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PHAR 123 > Osteoporosis/Bone and Joint > Flashcards

Osteoporosis/Bone and Joint Flashcards

1
Q

What are the functions of Osteocytes

A

Maintain mineral concentration of matrix

These will subdivide into osteoclasts/osteoblasts when needed

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2
Q

What are the functions of Osteoclasts

A

Bone resorption

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3
Q

What are the functions of Osteoblasts

A

Bone Formation

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4
Q

What are the functions of Osteogenic cells

A

Develop into osteoblasts

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5
Q

Most of the bone is composed of

A

hydroxyapatite crystal

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6
Q

What controls the metabolism of bone?

A

Parathormone levels

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7
Q

What is the definition of Osteoporosis

A

Multifactorial disease characterized by absolute reduction of the total bone mass. Bone density is significantly reduced.

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8
Q

What is the standerd criterion for the diagnosis of osteoporosis in postmenopausal women and older men

A

T score less then -2.5

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9
Q

What is the standard T score for someone with Osteopenia

A

by bone densitometry as a T score -1 to -2.5.

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10
Q

What are the risk factors for osteoporosis?

A

Low initial bone mass
Ethnicity
Bad dietary habits, smoking
Hormones
Age-related changes in metabolism

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11
Q

What are the two groups of etiology related to osteoporosis?

A

Primary and Secondary

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12
Q

What is Primary Osteoperosis?

A

cause unknown;
most common

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13
Q

What is secondary Osteoporosis?

A

Related to another disease affecting otherwise normal bone; rare.

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14
Q

What are some secondary causes of Osteroporosis

A

Autoimmune Disorders
Digestive and Gastrointestinal Disorders
Medical procedures
Cancer
Hematologic/Blood Disorders
Neurological
Blood and bone marrow
Mental illness
Endocrine/hormonal disorders

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15
Q

Osteomalacia is defined as

A

Normal Structure, under mineralized

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16
Q

Osteoporosis is defined as?

A

Structurally degraded, Fully mineralized

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17
Q

What is the MOA of Bisphosphonates

A

Bind to bone and slow down the bone resorbing action of osteoclasts

Promote osteoclast apoptosis

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18
Q

What are some of the Bisphosphonates available in the market (4)

A
  • alendronate (Fosamax ®)
  • etidronate (Didrocal ®)
  • risedronate (Actonel ®)
  • zoledronic acid (Aclasta®)

(Dronate)

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19
Q

What are some adverse effects of bisphosphonates?

A

esophageal irritation (must stay upright after administration), and osteonecrosis of the jaw

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20
Q

What is the MOA of denosumab?

A

prevents RANKL-RANK interaction and thereby inhibits osteoclast formation

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21
Q

What hormone therapy is used in osteoporosis treatment?

A

estrogen±progesterone to increase density

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22
Q

What are SERMs?

A

Selective Estrogen Receptor Modulators SERMs are non- hormonal, but they act like the hormone estrogen to increase bone density

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23
Q

What is one of the main purposes of estrogen that we emphasized?

A

Decreases RANKL induction differentiation

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24
Q

What does estrogen do? (3)

A

Decrease activation of bone remodelling
Continues maintenance of bone formation
Decrease bone resorption

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25
Q

What are the Four specific drug treatments for Osteoperosis?

BCPS

A

Bisphosphates
Calcitonin
Parathyroid Hormone
Sclerostin Inhibitor

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26
Q

What is the MOA of Calcitonin

A

Inhibits bone resorption by osteoclasts and promotes bone formation by osteoblasts

Not very effective, used when other treatments not tolerated

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27
Q

What is the MOA of Parathyroid Hormone

A

Activates osteoblasts. Teriparatide injection (Forteo) SQ daily, up to 2yrs for severe osteoporosis

Short term PTH has an anabolic effect on bone by acting on osteoblasts

Long term usage would lead to bone loss

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28
Q

What is the MOA of sclerostin Inhibitors?

A

Sclerostin is secreted by Osteoclasts and inhibits the maturation of osteoblasts

Binds an inhibits the release of sclerostin

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29
Q

What is the function of Osteoclasts?

A

Bone degredation

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30
Q

What is the function of Osteoblasts

A

Bone reformation

31
Q

What does rank ligand do?

A

Bind to RankL receptors on Osteoclasts and leads to activation

32
Q

What does OPG do?

A

Natural inhibitors secreted by osteoblasts that inhibits RankL. Regulates bone resportion

33
Q

Osteoblasts turn into what?

A

Osteocytes once new bone is created

34
Q

What does decreased levels of estrogen do to the levels of RPG

A

Increases and it overwhelms OPG leading to greater bone loss

35
Q

Define Osteomalacia

A

Softening of bones as a result of inadequate mineralization of the organic matrix

36
Q

Cause of Osteomalacia

A

deficiency of vitamin D, inadequate metabolic processing and activation of vitamin D, or disturbances of phosphate metabolism

37
Q

What is the recommended IU of Vitamin D a day?

A

200IU (May not be enough in Canada though)

38
Q

How is Hypophosphatemia caused?

A

Due to renal disease. The kidney is unable to retain phosphorus, and so it is lost in the urine.

