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BMS250 > wk 12, lec 3 > Flashcards

wk 12, lec 3 Flashcards

1
Q

osteopenia t score

A

-1 to -2.4

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2
Q

Causes of osteopenia

A

more osteoclasts

decrease estrogen in menopause or testosterone in men

vit d and calcium deficient

old age

genes

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3
Q

testosterone impacts on bone

A

increase osteoblast, inhibit osteoclast, muscle mass and strength

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4
Q

clinical features of osteopenia

A
  • Asymptomatic
  • Height Loss
  • Bone Pain
  • Fractures (MC: vertebrae, hips,
    wrists, metatarsals, and ribs)
  • Decreased Grip Strength
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5
Q

labs for osteopenia

A

serum BUN,
creatinine, albumin, calcium,
phosphate, alkaline phosphatase,
and 25-OH vitamin D

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6
Q

check DXA every 1-2 year if T score

A

below 2

and if using prednisone./ corticosteroid

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7
Q

osteoporosis t score

A

< -2.5

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8
Q

causes of osteoporosis

A

nutrient deficient
age
genes

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9
Q

change in osteoporosis

A

decrease BMD
microartchitectral changes (thin trabecular, increased porosity, decreased connectivity of bone tissue)

imbalance in bone formation and resorption

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10
Q

which bone effected in osteoporosis

A

trabecular (spongy) and cortical (bone) – trabecular more metabolically active and effected more

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11
Q

features of osteoporosis

A
  • Fractures (hip, wrist, spine)
  • Back Pain
  • Loss of Height (kyphosis)
  • Decreased Mobility and Function (hip fracture)
  • Risk of Secondary Complications. (pneumonia, DVT, pressure ulcers)
  • Asymptomatic Osteoporosis
  • Reduced Grip Strength and Muscle Weakness
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12
Q

pagets disease of the bone (osteitis deforming)

A

abnormal bone remodelling, excess breakdown and formation = large and weak bones

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13
Q

causes of paget’s disease of bone

A

genes, viral (paramyxoviruses i.e. measles and respiratory synctitial virus)

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13
Q

features of pagets disease of bone

A

excess bone resorption via osteoclast

disorganized bone formation (weak)

increase vascularity; hyperemia

abnormal bone architecture ( mixture of lamellar and woven bone, with
disorganized trabeculae and irregular cement lines)

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14
Q

phases of pagets disease of bone

A
  1. initial osteolytic phase = bone resorption and hypervascularization

2.s Econ phase= bone formation and resorption - replace normal lamellar bone with woven bone

  1. sclerotic phase; bone resorption declines and leads to hard, dense, less vascular bone (burn out phase)

-all 3 phases can happen at same time in different bones

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15
Q

symptoms of pagets disease

A

asymptomatic
bone pain
bone deformtion
fractures
neurolgocail if compress nerves (headache, hearing)
arthritis

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16
Q

labs in pagets disease of bone

A

elevated alkaline phosphatase levels

a marker of increased bone turnover

17
Q

scoliosis

A

abnormal lateral curvature
of the spine

usually in childhood

18
Q

4 categories of scoliosis

A
  1. idiopathic (80%)
  2. congenital
  3. neuromuscular (associated with neuropathy or musclular disease)
  4. syndromic (associated with other syndrome)
19
Q

scoliosis features

A

spinal curvature C or S shape

vertebral rotation

imbalance of muscles and ligaments

  • Visible Curvature
  • Asymmetry of the Shoulders, Hips, or Waist
  • Uneven Leg Length
  • Back Pain
  • Reduced Range of Motion
  • Breathing Difficulties (thoracic spine, reduce lung capacity)
20
Q

osteogenesis imperfecta (brittle bone disease)

A

fragile bones

genetics

21
Q

mutrations in which gene for osteogenesis imperfecta (brittle bone disease)

A

mutations in the genes responsible for producing
type I collagen

22
Q

osteogenesis imperfecta features

A

type I collagen synthesis mutation

abnormal bone matrix; weak

blue sclera (from CT abnormalities)

dentinogenesis imperfecta (tooth discoloured and weak)

short stature

skeletal deformities; bowed limbs, scoliosis,

joint hypermobile (lax ligaments)

hearing loss (from collagen dysfunction)

pulmonary (pneumonia, restrictive or obstructive lung disease)

cardiovascular (collagen in cardiac valves and aortic wall deformed) i.e. mitral regurgitation

23
Q

osteomyltiits

A

bone infection; usually bacteria

mainly in vertebrae; hematogenous spread

secondary infections if neuropathy or vascular insufficient

body tries to make new bone; sclerosis; but is irregular

bone pain, warm and swollen, fever and chills, limited ROM, drainage or sinus tracts

systemic: septicemia (bloodstream infection), septic arthritis, or even spread to
distant organs, posing a risk of life-threatening complications

