disease

Less mineralisation of bone as a result


Seen mostly in long bones (where the weight of the body is supported)

 N.b In osteoporosis – density is diminished, yet a normal bone

Osteomalacia – soft, bones actaully bent.


Children's Vitamin D levels are worse than in previous years. A change in public health policy is required.’

He added: 'We believe that a more robust approach to statutory food supplementation with vitamin D, for example in milk, is needed in the UK



What can Vitamin D be obtained from?

Can be made in skin under UV light

can take it in in the food and unsupplements, diary products, potatoes, eggs, cheese, oily fish.



  1. What is it produced by?
  2. What is it's regulator?
  3. What are it's actions?

(not particularly important in adults, no known pathological deficiency)

1. Parafollicular cells (C cells) in thyroid gland

2. High Calcium


Bone: inhibits resorption

Kidneys: increases Ca excretion



Other hormonal influences on bone

What are the actions of each of the following? What do excesses cause?

  1. GH, IGFs
  2. Thyroid Hormone
  3. Glucocorticoids
  4. Oestrogen and Testosterone
  5. Prolactin


  1. Promotes positive Ca balance, Gigantism

  2. essential for normal bone maturation in utero, osteoporosis

  3. Small amounts essential for normal bone development, osteoporosis

  4. Increase bone formation

  5. Increases Ca absorption


Give an overview of calcium balance

  1. What are the mechanisms behind hypercalcaemia?
  2. What are the mechanisms behind hypocalcaemia?

  1. Increased GI absorption, Increased bone resorption, decreased bone mineralisation, decreased urinary excretion
  2. decreased GI absorption, decreased bone resorption, increased bone mineralisation, increased urinary excretion.



  1. What is it?
  2. What are the causes?
  3. What are the clinical signs?
  4. Which sign is the earlier one, and diagnostic?
  5. Why does tetany occur?

  1. A fall in serum Ca2+
  2. Hypoparathyroidism (decreased PTH)

    Pseudohypoparathyroidism (postR resis)

    Vitamin D Deficiency

  3. Chvostek's Sign - tapping on face just ant to ear below zygomatic bone will cause twitching of the ipsilateral facial muscles, suggesting neuromuscular excitability caused by hypocalcaemia                                                           Trousseau's Sign - Inflating a sphyg cuff above systolic BP for several minutes will give muscular contraction including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm suggesting neuromuscular excitability caused by hypocalcaemia 

  4. Trousseau's Sign

  5. Low ECF levels – cell membranes become more permeable to sodium ions. HypoC allows Na to enter cells, brings resting membrane potential close to threshold, can fire. Can cause numbness, pins and needles (sensory neurons affected) Sponatnous contraction of muscles (motor neurons affected) – in the most severe cause can cause tetany. 



  1. What is it?
  2. What are the causes?
  3. What are the clincal signs?

1. A rise in serum Ca2+

2. Hyperparathyroidism (increased PTH levels)

Secondary Hyperthyroidism (GI tract problems, Kidney failure, reabsorption issues)

3. Bones, Stones, Groans and Moans

Bones- Bone disease eg Osteoporosis, osteomalacia

Stones- Kidney stones

Groans- GI Disruption eg. abdominal pain, peptic ulcer, lack of appetite, constipation 

Moans- CNS Disturbance - depression of nerves, muscle weakness, lethargy, cardiac conduction abnormalities


Summary (for general perusal)

Decks in Physiology Class (46):