Class 4 (1/28/21) Flashcards
Osteoporosis
Characterized by low bone density leading to bone fragility and an increased susceptibility to fractures, especially of the hip and and spine osteoporosis develops due to an imbalance between bone formation & bone degeneration.
Types of osteoporosis
- Postmenopausal osteoporosis: specific to women.
- Senile osteoporosis: occurs in both men and women because of reduced bone formation (aging).
- Secondary osteoporosis: secondary to medication, particularly corticosteroids (prednisome/cortisol).
Bone cells
Osteoblasts: build
Osteocytes: maintain
Osteoclasts: degrade
Maintenance of bone mass
Bone production
Stress (activity)
Nutrition (Ca, Mg, Vit. D)
Hormones (estrogen, testosterone, HGH)
Bone loss
Inactivity
Inadequate nutrition
Hormones (decreased/low estrogen and testosterone)
Risk factors of osteoporosis
- Gender: osteoporosis is more common in women than men.
- Age
- Race
- In women: estrogen deficiency as a result of premature menopause (onset before age 45)
- In men: low testosterone levels
- Family history
- Alcohol
- Nutrition: low Ca intake, Vit. D deficiency
- Cigarette smoking
- Low body weight
- Current low bone mass
- Drugs: Glucocorticoids (cortisone/prednisone), Progestin (w/o estrogen), Anticonvulsants (phenytoin, Dilantin)
Presentation of osteoporosis
A development of “fragility fracture” is regarded as the hallmark, e.g. hip fracture after falling from less than standing height or a vertebral fracture with activities of daily living.
Collapsed vertebrae may initially be seen as kyphosis (stooped posture = “Dowager’s hump”)
Diagnosis of osteopororsis
Bone mass/mineral densitometry (BMD) = DEXA scan
- A fracture sustained after a fall from less than standing height or with minimal trauma should suggest the diagnosis.
- Radiographic evaluation: a compression fracture causes reduction in vertebral body weight.
DEXA scan
Bone density scanning, also called dual-energy x-ray absorptiometry (DEXA) or bone densitometry, is an enhanced form of x-ray technology that is used to measure bone loss. DEXA is today’s established standard for measuring bone mineral density (BMD).
Prevention
- The MOST critical time for formation of the calcium matrix ofbone which is specific for women is from about 2 years beforethe menses starts to about 5 years after, approximately age 9-16.
- Adequate calcium and vitamin D intake and regular weight-bearing exercise.
Vitamin D: Adequate intake, 600 IU/day; maximum safe upper level of intake, 4,000 IU/day.
Calcium: The amount you need depends on your age and sex. But, around 1000 mg.
Initial BMD screening
BMD screening in postmenopausal women is widely recommended for those 65 and older
BMD screening in men: age 70 and over
Non-Dairy Sources of Calcium
Dark green leafy vegetables
Sea vegetables (seaweed)
Seafood
Seeds
Medication for osteoporosis
- Bisphosphonates (=Bisphosphonates slow down the osteoclasts, increase bone density).
- (Alendronate = Fosamax. Problem of Fosamax? Difficulty swallowing (dysphagia)).
- Calcitonin (it is a natural hormone made by the thyroid gland and controls the activity of the osteoclasts. It increases bone density).
- Hormone Replacement Therapy (HRT) that has estrogen in women.
- Testosterone Replacement Therapy in men.
- Testosterone Replacement Therapy: osteoporosis in men can be the result of a medical condition called hypogonadism (meaning low levels of the male hormone testosterone with associated symptoms e.g. sexual dysfunction). Increasing androgen levels increases bone density
Rheumatology
It focuses on the treatment of any painful disorder affecting the loco-motor system including joints, muscles, connective tissues, soft tissues around the joints and bones.
Osteoarthritis (OA)
- It is also known as degenerative joint disease (DJD).
OA is the most common pathology of the joints. OA involves mechanical abnormalities involving degradation of joints, including articular cartilage and the subchondral bone. - Subchondral bone ( it is the layer of bone just below the cartilage in a joint).
Risk factors of OA
- Age: the prevalence of OA increases with age.
- Trauma or cumulative mechanical stresses abnormal physical forces lead to altered joint function and damage.
- Obesity
- Muscle weakness
Pathogenesis of Osteoporosis
- The primary event is deterioration of articular cartilage.
- The joint lining, or the synovium, becomes inflamed due to cartilage breakdown causing cytokines (inflammatory cascade proteins) and enzymes that damage cartilage further (synovitis).
- Wear of cartilage causes changes to underlying bones.
- As the articular cartilage wears away, there is increased stress on the articular surfaces of the bone.
- This creates inflammation at the joint and the additional stress can cause local bone remodeling leading to the formation of bone spurs or osteophytes.
Presentation of Osteoarthritis
- OA commonly presents over age 40.
- Signs and symptoms localized to affected joints (not a systemic disease).
- Pain is often insidious and gradually progresses over years.
- Osteoarthritis most commonly occurs in the weight-bearing joints of the hips, knees and lower back.
- Joint soreness after periods of overuse or inactivity.
- Relieved with rest.
- Stiffness after periods of rest that goes away quickly with movement.
- Morning stiffness, which usually lasts no more than 30 minutes.
- Deterioration of coordination, posture and walking due to pain and stiffness of large joints such as knee.
- Loss of function.
- Limited ROM.
Lab results
It is normal in OA, whereas it is abnormal in rheumatoid arthritis.
X-ray in OA
Narrowing of joint space, osteophytes.
Treatment plan of OA
- Exercise
- Weight control
- Joint protection
- Physical and occupational therapy
Medications of OA
- Analgesics (NSAIDS)
- Injectable glucocorticoids (Cortisone)
- Glucosamine and Chondroitin Sulfate
- Topical Analgesics: Tiger Balm, etc.
Analgesics
- Nonsteroidal anti-inflammatory drugs (NSAIDs)
- NSAIDs reduce inflammation and swelling as well as aid in pain relief.
- Examples of NSAIDs include: ibuprofen, naproxen, COX-2 inhibitors.
- Older NSAIDs (for example, aspirin, ibuprofen, naproxen, etc.) all act by blocking the action of both the COX-1 and COX-2 enzymes.
- COX-2 inhibitors selectively block the COX-2 enzyme and therefore have a lower risk of causing ulcers of the stomach or intestine.
- > > COX-2 inhibitors (blocks the enzyme cyclooxygenase-2 (COX-2). This action impedes the production of the prostaglandins that cause the pain and swelling of arthritis inflammation. Celebrex (celecoxib) is the only COX-2 painkiller still on the market.
Injectable glucocorticiods (cortisone)
For fast, targeted pain relief.
Glucosamine and Chondroitin Sulfate
Glucosamine sulfate - it is thought to help with cartilage formation and repair.
Chondroitin sulfate - have an anti-inflammatory effect.
Joint replacement surgery
Indications for joint replacement are severe, unremitting pain with loss of joint function in the presence of radiographic evidence of articular damage.
