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General Anatomy > Osteoporosis > Flashcards

Osteoporosis Flashcards

1
Q

What are osteoprogenitor cells

A

precursors for othe bone cells
undifferentiated cells
can divide to replace themselves
found in inner layer or periosteum and endosteum

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2
Q

What are osteoblasts

A

builder cells
secrete collagen and other matrix components
from mesenchymal stem cells
secrete mand mineralise osteoid
some control over osteoclasts–> building and reabsorbing needs to be balanced

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3
Q

What do mesenchymal cells differentiate into

A

osteoblasts, chondrocytes, myocytes, adipocytes

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4
Q

What are osteocytes

A

mature bone cells located in lacunae (area surrounding an osteoblast bacomes calcified and results in osteoblast becoming encapsulated
Carry out daily maitenance of bone, nutrients and removal of wastes
Maintain mineral concentration of matrix
Direct the timing and location of remodelling

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5
Q

What are osteoclasts

A

Reabsorb bone and release calcium into blood stream
Work at surfaces such as endosteum
From hematopoietic precursors (stem cells that are precursors for blood cells)

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6
Q

When do you reach PBM/PBD

A

approx 30yrs

after 30yrs, reabsorption>formation

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7
Q

What role does collagen protein play in bone strength

A

Collagen proteins provides tensile strength= able to twist and bend without breaking

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8
Q

What role does mineralised osteoid play in bone strength

A

calcium gives compressive strength

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9
Q

Cells with mesenchymal cells origin

A 
Structural/muscle cells
Osteoblasts
chondrocytes
fibroblasts
adipocytes
muscle cells
due to same origin, they produce the same cytokines and colony stimulating factors as fibroblasts--> hence build bone/muscle
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10
Q

Cells with hematopoietic cells origin

A 
Blood cell line
Monocytes
macrophages
osteoclasts
due to same origin, they produce the same cytokines which are destructive--> stimulating osteoclastic activity
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11
Q

What is the time frame within which osteoblasts and osteoclasts work

A

osteoblasts= take months to produce new bone

osteoclasts=take weeks to reabsorb

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12
Q

What influences the difference in PBM b/w individuals

A

Activity
nutrition
Sunlight
Hormones

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13
Q

What is osteoporosis

A

The failure to reach optimal PBM as a result of bone reabsorption > bone formation
Normal mineralisation occurs, but decreases bone mass and decreased bone quality–> predisposing it to #’s

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14
Q

What type of disease is osteporosis

A

Progressive

common and systemic

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15
Q

What is the epidemiology of OP

A

Elder white women most common
Majority of cases affect women
Risk increases with age
Asia>white>black

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16
Q

What are the predisposing factors for OP

A

Genetics–> determines about *0% of PMB
decreased physical activity (sedentary lifestyle)
decreased vitamin D intake and calcium intake
Oestrogen and androgen deficiency (postmenopausal women at higher risk of OP, prevented with oestrogen supplement)
Increased parathyroid hormone level or function

17
Q

How does parathyroid hormone affect calcium levels in blood

A

Parathyroid hormone promotes mobilisation of calcium from bone to blood, hence increased parathyroid hormone decreased calcium in bone, which results in softening of bone

18
Q

What is primary juvenile OP

A

Occurs b/w 8-14yrs
normal gonadal function
abrupt bone pant and/or # following trauma
Condition usually goes away spontaneously, although early diagnosis is important to protect child’s spine

19
Q

what is the cause of primary OP

A

idopathic hence no know cause–> occurs spontaneously

20
Q

What is postmenopausal primary OP

A

Primary OP–> type I
Accelerate loss of bone post menopausal
Occurs as a result of oestrogen deficiency
Thin, white, sedentary smoker female at greatest risk
(sedentary affects PMB and wolffs law; smoking has toxins which cause inflammation)
Brest feeding-> lose calcium and hence reduced bone mass
females lose 30-40% cortical and 50% trabecular bone in their lifetime–> hence trabecula will contribute 50% less to weight
generally takes 10yrs post menopause for effects to start showing

21
Q

What is senile OP

A

Primary OP–> type II
Age associated bone loss and calcium deficiency
Hence deterioration of bone structure
Decreased activity–> therefore decreased stress on bones (Wolffs law)

