10.3 Flashcards
(10 cards)
- What cellular imbalance drives bone loss in osteoporosis?
In osteoporosis, bone resorption by osteoclasts exceeds bone formation by osteoblasts.
- Which serum markers indicate bone formation and how do they respond to anabolic treatment?
Markers like P1NP (Procollagen type I N propeptide) increase with anabolic agents.
- Which serum markers indicate bone resorption and how do they respond to anti-resorptive therapy?
Markers such as CTX (C-terminal telopeptide) decrease with anti-resorptives.
- What distinguishes anti-resorptive treatments from bone anabolic treatments in osteoporosis?
Anti-resorptives reduce osteoclast activity, while anabolics stimulate osteoblast function to build new bone.
- What is the mechanism of action for bisphosphonates?
They bind to bone mineral and, when taken up by osteoclasts, impair their function and promote apoptosis.
- How does denosumab act as an anti-resorptive agent?
It is a monoclonal antibody that binds RANKL, preventing osteoclast formation, function, and survival.
- What is the mechanism of action of teriparatide, a bone anabolic agent?
Teriparatide (a PTH analog) given intermittently promotes osteoblast differentiation and activity, increasing bone formation.
- How does romosozumab work as an anabolic therapy?
Romosozumab blocks sclerostin, lifting its inhibitory effect on osteoblasts, thereby enhancing bone formation while reducing resorption.
- Why are these serum markers useful in monitoring osteoporosis treatment?
They reflect the balance between bone resorption and formation, allowing assessment of treatment efficacy.
- Why is it important to balance anti-resorptive and anabolic treatments in managing osteoporosis?
A balanced approach improves bone density and strength, effectively reducing fracture risk.
