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Block 2 - MSK > WEEK 4 - MINI LECTURES - OSTEOPOROSIS > Flashcards

WEEK 4 - MINI LECTURES - OSTEOPOROSIS Flashcards

(58 cards)

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1
Q

What are the short terms of decrease calcium in extracellular fluid

A
  • increase Na+ permeability of cells

- leads to partial depolarisation which in turn leads to muscle spasm tetany and pins and needles and seizures

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2
Q

What are the short term effects of increase calcium concentration in ECF

A
  • decrease Na+ permeability of cells
  • hyperpolariation -> neurolgical dysfunciton, cardiac arrythmias, constipation, anorexia, nausea -> dehydration
  • long term effects induce diuresis -> Dehydration
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3
Q

Normal range of serum inorganic phosphate

A

0.8-1.4 mmol/L

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4
Q

High PO4 in the long term

A

Soft tiussue mineral deposition

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5
Q

Low PO4 in the long term

A

Inadequate bone mineralisation

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6
Q

Three systems involved in calcium homeostasis

A
  • gut
  • kidney
  • bone
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7
Q

Role of bone in caclium homeostasis (2)

A
  • structural requirement for hydroxyapaetite laying -> gives comrpessive strength
  • alternative store: release in blood to make up for daily losses
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8
Q

Parathyroid hormone

A
  • Peptide
  • released from parathyroid glands
    Can be synthesized by Vit D precursor
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9
Q

What triggers the release of PTH

A
  • low Ca2+ via calcium sensing receptor
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10
Q

What inhibits the release of PTH

A
  • calcitriol

- high Ca2+

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11
Q

Sources of Vit D

A
  • sun exposure is the main source
  • Diet as a minor source: fatty fish, meat, liver, eggs, fortified food
  • supplements: 1000 daily
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12
Q

Vitamin D metabolism

A

7 dehydrocholesterol -> Vit D -> 25(OH) vit D -> 1.25(OH)2D (= calcitriol)

  • the last conversion is promoted by PTH, low Ca 2+, low PO43-, growth and pregnancy mainly by kidney and other tissues
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13
Q

Groups at high risk of Vit D deficiency

A
  • old people in hospital or care
  • dark skinned people
  • infants of motherswith low vit D are at risk of rickets
  • ## chronically ill individuals
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14
Q

FGF 23

A
  • produced predominantly in bone by osteocytes
  • also produced by rare tumours
  • acts predominantly in kidneys: increase phosphate wasting, decrease calcitriol production and increase calcitriol degradation
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15
Q

FGF23 production is stimulated by

A
  • calcitriol
  • PTH
  • high phosphate
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16
Q

Calcitonin

A
  • inhibits bone resorption
  • peptide
  • produced by parafollicular cells
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17
Q

What promotes the release of calcitonin

A
  • gastric hormones
  • pentagastrin
  • increase Ca2+
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18
Q

Gut: role in mineral homeostasis

A
  • ingestes calcium and phosphate
  • absorb Ca2+ passively or actively ( when stimulated by calcitriol)
  • main function of calcitriol is to acquire Ca 2+ and PO4 from food for bone mineral
  • Vit D role: acquire calcium and phosphate from food
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19
Q

Bone: role in mineral homeostasois

A
  • calcium and phosphate required for bone mineral and compressive strength
  • acts as a store of cacium and phosphate in bone turnover
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20
Q

Short term release of calcium from bone

A
  • increased by PTH and calcitriol

- inhibition of release by calcitonin

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21
Q

Kidney: role in mineral homeostasis

A
  • modulate Ca 2+ and PO4 losses
  • calcium filtration and reabsorption by PTH
  • filter PO4 and reabsorb
  • PTH: reduces PO4 reapsorption and causes dumping of PO4 in urine
  • PTH also increases calcitriol production
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22
Q

Summary: 2 role of gut

A
  • increase Ca 2+ abosrption
  • increase PO4 absorption
  • both of these effects are induced by calcitriol
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23
Q

SUMMARY: kidney role

A
  • low blood calcium -> increase PTH
  • PTH Acts on kidney
  • increase calcitriol
  • conserve Ca 2+
  • dump PO4 in urine
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24
Q

