Pathophysiology of Bone Disorders and Osteoporosis Flashcards
what happens to bones as we age?
they become thinner and weaker
what is Wolff’s law?
Every change in function of bone is followed by certain definite changes in its internal architecture and its external conformation.
how does the parathyroid hormone regulate calcium?
it increases calcium levels by:
- Stimulating osteoclasts to degrade bone and release Ca2+ into blood
- Increasing intestinal absorption of calcium
- Decreases calcium excretion at kidneys
what is secreted from the thyroid gland to reduce calcium ion levels and how does it do this?
Calcitonin is secreted and it reduces calcium ion levels by:
- inhibiting osteoclast activity
- increasing calcium excretion at kidneys
what effect does a rise in blood calcium have on the thyroid gland to then reduce calcium levels?
It triggers the thyroid to release calcitonin which then stimulates Ca2+ salt deposit in bone
what is the most common cause of Rickets/Osteomalacia?
severe, prolonged vitamin D deficiency
what is the pathogenesis of rickets?
- normal bone is formed
2. the body can not fully mineralize the newly formed osteoid tissue, resulting in decreased bone strength
how is rickets treated?
with high-doses of vitamin D
what are the main areas affected by Paget’s disease?
skull, spine, pelvis, femur, and tibia
what is the pathogenesis of Paget’s disease?
- An accelerated bone formation does not allow for proper layering of collagen leading to disorganized or woven collagen.
- this causes reduced mineralization causing spotty weakening of bone
how is Paget’s disease treated?
- Bisphosphonates as they work directly on osteoclasts to slow down bone turnover, allowing more time for proper bone formation
- Subcutaneous or intramuscular calcitonin can be used if bisphosphonates therapy is contraindicated.
which two hormones help maintain bone mass to prevent osteoporosis?
Estrogens and androgens
what is postmenopausal osteoporosis (type I)?
When oestrogen deficiency causes:
• increased proliferation and activation of osteoclasts
• prolongs survival of osteoclasts
Therefore more bone breakdown
what is senile osteoporosis (type II)?
Bone loss due to:
• increased bone turnover
• Malabsorption
• Mineral and vitamin deficiency
what is used to diagnose osteoporosis?
Bone mineral density (BMD)
where are Bone mineral density (BMD) measurements usually taken?
at lumbar spine and hip
what does a T score between -1 and -2.5 indicate?
osteopenia
what does a T score equal to or less than -2.5 indicate?
osteoporosis
what does a T score less than -2.5 with a fracture indicate?
established osteoporosis
what is the active form of vitamin D?
1,25-(OH)2-D = calcitriol
where is RANKL released from and what does it do?
- secreted by osteoblasts and bone marrow stromal cells
- mediates osteoclast differentiation, activation, and survival and primary mediator of bone resorption.
what does Osteoprotegerin (OPG) do?
provides alternative binding site for RANKL acting as decoy receptor, so it cannot activate osteoclast cellular signalling preventing bone resorption/breakdown
