Bones

Question 1

What are the major proteins making up the bone matrix?

Answer 1

Type 1 collagen. Also proteoglycans and phosphoproteins.

Question 2

What is the mineral found in the bone matrix called?

Answer 2

Hydroxyapatite - calcium phosphate crystals.

Question 3

Name the cell involved in bone resorption.

Answer 3

Osteoclast, derived from monocytes.

Question 4

Name the cell involved in bone formation.

Answer 4

Osteoblasts.

Question 5

Which hormone stimulates osteoclastic activity, and which cell does it act through?
Where is it released from?

Answer 5

Parathyroid hormone (acts via PTH receptors on osteoblasts).
Released from chief cells in the parathyroid glands.

Question 6

Which hormone inhibits osteoclasts and where is it released from?

Answer 6

Calcitonin, released from parafollicular cells in the thyroid gland.

Question 7

What is another name for the bone matrix?

Answer 7

Osteoid.

Question 8

Which hormones promote bone growth?

Answer 8

Growth hormones, male and female sex hormones (oestrogen and androgens), thyroid hormones.

Question 9

How does calcium exist in circulation?

Answer 9

Ionic form - Ca2+
Bound to plasma proteins
Combined in unionised salts with citrate and phosphate

Question 10

Name the hormones that regulate calcium levels.

Answer 10

Parathyroid hormone, calcitonin.

Question 11

Name three physiological processes requiring calcium.

Answer 11

Blood coagulation
Nerve impulse transmission (exocytosis in presynaptic terminal)
Muscle contraction (excitation-contraction coupling)
Enzyme regulation

Question 12

Where is calcium absorbed from?

Answer 12

The duodenum and jejunum, stimulated by 1,25-(OH)2 vitamin D3.

Question 13

State three factors which can alter calcium absorption.

Answer 13

A deficiency of vitamin D (osteomalacia).
A decrease in oestrogen levels due to the menopause.
Age-related decrease in Ca2+ absorption from the gut.

Question 14

How is vitamin D synthesised?

Answer 14

7-dehydrocholesterol in the skin is converted to vitamin D3 (cholecalciferol), which is the converted to 25-(OH) vitamin D3 in the liver by 25-hydroxylase. This is then converted to 1,25-(OH)2 vitamin D3 in the kidneys by 1alpha- hydroxylase.
It is broken down to 1,24,25-(OH)3 vitamin D3 by 24-hydroxylase in the liver.

Question 15

What are the physiological actions of parathyroid hormone?

Answer 15

PTH increases Ca2+ levels in the plasma by:
Increasing osteoclastic activity to increase Ca2+ and (HPO4)2- in the blood.
Increasing Ca2+ reabsorption by the kidneys, and increasing phosphate excretion by kidneys.
Increasing the formation of vitamin D3, which increases the absorption of Ca2+ from the duodenum and jejunum.

Question 16

What are the physiological actions of calcitonin?

Answer 16

Calcitonin decreases plasma Ca2+ by increasing mineralisation of bone.
Calcitonin stimulates osteoblastic activity.
Inhibits osteoclasts.
Increases Ca2+ excretion by kidney.

Question 17

What are the physiological actions of vitamin D3?

Answer 17

Increases absorption of Ca2+ and (HPO4)2- from the intestine.
It induces marrow monocytes to form osteoclasts.
High 1,25-(OH)2 vitamin D3 levels stimulate 24-hydroxylase activity in the liver so vitamin D toxicity is prevented.

Question 18

What is secreted cancer cells and causes hypercalcaemia?

Answer 18

Parathyroid hormone-related protein.

Question 19

What’s the difference between primary hyperparathyroidism and secondary hyperparathyroidism?

Answer 19

Primary hyperparathyroidism is too much secretion of parathyroid hormone (e.g due to a parathyroid adenoma) which causes hypercalcaemia.
Secondary hyperparathyroidism is a physiological response to hypocalcaemia and produces similar symptoms.

Question 20

What elevates alkaline phosphatase levels?

Answer 20

Osteomalacia and rickets.

Question 21

Name some treatments of osteoporosis.

Answer 21

Bisphosphonates.
HRT.
Calcium supplements.
Selective oestrogen receptor modulators - SERMs (which only bind to oestrogen receptors in bone

Question 22

Describe the 5 stages of fracture repair.

Answer 22

1) Haematoma forms - broken blood vessels leak blood which forms a clot and impedes circulation at the fracture site, this leads to some bone cells dying, and inflammation as osteoclasts and phagocytes clear away dead cells.
2) Subperiosteal and endosteal cell proliferation - fibroblasts from periosteum invade fracture site and begin producing collagen fibres. Cells in the periosteum and endosteum develop into chondroblasts and begin forming fibrocartilage to produce the fibrocartilaginous (SOFT) callus.
3) Woven bone callus - in areas close to the well-vascularised bone tissue, osteoprogenitor cells develop into osteoblasts which produce trabecular which join up the living and dead bone. Fibrocartilage is converted to spongy bone to form a HARD callus.
4) Consolidation of woven bone to lamellar bone - more organised compact bone replaces the spongy bone, but this can only really happen when the bone in load bearing, so it knows where to resorb and where to build bone.
5) Remodelling - osteoclasts resorb fragments of broken bone, and compact bone replaces spongy bone. Only a thickened area on the bone surface remains as evidence of fracture.