This is a short video on five bone diseases caused by altered bone metabolism.
I created this presentation with Google Slides.
Image were created or taken from Wikimedia Commons
I created this video with the YouTube Video Editor.
ADDITIONAL TAGS:
Metabolic bone disorders
Bone diseases caused by disturbed bone metabolism
Osteitis
fibrosa
cystica
Paget’s disease
of bone
Osteogenesis imperfecta
Osteomalacia
/ rickets
Osteoporosis
Osteitis fibrosa cystica
AKA brown tumor of hyperparathyroidism
Excessive bone resorption (mediated by osteoclast activity)
Hyperparathyroidism → increased PTH → resorp bone
Pathology → diminished bone strength
Subperiosteal (below connective tissue) resorption
Bone cysts
Radiology: cyst formation, mimics bone neoplasms
Histology: fibrous tissue, hemorrhage (hemosiderin pigment)
Treatment: underlying cause of hyperparathyroidism
Osteitis
fibrosa
cystica
Paget’s disease
of bone
Excess bone resorption and formation
Repetition and acceleration of cyclic osteon breakdown and rebuilding
Results in disorganized bone (“jigsaw puzzleâ€, “mosaicâ€)
Epi: prevalence increases with age
Pathology: larger, weaker, less dense, more vascular bones
Affects axial skeleton and proximal long bones
Clinical: isolated AP increase
Symptoms: usually asymptomatic, but some get bone pain/fracture/deformity, arthritis, neuro complications (compression)
Radiology: cotton wool spots (sclerosis, whiter areas);
Nuc: increased uptake in affected bones
Treatment: bisphosphonates (antiresorptive)
Osteogenesis imperfecta
AKA brittle bone disease or Lobstein syndrome
Inadequate bone formation with defective bone matrices
Due to mutation in bone collagen gene (8 variants)
Clinical: unexpected fractures, family hx, blue sclera
Diagnose with DNA tests or collagen analysis
Treatment: bisphosphonates, surgery; no cure
Inadequate bone formation with defective bone matrix mineralization
Due to insufficient calcium or phosphorus
Most frequently caused by vitamin D deficiency
Also caused by chronic kidney disease → kidney converts inactive to active vit D
25-OH-D → 1,25-OH2-D
Pathology: softening of bone
Adults (osteomalacia)→ bone pain, muscle weakness, fracture risk
Children (rickets) → bone deformities (ie bowing), dental issues
Treatment: restore vitamin D levels (or active form (calcitriol)), calcium and phosphorus if necessary
Osteoporosis
Reduced bone matrix and mineralization secondary to various factors
No single etiology → 50% hereditary, 50% acquired (diet, age, exercise, comorbidities)
Epi: most common metabolic bone disorder
Pathology: increased fragility, fractures
Decrease in bone density (2.5 std dev)
Osteopenia is milder form (1 to 2.5 std dev)
Bone mineral density (BMD) measured with dual-energy X-ray absorptiometry (DEXA) scan
T-score is std dev multiple difference from avg ethnicity/gender-matched 30 yo
Z-score is std dev multiple difference from avg ethnicity/gender/age-matched pt
Primary osteoporosis
Inherent risks: fracture hx, female, white, age, genetics, fam hx
Modifiable risks: smoking, alcohol, low estrogen, low Ca, sedentary, low BMI
Secondary osteoporosis → due to other diseases, surgeries, medications
Hormones: corticosteroids (net resorption); thyroid/growth hormone (net formation)
Dzs: Cushing’s; hyper-parathyroid/thyroid/prolactin; hypo-gonad/pituitary; gastric bypass and other malabsorption; Ehlers-Danlos; OI; myeloma, lymphoma/leukemia
Drugs: ethanol, glucocorticoids, heparin
Clinical: kyphosis (hump-back), scoliosis (S-spine), height loss, gait/balance issues
Radiology: x-ray only detects 30-50% loss → DEXA preferred
Treatment: Ca, vit D, estrogen replacement; calcitonin; selective estrogen receptor modulators (SERMs, ie raloxifene and tamoxifen), bisphosphonates, denosumab (RANK Ab); teriparatide (PTH analog, anabolic)
Osteitis
fibrosa
cystica
Paget’s disease
of bone
Osteogenesis imperfecta
Osteomalacia
/ rickets
Osteoporosis
I created this presentation with Google Slides.