Bone SUMMARY

Study These Flashcards
A
  • PTH increases resorption
  • stimulates release of Ca2+
  • stimulates release of PO4
25
Low blood phosphate mechanism
- sensed directly by kidney -> increase calcitriol production - calcitriol acts on gut to increase PO4 absorption and on bone to increase resorption - calcitriol also modulates PO4 losses in kidney
26
Affect of changes in hormones - high PTH - Low PTH - High FGF23 - mild- mod low vitD - severe low Vit D
- hypercalcemia - hypocalcemia - hypophosphatemia (RARE) - increase in PTH which maintains blood ca for some time at the expense of bone resorption - cant resorb bone anymore -> osteomalacia and rickets
27
Bone mass determinants
- genetics - age - mechanical loading - mineral balance: vit D, PTH, Sex steroids - balance between rate of bone resorption and rate of bone formation
28
Contributors to fracture risk
- bone mass (density) - measured usually with DEXA - T-score: bone mineral density less than 2.5SF below young normal mean - osteoporosis - bone quality Bone gometry - propensity to fall - loss of horizontal struts
29
Minimum requirements for bone health
- adequate exercise - adequate calcium intake - adequate vit D - normal sex steroids - avoid smoking, excess alcohol, glucocoricoids
30
Adequate exercise
- mechanical loading -> resistance to deformity - large changes at low activity levels - gravity, weight bearing exercises
31
Regulation of bone mass by osteocytes and sclerostin
- osteocytes is 90% of bone cells - secrete sclerostin - negative regulator of bone mass - with deformity of bone - sclerostin secretion decreases
32
Wnt pathway in bone
- Wnt 3b secreted by bone cells - when binds to receptor, inhibits GSK3b -> b catenin is freed from complex APC -> goes to nucleus -> acts on TF to stimulate bone cell and proliferation - Wnt Signalling inhibited by Sclerostin -> b catenin is targetted for defradation
33
Adequate Vit D
- needed to absorb clacium from diet, to mineralize bone and for normal muscle function - D3: cholecalciferol - animal sources - D2: ergocaciferol: plant sources
34
Mild-moderate deficiency in Vit D
- increased. PTH - increased bone resorption, decreae bone density - impaired muscle function and increased risk of falls and fracture
35
Severe deficiency in but D
- gut calcium absorption impaired - a lot of increase in PTH - bone resorption impaired, no capacity to increase gut calcium or phosphate absorption - phosphate loss in urine - insufficient calcium and phosphare -> impaired bone mineralisation -> rickets and osteomalacia, impaired muscle function
36
Intermittent PTH stimulates bone formation
- main effect is on osteoblasts - anabolic effect on bone - unclear why, but suppresses sclerostin and stimulation of Wnt pathway
37
Sex steroids: estrogens, androgens
- help to maintain normal balance between bone formation and resorption - help to keep bone cells alive - estrogen are probably important in men as well - androgens give men bigger, more mechanically strong bones
38
Actions of estrogens in bone
- reduce osteoclast generation and lifespan - reduces rates of bone turnover - promote coupling - some evidence of increase formation - keep osteoblasts and osteocytes alive longer
39
Glucocorticoids effects
- decrease calcium absorption in gut - increase calcium loss in kidney - decrease osteoblast and osteocyte viability in bone
40
Non modifiable risk factor for fracture
- advanced age - female gender - prevalent fractrures - bad genes - early menopause - past comorbidity - disability
41
Most important risk factor for fracture
- previous fractures
42
Modifiable risk factors for fracture
- life style and nutrition - low bone mass - high bone turnover - high fall propensity - treatable comorbidities - bone adverse medicatin
43
T score
- comapred to mean peak bone mass | - used to assess fracture risk
44
Z score
- compared to age and gender matched congtrols | - used to assess what is expected
45
When is a bone density scan recomeded?
- in any person with a minimal trauma fracture | - in any person with significant risk factors for bone loss without a fracrture
46
Clinical examination of osteoporosis:
- early stages are asymptomatic - late stages: complication and fracture - severe acute or chronic back pain - loss of height, stooped posture - cardiovascular and respiratory complications
47
Thoracolumbar spine examination
- change in posture, height loss - thoracic kyphosis - abdominal distension - lower ribs to pelvis distance - para-spinal skin folds - localised tenderness - spinal mobility
48
Balance and risk of falling
- neuro-muscular examination - sarcopenia, proprioception - time-up-and-go - gait and tandem speed - visual acuity - mini mental state
49
Laboratory investigations to exclude secondary causes
- ESR: exclude muyeloma - C,P, M: look for problems with homeostasis metabolism - Creatinine for renal function - 25OH Vit D - TFT - urine: calcium, phosphate, creatinine
50
Management strategy
- analgesia -> physiotherapy -> life style changes -> Fall prevention -> calcium balance -> Vit D sufficiency -> pharmacotherapy
51
Non pharmaological management
- weight bearing exercise programs improve muscle strength, mobility, balance, bone density, future fracture risk
52
Calcium supplement effect
- decrease PTH secretion | - decrease bone resorption
53
Calcium and Vit D supplement and fracture risk
- each individually has no effect on fracture risk | - in combination can decrease fracture risk by 12%
54
Pharmacotherapy: Inhibitors of bone resorption
- SERM - Biphosphonates - Strontium Ranelate - RANKL inhibitors
55
Specific pharmacotherapy: Stimulators of bone formation
- PTH
56
Effect of oral biphosphonates on incidence of vertebral fracture risk
- risk reduction of 50-60% for vertebral fractures | - 20-40% for non vertebral fractures
57
Persistence with oral anti-osteoporosis treatment is generally poor
- 50% after 1 year - 40% after 2 years - 20-35% after 5 years - if miss half of the dose, its the same thing as not taking it - solution is a non oral treatment
58
The true problem: we dont treat patients with osteoporosis
- 70% of patients who have suffered an osteoporotic fracture go untreated - 30-50% of these patients fracture again, usually within 3-5 years: domino effect - all osteoporotic fractures are associated with increased morbidity and excess mortality

Block 2 - MSK (38 decks)

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