seminar on pharmacotherapy of osteoporosis copy
TRANSCRIPT
FACILITATED BY:DR.RAJU KONERI SIR
HOD of Pharmacology
department
SUBMITTED BY:Dipankar acharjee
M.Pharmacy 1st year
Department
pharmacology
Osteoporosis is defined as a “skeletal
disorder characterized by compromised bone
strength predisposing a person to an increased risk
of fracture’’
The development of osteoporosis is multifactorial,
beginning with genetics and unhealthy bone
lifestyles, along with other skeletal factors, which
lead to compromised bone strength, and nonskeletal
factors
PATHOPHISIOLOGYBone is comprised of three types of cell.
Osteoblasts.
Osteocytes.
osteoclasts.
Osteoblast:-These are mononucleate bone-forming cells.
Osteoblasts also manufacture hormones.
Osteocytes:- These are mostly inactive osteoblasts.
Osteoclast:-These are the cells responsible for bone
resorption, thus they break down bone. New bone is then
formed by the osteoblasts. Bone is constantly remodelled by
the resorption of osteoclasts and created by osteoblasts.
Bone remodelling
o Bone remodelling is a dynamic process that occurs
continuously throughout life.
o The purpose of remodelling is to regulate calcium
homeostasis, repair micro-damaged bones from
everyday stress.
o The action of osteoblasts and osteoclasts are
controlled by a number of chemical enzymes that
either promote or inhibit the activity of the bone
remodeling cells, controlling the rate at which
bone is made, destroyed, or changed in shape.
In osteoporosis,, bone mass (the amount of bone
tissue) is reduced because its deposition does not keep
pace with resorption. Peak bone mass occurs around 35
years and then gradually declines in both sexes. Lowered
oestrogen levels after the menopause are associated with
a period of accelerated bone loss in women. Thereafter
bone density in women is less than in men for any given
age. Bone is progressively weakened with cancellous bone
affected first by thinning and loss of trabeculae. In the
postmenopausal period an imbalance of hormones probably
causes bone weakening.
The accelerated bone loss during perimenopauseand postmenopause results from enhanced resorption mainly as a result of the loss in ovarian hormone production, specifically estrogen.
Estrogen deficiency increases proliferation, differentiation, and activation of new osteoclasts and prolongs survival of mature osteoclasts.
The number of remodeling sites increases and resorption pits are deeper and inadequately filled by normal osteoblastic function.
Men are at a lower risk for developing osteoporosis and osteoporotic fractures because of larger bone size, greater peak bone mass, and fewer falls
The etiology of male osteoporosis tends to be multifactorial with secondary causes and aging being the most common contributing factors
SECONDARY CAUSES OF
OSTEOPOROSIS
CAUSES
CausesThe major factors influencing bone losses are hormonal status,
exercise, aging, nutrition, lifestyle, disease states, medications,
and some genetic influences. Non hormonal risk factors are
similar between women and men.
LOW BONE DENSITY: Bone loss occurs when bone
resorption exceeds bone formation. Bone resorption sites
greatly exceed the rate and ability of osteoblasts to form new
bone. During peri-menopause and for up to 5 to 7 years after
menopause, women can experience an accelerated rate of
bone loss because of the drop in circulating estrogen and an
increase in bone resorption
IMPAIRED BONE QUALITY
The strength of bone is highly impacted by the quality
of the bone’s material properties and its structure. . Bone quality assessment is important because changes
in bone quality effect bone strength much more than
bone mass changes
FALLS
Risk of falling increases with advanced age
predominantly as a result of balance, gait, and mobility
problems, poor vision, reduced muscle strength,
impaired cognition, multiple medical conditions
PREVENTION AND TREATMENTOsteoporosis prevention and treatment begins with a
bone-healthy lifestyle and uses non prescription and
prescription medications as needed.
The primary goal of osteoporosis management
should be prevention.
Once osteopenia or osteoporosis develops, the
objective is to stabilize or improve bone mass and
strength and prevent fractures.