39
Q

Excessive losses or failure to add phosphate to bone leads to

A

Osteomalacia

40
Q

Pathology of Osteomalacia

A
  • Excess nonmineralized osteoid
  • Bone deformities and fractures
  • Serum calcium and phosphorus low * Rickets = osteomalacia in children
41
Q

Consequences of Rickets? (4)

A
  • Bowlegs
  • Widened costochondral junction (“rachitic rosary”)
  • Craniotabes (bulging forehead)
  • Delayed dentition
42
Q

Symptoms of Osteomalacia

A

Easy fractures
Muscle weakness
Bone pain (esp in hips)
Abnormal heart rhythms
Spasms

43
Q

What is Degenerative Joint Disease (DJD)

A

Most common joint disease also known as Osteoarthritis

Affects larger people

Most prevalent chronic health conditions in Canada

44
Q

What is the Difference in structure between Osteoarthritis and Advanced Osteoarthritis?

A

Bone cysts and Osteophytes still occur

Calcified cartilage
Periarticular fibrosis (Enlargement of tendons)

45
Q

What is/are osteophytes

A

Calcified regions that stab into cartilage/fibrosis regions

46
Q

What is the management of OA?

A

Exercise
PT/OT
Analgesics, NSAIDs, corticosteroids or hyaluronic acid
Surgery

47
Q

What is Rheumatoid Arthritis?

A

the chronic multisystem disease primarily involving the joints.

48
Q

What happens in terms of pathogenesis with RA?

A

Ankylosis
Peri-Articular osteopenia
Joint deformity

49
Q

What is Peri-articular osteopenia

A

Degeneration of the bone
Holes near the joint

50
Q

What is ankylosis?

A

Muscular atrophy in the region of the joints of RA causing stiffness

51
Q

Rheumatoid synovium is characterized by

A

number of secreted products of activated lymphocytes, macrophages, and altered fibroblasts

52
Q

What are the Mild treatments of RA?

A

NSAIDS
Plaquenil
Sulfasalazine
Minocycline
Methotrexate

53
Q

What is the moderate treatment of RA?

A

DMARDS
Methotrexate
Anti TNF
Anti IL1

54
Q

What is the severe treatment of RA?

A

DMARDs, Steroids, prosorba

55
Q

What is the MOA of Plaquenil (hydroxychloroquine), RA treatment

A

Raises lysosomal pH in antigen-presenting cells, thereby reducing antigen processing efficiency

Slow

56
Q

MOA of Sulfasalazine

A
  • effects inflammatory cell function, cytokine and antibody production
57
Q

MOA of Minocycline

A

tetracycline class antibiotic with anti-inflammatory properties.

Reduces IL-10, suppresses B and T cells

Synergistic with NSAIDS***

58
Q

MOA of Methotrexate

A

immunosuppressant

  • Inhibits purine and pyrimidine synthesis.
  • Anti-inflammatory - Adenosine receptor agonist.
  • Reduces IL-6, IL-1 and TNF-alpha.
  • Complex effects on immune cell proliferation and activity. Acts quickly.
59
Q

What is a difference between RA and OA (Physical symptoms)

A

OA: patients tend to be transiently stiff for seconds to minutes after waking and problems are worse through the day and on activity. Post rest stiffness called gelling is typical lasting seconds to minutes in osteoarthritis patients.

RA: Patients with inflammatory arthritis, typically, are very stiff and this lasts longer than 1 hour after waking. The pain and stiffness in these patients gets better with mobilisation and as the day progresses.

60
Q

What is Ankylosing Spondylitis

A

Chronic inflammation in these areas causes pain and stiffness in and around the spine. Over time, chronic inflammation of the spine (spondylitis) can lead to a complete fusion of the affected vertebrae (ankylosis). Fatigue is common during active inflammation.

61
Q

Pathogenesis of Ankylosing Spondylitis

A

activation of the body’s immune system, perhaps by a preceding bacterial infection (Yersinia, Salmonella) or a combination of infectious microbes.

Ligaments more affected than bones.***

62
Q

Psoriatic Arthritis define

A

Inflammatory Psoriasis usually that causes swelling of joints, lifting/crack of nail, and inflammation associated with psoriasis

63
Q

What does DMARDS stand for?

A

Disease modifying antirheumatic drugs

64
Q

What are the main three DMARDS

A

Methotrexate, Leflunomide, Sulfasalazine

65
Q

What are the 2 main Immunosuppressants discused?

A

Azathioprine, cyclosporine

66
Q

What is septic arthritis?

A

Joints may be infected with pyogenic bacteria or TB.

Left untreated= joint destruction

67
Q

Pathogenesis of osteomyelitis

A
  • Pathogens are seeded into the bone
  • Infection established
  • Inflammatory response, with pus formation,tissue destruction and systemic symptoms of acute inflammation.
  • Local edema puts pressure on vascular supply, compromising blood flow
  • Local necrosis can result (the trapped dead area is the “sequestrum”)
68
Q

Where does bone changes usually occur?

A

Senile osteoporotic bone

69
Q

What is the overarching defn of osteoperosis pathogenesis?

A

More bone cells being resorbed than being deposited

70
Q

What does estrogen do to Osteoclasts?

A

Decreases bone resorption

71
Q

What is crepitus?

A

Degeneration of cartilage

72
Q

What is Apremilast?

A

Anti-inflammatory

73
Q

What is Ustekinumab?

A

Reduces T cell activation

74
Q

What is Secukinumab?

A

Acts against proinflammatory cytokines

PHAR 123 (11 decks)

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