Osteoporosis Flashcards
1
Q
Osteoporosis
A
- most common metabolic bone disease
- low bone mass but normally mineralized bone
- Microarchitectural disruption –> skeletal fragility
- Major risk factor for fracture
2
Q
Epidemiology of osteoporosis
A
- 8mill women, 2mill men (more women bc of menopause)
- 43mill w/ bone mass that puts them at risk (called osteopoenia), 10mill with osteoporosis
- 30% women >50yo have low bone mass
3
Q
osteopenia
A
precursor for osteoporosis
4
Q
At what age does bone mass typically decrease
A
30-40yo
5
Q
what causes osteoporosis
A
- bones naturally get thinner as you age because existing bone cells are reabsorbed faster than new bone is made
- the thicker your bones at age 30, the longer it takes to develop osteopenia or osteoporosis
6
Q
types and percentages of osteoporotic fractures
A
- 50% vertebral fractures (700k per yr) –> mostly asymptomatic, height loss, kypohosis, back pain
- 25% hip fractures (300k per yr) –> a lot of older pts, risk for DVT, PE; HIGH MORTALITY!!
- 25% colles’ fractures (250k per yr) –> fall onto outstretched hand (younger pt), fracture of distal radius
- increased fracture risk in spine, hip, wrist, humerus, and pelvis
- osteoporotic fractures = fragility fractures (falls from standing height or less)
- fractures of hip or spine are associated with 10-20% increase in mortality
7
Q
nonmodifiable risk factors
A
- h/o fracture
- family h/o fracture
- female
- old
- Caucasian/Asian
- Dementia (less likely to remember to take osteoporotic meds including vitamins)
8
Q
modifiable risk factors
A
- cigarettes (may inhibit osteoblast activity, interfere with calcium absorption)
- low body weight (high is better)
- low estrogen
- low calcium intake
- chronic steroids
- alcoholism
- poor eyesight
- recurrent falls
- low physical activity
9
Q
Protective factors
A
- high BMI
- black race
- estrogen or diuretic therapy (diuretics bc decrease calcium excretion by kidneys)
- exercise (start as a kid)
10
Q
Pathogenesis of osteoporosis
A
- slow loss of cortical and trabecular bone as you age
- rapid loss of trabecular bone postmenopause
- any process that increases rate of bone remodeling results in net bone loss over time
- Genetic component (40-80%) –> genes involving vitD synth, E receptors, bone forming proteins
- Environmental –> calcium intake, muscle strength and physical activity, chronic dz, meds, smoking
11
Q
coupling
A
resorption followed by formation (or mineralization)
12
Q
bone remodeling
A
- resorption followed by formation
- continually removes older bone and replaces it with new bone –> maintains healthy skeleton
- repairs microdamage in skeleton
- supply Ca from skeleton to body
- mass of the skeleton remains constant once peak bone mass is reached
13
Q
osteoporosis in trabecular bone
A
- osteoclasts penetrate trabeculae leaving no template for new bone formation
- age related loss of horizontal connections
14
Q
osteoporosis in cortical bone
A
- increased activation/remodeling leads to more porous bones
- decreased bone strength
15
Q
how does estrogen deficiency cause bone loss
A
- activates new bone remodeling sites
- exaggerates imbalance between formation and resorption
- increased osteoclast recruitment and activity
- increased osteoblast apoptosis
- AFFECTS TRABECULAR BONE FIRST
- in men, T is important because it is converted to E to build bones
16
Q
how does calcium deficiency cause bone loss
A
- increased rate of bone remodeling to maintain adequate serum calcium
- PTH is secreted when there is low calcium –> increases Ca resorption from bone, decreases renal Ca excretion, increases renal production of 1,25-dihydroxyvitamin D (hormonal form of vitD that optimizes Ca and phos absorption and inhibits PTH synth)
17
Q
vitD deficiency
A
- most common nutritional deficiency worldwide
- most underdiagnosed medical condition
- sever, prolonged deficiency can lead to hypocalcemia, rickets, osteomalacia, osteoporosis
- high risk: sun avoidance/sunscreen, poor nutrition, malabsorption, old, liver or renal dz, living in northern lats
- vitD promotes Ca absorption in GI and is needed by osteoblasts and osteoclasts for bone growth and remodeling
- may be a link between vitD deficiency and DM, cancer, autoimmune dz, CT dz, autism, childhood obesity, preg complications, depression, schizo
18
Q
vit D metabolism
A
- activation of vitD to calcitriol = increase in serum calcium and phosphate concentrations
- fat soluble that is naturally present in foods, added to others, available as dietary supplement
- produced endogenously via UV rays
- vitD from sunlight, food, and supplements is biologically inert and must undergo two hydroxylations in body for activation (first in liver converted to 25 hydroxyvitD aka calcidiol, second in kidney converted to 1,25 dihydroxyvitD aka calcitriol)
19
Q
sources of vitamin D
A
- body makes it when exposed to UV
- cheese, margarine, butter, fortified milke, healthy cereals, fatty fish, shitake mushrooms, cod liver oil
- vitamin D fortified milk - 400iu per quart
20
Q
rickets
A
- vitamin D deficiency
- decreased mineralization around epiphyses and bowing of lower extremities
- growth retardation
- only in GROWING children - before fusion of epiphyses
- Pregnant women and children must have sufficient vitD and Ca intake
- most common cause is nutritional deficiency of vitD - even in hot climates ppl avoid sun, cover skin, dark skinned ppl require more sun to synth vitD
21
Q
osteomalacia
A
- vitD deficiency
- incomplete mineralization of underlying mature bone matrix (osteoid) following growth plate closure in adults
22
Q
osteomalacia vs. rickets
A
- diff manifestations of same underlying pathologic process
- can occur concurrently when growth plates are open, osteomlacia cna continue after growth plates fuse