22
Q

What is secondary OP

A

OP as a result of an underlying drug/deficiency or disease

23
Q

What are genetic underlying causes of secondary OP

A

cystic fibrosis

Hypogonadal states

24
Q

what are endocrine causes of OP

A 
Acromegaly--> disorder where pituitary produces too much growth hormone
Oestrogen deficiency
Diabetes mellitus
Hyperparathyroidism
Hyperthyroidism
25
Q

What are chronic inflammatory conditions of secondary OP

A 
AS
RA
SLE--> systemic lupus erythematosus (autoimmune, affects skin, joints kidneys brain and other organs)
Alcoholism
Depression
Emphysema
Kidney disease--> reabsorbs calcium
Pregnancy/lactation
26
Q

What sort of deficiences contribute to OP

A 
Malabsorption
Malnutrition
Calcium
Magnesium
Protein
Vitamin D
27
Q

How does celiac disease affect OP

A 
An autoimmune disease
immune response to eating gluten
creates inflammation
damages small intestine lining
prevents absorption of some nutrients (e.g. Ca)
associated with diabetic pts
28
Q

How will OP present clinically

A

Asymptomatic
Usually silent and not clinically apparent till well advanced or spontaneous #
Small stress will cause #
Pain in thoracic and lumbar–> usually as a result of vertebral #’s caused by loss of beams (trabeculae)
Height loss and spine deformity–> kyphosis, lordosis, kyphoscoliosis

29
Q

What are some common # risk sites

A

NOF
wrist
vertebrae
WB exercises and diet help in prevention

30
Q

How can OP be identified from x-rays

A

not apparent in x-rays till 30% bone mass gone
thin cortices–> loss of cancellous bone
vertebral bodies–> anterior wedging and #

31
Q

Changes in vertebrae from OP

A

WB in vertebral body is longitudinal forces
Greater loss of beams therefore less support for compressive forces–> only left with struts which break from longitudinal forces causing them to collapse and hence #

32
Q

What is the oestrogen independent mechanism of OP

A

Parathyroid hormones regulates calcium
physical stress on bone
vitamin D intake/synthesis
calcium intake

33
Q

What are oestrogen dependent mechanisms of OP

A

Menopause–> decrease in oestrogen
osteoblasts/clasts/cytes–> all have oestrogen receptors
oestrogen moderates osteoclast production, activity and apoptosis (keeps osteoclasts under control)
hence decreasedoestrogen = increased osteoclast production and activity (also prolonged survival of osteoclasts)
oestrogen also affects bones indirectly through cytokines and local growth factors which have a ‘turn-off’ effect on osteoblasts and osteoclasts

34
Q

Affect of exercise on OP

A

Works/benefits only when regular exercise

Spinal density is shown to increase by 4% in exercisers

35
Q

What is the final common pathway of bone reabsorption

A

RANKL-RANK (OPG System)

36
Q

What is RANKL

A

RANKL= recetor activator of nuclear factor-Kappa B Ligand–> a cytokine produced by osteoblasts and activated by T cell lymphocytes
RankL is moderate by estrogen

37
Q

What is RANK

A

Receptor Activator of Nuclear factor-kappa B–> on osteoclasts

38
Q

What is OPG system

A

Osteoprotegerin system
OPG secreted by stromal cells and osteoblasts a soluble decoy receptor
Receptor inhibits RANK-RANKL by binding and sequestering RANKL
Takes RANKL receptor spot for RANKL binding to RANK therefore blocking or decreasing bone reabsorption cycle, therefore more OPG promotes bone formation

39
Q

Explain the RANK-RANKL pathway/process

A

RANKL binds to RANK expressed on osteoclasts and osteoclast precursors to promote osteoclast differentiation
Increased RANKL results in recruitment of higher numbers of preosteoclasts as well as increased activity, vigor and lifespan of mature osteoclasts
osteoporotic menopausal changes= increased bone turnover as a remodelling imbalance with increased bone reabsorbing osteoclast activity with pro-inflammatory cytokines and decrease bone forming osteoclast activity

General Anatomy (13 decks)

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