24
multiple myeloma
cancer that affects plasma cells (a WBC that makes antibodies) causes them to profligate in bone marrow and crowd out normal blood cells and make abnormal antibodies
25
myeloma common in
among farmers, wood workers, leather workers, and those exposed to petroleum products
26
multiple myeloma cells involved
MM cells bind via cell-surface adhesion molecules to bone marrow stromal cells (BMSCs) and extracellular matrix (ECM) * Triggering MM cell growth, survival, drug resistance, and migration in the bone marrow milieu cytokines: IL6, IGF1, VEGF, SDF-1a ras/raf/protein kranse, PI3K/.Akt, PKC Immune cells such as plasmacytoid dendritic cells (pDC), myeloid-derived suppressor cells (MDSC), and T helper 17 (TH17) cells are increased in number and support myeloma growth
27
multiple myeloma feature
plasma cell proliferate via monoclonal immunoglobulins (m proteins) infiltrate bone marrow and crowd out normal hematopoietic cells osteolytic lesions, stimulate osteoclasts monoclonal protein production bone pain anemia renal dysfunction (proteinuria, hematuria) hypercalcemia (ca in blood- N/V, constipation, confusion, dehydration) recurrent infections neurological (weak, numb, tingle if compress spinal cord)
28
akylosing spondylitis cause
infalmmation of spine and sacroiliac joints HLA-B27 gene
29
features of ankylosing spondylitis
infalmamtion' ossification TNFalpha bone formation; ossification --> syndesmophyte formation --> fusion of adjacent vertebrae and lose spinal mobility --> bamboo spine SI joint most effected (sacroilitis) back pain, morning stiffness >30min, reduce spine mobility, enthesitis (inflamed ligament andtendons) esp achilles and chest/costochondral, fatigue, system (fever, weight loss, malaise), extra articular (uveitis, IBD, CVD)
30
joints for anklosing spondylitis
mostly sacroiliac
31
osteomalacia and rickets
soften and weaken bones from impaired mineralization of bone matrix inadequate deposition of calcium and phosphorus osteromalacia= adults rickets= kids during rapid growth (before epiphyseal fusion, vitamin D deficiency)
32
rickets cause
in children during periods of rapid growth * Before epiphyseal fusion, vitamin D deficiency results in growth retardation associated with an expansion of the growth plate known as rickets
33
features of osteomalacia and rickets
mineralization defect inadequate intake or absorb phosphorus and calcium and vitamin D hypercaleamia (muscle cramp, tetany, numb, tingle, seizure) other: fatigue, weak, secondary hyperparathyroidism
34
causes of osteomalacia and rickets
* Inadequate dietary intake of vitamin D or calcium * Malabsorption disorders (such as celiac disease or inflammatory bowel disease) * Renal disorders affecting vitamin D metabolism * Liver disorders impairing vitamin D activation * Insufficient sunlight exposure.
35
osteomlalcia in adults features
bone pain muscle weak secondary hyperparathyroid from low serum calcium fractures skeletal deformities; bowed legs, pelvic
36
rickets (kids) features
delayed growth and development skeletal deform; bowed legs (genu varum), knock knees (genu valgum), and deformities of the chest (e.g., pigeon chest or Harrison's groove) delayed dentition (teeth) muscle weak
37
fracture repair steps
* Hematoma Formation (blood vessels rupture and make blood clot for inflammatory cells to come) * Inflammatory Phase (heal hematoma; TNFa, IL1, IL6, IL11, IL18, TNFa) * Granulation Tissue Formation (mesenchymal stem cells differentiate to chondroblasts or fibroblasts) (chrondroblasts form temporary cartilaginous callus and fibroblasts make collagen) * Callus Formation (cartilage is apoptosis, then VEGF from osteoblasts comes in; M-CSF, RANKL, OPG, TNFa) (replace cartilaginous callus with bony callus and osteoblasts make new bone matrix, osteoid) --> chondrocytes hypertrophy and calcify ECM -->ca2+ binds phospahte and make hydroxyapatite crystals -->type 1 collagen bind hydroxyapatite * Bone Remodelling (osteoclasts resorb excess bone tissue, osteoblast make new deposits, hard callus woven bone replaced by lamellar bone, haversian system, IL1 and TNFa)
38
fracture repair steps
* Hematoma Formation * Inflammatory Phase * Granulation Tissue Formation * Callus Formation * Bone Remodelling
39
frature repicar in osteoporosisi
reduced bone density and altered bone metabolism associated with osteoporosis, the healing process may be slower and less robust compared to fractures in individuals with normal bone density * The formation of a stable callus and subsequent bone remodelling may take longer in osteoporotic fractures support via nutrition, weight bearing, smoking cessation, less alcohol
40

BMS250 (52 decks)

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