NONPHARMACOLOGIC THERAPY
Diet:- Overall, a diet well balanced in nutrients and
minerals is important for bone health. In addition, limiting
intakes of caffeine, alcohol, sodium, cola, and other
carbonated beverages.
Excessive caffeine consumption is associated with
increased calcium excretion, increased rates of bone loss,
and a modest increased risk for fracture.
Calcium:- Data clearly indicate that adequate calcium
intake is necessary for the development of bone mass
during growth and for its maintenance throughout life.
Vitamin D:- The three main sources of vitamin D
are sunlight, diet, and supplements. Because few
foods are naturally high or fortified with vitamin D .
(at least 800 to 2,000 units of vitamin D daily are needed)
Other Nutrients and Minerals:-
Protein :-
Dietary protein represents a key nutrient for bone
health , evidence suggests that low protein intakes
increase osteoporosis risk and that higher protein
intakes are protective against bone.
Dietary Soy
Isoflavone phytoestrogens are plant-derived
compounds that possess weak estrogenic agonist and
antagonist effects. The most common source for
isoflavone is dietary soy products. Genistein is the
most abundant and biologically active isoflavone in
soybeans.
Smoking
Smoking cessation can help to optimize peak bone
mass, minimize bone loss, and ultimately reduce
fracture risk
Exercise
Physical activity or exercise is an important
nonpharmacologic approach to preventing
osteoporotic fractures. Exercise can decrease the risk
of falls and fractures by improving muscle strength,
coordination, balance, and mobility.
Fall Prevention
Because of the link between falls and fractures,
homes should be made safe and potentially harmful
medications eliminated.
PHARMACOLOGIC THERAPY
Non-pharmacologic interventions alone frequently are
insufficient to prevent or treat osteoporosis, drug
therapy is often necessary.
Antiresorptive
Antiresorptive therapies include calcium, vitamin D,
bisphosphonates, estrogen agonists/antagonists and
calcitonin.
Calcium Supplementation
Calcium imbalance can result from inadequate dietary
intake, decreased fractional calcium absorption, or
enhanced calcium excretion. Adequate calcium intake
is considered the minimal standard for osteoporosis
prevention and treatment and should be combined
with vitamin D and osteoporosis medications when
needed.
Adverse Events/Precautions:- Calcium’s most
common adverse reaction constipation.
Vitamin D Supplementation
Vitamin D intake is critical for the prevention and
treatment of osteoporosis because it maximizes
intestinal calcium absorption.
Seniors and patients being treated for osteoporosis
should take at minimum 800 units of vitamin D
through food and supplementation.
Bisphosphonate
Bisphosphonates mimic pyrophosphate, an endogenous
bone reabsorption inhibitor. Bisphosphonates
consistently provide the greatest fracture risk reductions
and BMD increases
Adverse Events/Precautions;-Bisphosphonate GI adverse
effects are minimal if the medication is taken correctly.
Intravenous bisphosphonates include fever, flu-like
symptoms.
Each oral dose should be taken with at least 6 ounces
of plain tap water at least 30 minutes before
consuming any food.
Mixed Estrogen Agonists/Antagonists
Raloxifene, a second generation mixed estrogen
agonist/antagonist (EAA) approved for prevention and
treatment of postmenopausal osteoporosis, is an
estrogen agonist on bone. Raloxifene decreases
vertebral fractures and increases spine and hip BMD
Calcitonin
Calcitonin is FDA indicated for osteoporosis treatment
for women who are at least 5 years past menopause.
Estrogen Therapy
Although estrogens are FDA indicated for prevention
of osteoporosis, they should only be used short-term in
women who need estrogen therapy for the management
of menopausal symptoms such as hot flushes.
Thiazide Diuretics
It increase urinary calcium reabsorption.
Observational studies suggest that patients who receive
thiazide diuretics have a greater bone mass, lower rates
of bone loss, and fewer fractures
REFERENCES
Dipiro J.T. et al., Pharmacotherapy. A
Pathophysiologic Approach. 7th ed.
Pg. no. 1483-1504
Waugh A, Grant A., Ross and Wilson
Anatomy and Physiology in Health
and Illness. 9th ed. Pg. no. 494