Lec 17: Osteoporosis, Renal Osteodystrophy, Hyperparathyroidism Flashcards
OSTEOPOROSIS
Primary vs Secondary
What is the mechanism in Menopause vs Aging
What is the most affected bone in postmenopause vs in senile osteoporosis?
Clinical features of post menopausal vs senile?
Prevention?
Increased porosity of the bones & reduced bone mass
Primary - post menopausal & senile
Secondary - endocrine disorders (ex: cushing), metastasis, GI, rheum, drugs
In menopause, there is
decreased serum estrogen
increased IL-1, IL-6, TNFa
increased expression of RANK/RANKL
increased osteoclast activity
= - estrogen and + everything else
the osteoblast displays the RANK-Ligand which binds to RANK (induced by NF-kB) on an osteoclast precursor—> differentiation into an osteoclast is stimu by IL1/IL6/TNFa—> bone degradation
Senile - caused by everything to do with osteoblasts thriving is now decreased along with reduced physical activity
Menopause = cancellous compartment of vertebral bodies (compression fx) = trabecular thinning
Senile = Cortical thinning and widened Haversian systems
Post menopausal osteoporotic symptoms: back pain, shortening of stature, dorsal kyphosis, cervical lordosis
Senile osteoporotic symptoms: painful thoracic and lumbar regions, fractures in the femoral neck and pelvis. Yikes.
Prevention: Exercise, calcium and vitamin D intake, bisphosphonates, recombinant PTH
PAGET DISEASE aka osteitis deformans
PHASES
Pathogenesis/Mutations
Bone mass is increased, disordered and structurally unsound
PHASES
1. Osteolytic
2. Mixed osteoclasts-osteoblastic
3. Osteoblastic burn out / Osteosclerotic stage
+activity of NF-kB = increases osteoclast activity
RANK mutations
Morphology hallmark = mosaic pattern (lamellar bone in the sclerotic phase) and jigsaw-puzzle like appearance
Axial skeleton or proximal femur involved in 80% of cases
Pain localized to affected bone + micro fractures and bony overgrowth compressing the spinal/cranial nerve roots
Complications:
Bowing of femur or tibia: distorts femoral head
Severe secondary osteoarthritis
Chalk-stick type fractures
Compression fractures of the spine —> spinal cord injury & development of kyphosis
PTH effects ?
Pathology of hyperparathyroidism
Osteoclast activation
Indirectly inc RANKL expression on osteoblast
Bone resorption
Calcium mobilization
Inc reabsorption of calcium by renal tubules
Inc urinary excretion of phosphates
Inc synthesis of active vitamin D
-Micro fractures & secondary hemorrhages
-brown tumor —> vascularity, hemorrhage, and hemosiderin, deposition by macrophages*
-Cystic degeneration
What is the condition called that has skeletal abnormalities in kidney disease?
How does that happen?
RENAL OSTEODYSTROPHY
-tubular dysfunction l/et renal tubular acidosis and the low pH dissolves hydroxyapatite —> bone demineralization
-reduced phosphate excretion l/t chronic hyperphosphatemia
-hypocalcemia
Just in general relation of kidney to bone…
Chronic renal failure will result in hyperphosphatemia which causes secondary hyperparathyroidism, hypocalcemia logically develops, causing PTH secretion to increase and this increases osteoclast activity and also metabolic acidosis