Image were created or taken from Wikimedia Commons
I created this video with the YouTube Video Editor.
ADDITIONAL TAGS:
Metabolic bone disorders
Bone diseases caused by disturbed bone metabolism
Osteitis
fibrosa
cystica
Paget’s disease
of bone
Osteogenesis imperfecta
Osteomalacia
/ rickets
Osteoporosis
Osteitis fibrosa cystica
AKA brown tumor of hyperparathyroidism
Excessive bone resorption (mediated by osteoclast activity)
Hyperparathyroidism → increased PTH → resorp bone
Pathology → diminished bone strength
Subperiosteal (below connective tissue) resorption
Bone cysts
Radiology: cyst formation, mimics bone neoplasms
Histology: fibrous tissue, hemorrhage (hemosiderin pigment)
Treatment: underlying cause of hyperparathyroidism
Osteitis
fibrosa
cystica
Paget’s disease
of bone
Excess bone resorption and formation
Repetition and acceleration of cyclic osteon breakdown and rebuilding
Results in disorganized bone (“jigsaw puzzleâ€, “mosaicâ€)
Epi: prevalence increases with age
Pathology: larger, weaker, less dense, more vascular bones
Affects axial skeleton and proximal long bones
Clinical: isolated AP increase
Symptoms: usually asymptomatic, but some get bone pain/fracture/deformity, arthritis, neuro complications (compression)
Radiology: cotton wool spots (sclerosis, whiter areas);
Nuc: increased uptake in affected bones
Treatment: bisphosphonates (antiresorptive)
Osteogenesis imperfecta
AKA brittle bone disease or Lobstein syndrome
Inadequate bone formation with defective bone matrices
Due to mutation in bone collagen gene (8 variants)
Clinical: unexpected fractures, family hx, blue sclera
Diagnose with DNA tests or collagen analysis
Treatment: bisphosphonates, surgery; no cure
Inadequate bone formation with defective bone matrix mineralization
Due to insufficient calcium or phosphorus
Most frequently caused by vitamin D deficiency
Also caused by chronic kidney disease → kidney converts inactive to active vit D
25-OH-D → 1,25-OH2-D
Pathology: softening of bone
Adults (osteomalacia)→ bone pain, muscle weakness, fracture risk
Children (rickets) → bone deformities (ie bowing), dental issues
Treatment: restore vitamin D levels (or active form (calcitriol)), calcium and phosphorus if necessary
Osteoporosis
Reduced bone matrix and mineralization secondary to various factors
No single etiology → 50% hereditary, 50% acquired (diet, age, exercise, comorbidities)
Epi: most common metabolic bone disorder
Pathology: increased fragility, fractures
Decrease in bone density (2.5 std dev)
Osteopenia is milder form (1 to 2.5 std dev)
Bone mineral density (BMD) measured with dual-energy X-ray absorptiometry (DEXA) scan
T-score is std dev multiple difference from avg ethnicity/gender-matched 30 yo
Z-score is std dev multiple difference from avg ethnicity/gender/age-matched pt
Primary osteoporosis
Inherent risks: fracture hx, female, white, age, genetics, fam hx
Modifiable risks: smoking, alcohol, low estrogen, low Ca, sedentary, low BMI
Secondary osteoporosis → due to other diseases, surgeries, medications
Hormones: corticosteroids (net resorption); thyroid/growth hormone (net formation)
Dzs: Cushing’s; hyper-parathyroid/thyroid/prolactin; hypo-gonad/pituitary; gastric bypass and other malabsorption; Ehlers-Danlos; OI; myeloma, lymphoma/leukemia
Drugs: ethanol, glucocorticoids, heparin
Clinical: kyphosis (hump-back), scoliosis (S-spine), height loss, gait/balance issues
Radiology: x-ray only detects 30-50% loss → DEXA preferred
Treatment: Ca, vit D, estrogen replacement; calcitonin; selective estrogen receptor modulators (SERMs, ie raloxifene and tamoxifen), bisphosphonates, denosumab (RANK Ab); teriparatide (PTH analog, anabolic)
Osteitis
fibrosa
cystica
Paget’s disease
of bone
Osteogenesis imperfecta
Osteomalacia
/ rickets
Osteoporosis
Metabolic Bone Disorders camera iphone 8 plus apk | |
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Education YouTube Video Editor View attributions | Upload TimePublished on 28 Aug 2016 |
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