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PHAR 123* > Bone > Flashcards

Bone Flashcards

1
Q

What are the functions of the main types of bone cells?

A

Osteogenic cells: Develop into osteoblasts

Osteoblasts: bone formation (build)

Osteoclasts: Bone resorption

Osteocytes: maintain mineral concentration of the matrix

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2
Q

What are osteons?

A

They are a subunit of bone structure. Osteons are composed of concentric rings of osteocytes with their dark nuclei in lacunae and this processes called canaliculi

Each osteon has a central Haversian canal with the vascular supply that reaches osteocytes via the canaliculi

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3
Q

What mineral primarily composes the bones?

A

Hydroxyapatite crystal

Serum calcium, Vitamin D, and PTH levels control the metabolism of bone

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4
Q

What is the definining characteristic of trabecular bone?

A

This part of the bone is spongy and it serves an absorbent of stresses put on the bone. They also provide rigidity without conferring a lot of weight

The pores in trabelular bone contain either yellow or red marrow

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5
Q

What is osteoporosis?

A

Multi factorial disease characterized by absolute reduction of the total bone mass. Bone density is significantly reduced. The bones are the same size, but contain less mineral material, effectively reducing bone density and strength

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6
Q

What is the incidence of osteoporosis?

A

1.4 Million Canadians are affected, mainly postmenopausal women and the elderly

Affects 1/4 of women over 50, but only 1/8 of men over 50

70-90% of hip fractures are caused by osteoporosis

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7
Q

What are the clinical criteria for osteoporosis diagnosis?

A

Reduction in bone mineral density by 2.5 STDEVs at the lumbar spine, femur neck, or total hop

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8
Q

What is the clinical criteria for osteopenia diagnosis?

A

This is a less severe version of osteoporosis

Reduction of bone mineral density between 1 and 2.5 STDEVs

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9
Q

What are the risk factors for primary osteoporosis?

A

Unknown etiology, but certain factors predispose patients to osteoporosis:

Age-related changes in metabolism (primary cause)

Low initial bone mass (small frame)

Ethnicity (affects White and Asian more than Black people)

Bad dietary habits (smoking, low Ca2+ and Vitamin D)

Hormones (menopause=low estrogen)

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10
Q

What is the difference between primary and secondary osteoporosis?

A

In primary osteoporosis, the etiology is unknown, but it is the most common form

In secondary osteoporosis, it is usually related to another disease (autoimmune, inflammatory, or nutrient deficiencies)

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11
Q

What are some diseases that may cause secondary osteoporosis?

A

Essentially any disease that can reduce activity and load on bones = decreased bone mass = increased osteoporosis risk

Autoimmune Disorders (inflammatory factors affect bone turnover):
Rheumatoid Arthritis
Lupus
Multiple Sclerosis
Ankylosing spondylitis

GI Disorders (absorption of nutrients is decreased):
Celiac disease
IBD
Weight loss surgery

Medical procedures:
Gastrectomy
GI bypass

Cancer (invasion of bone):
Breast cancer
Prostate Cancer

Hematologic/Blood disorders:
Leukemia
Multiple myeloma
Sickle cell disease

Neurological Disorders (limits mobility and weight bearing activities):
Stroke
Parkinson’s disease
MS
Spinal injuries

Mental health (poor nutrition and activity):
Depression
Eating disorders

Endocrine function (hormonal effects):
Diabetes
Hyperparathyroidism
Hyperthyroidism
Cushing’s syndrome
Premature menopause

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12
Q

What is female athlete triad?

A

This is a situation where a young woman does excessive exercise, whilst not maintaining nutrition. She also has looses nutrients during menstruation

This can greatly increase her risk of developing osteoporosis in the future

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13
Q

What is the pathogenesis of osteoporosis?

A

Osteoporosis is caused by more more cells being resorted than being deposited

This imbalance causes a progressive loss of bone density and thinning

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14
Q

Review slide 17 for a detailed look at the regulation of bone remodelling and what can go wrong to cause osteoporosis

A
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15
Q

What is the relevance of RANKL in osteoporosis?

A

RANKL is a ligand produced by osteoblasts, it production is unregulated when estrogen levels decline. When RANKL binds to osteoclasts, it stimulates their activity an inhibits osteoblast activity

In postmenopausal women, estrogen levels decline, which up-regulates the production of RANKL. More RANKL binding to osteoclasts causes (bone resorption) to go into overdrive.

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16
Q

What are some consequences of osteoporosis?

A

Hip(falling, normal movement) and vertebral (kyphosis) fractures

Radial fractures (break while catching yourself fall)

Loss of height and stooped posture (successive vertebral fractures)

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17
Q

What treatments are available for osteoporosis?

A

BIsphosphonates

Denosumab

Hormone Therapy

SERM (selective estrogen receptor modulators)

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18
Q

What is the mechanism of action for bisphosphonates?

A

Slow down the bone resorption action of the osteoclasts and promote osteoclast apoptosis.

These drugs need to be taken and stay in an upright position. If patient lies down, it can cause esophageal pain

Ex. Alendronate, etidronate, risedronate

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19
Q

Why is it a bad idea to be on bisphosphonates for an extended period of time without breaks (10 years straight)?

A

No bone remodelling due to inhibited osteoclasts can increase fracture risk (opposite effect of bisphosphonates)

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20
Q

What is the mechanism of action for Denosumab?

A

A monoclonal antibody that binds to RANKL. Once binded to RANKL, it prevents RANKL from promoting osteoclast activity

Effective and useful for patients that cannot tolerate bisphosphonates, but it is more expensive

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21
Q

What is the mechanism of hormone therapy in osteoporosis?

A

Increased estrogen down regulates the production of RANKL by osteoblasts. Due to this inhibition of RANKL, osteoclast activity isn’t downregulated

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22
Q

What is the utility of adding progesterone to hormone therapies?

A

Progesterone is added to reduce estrogen-induced tumour incidence

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23
Q

What is the mechanism of action for SERMs?

A

They are non-hormonal, but they mimic the actions of estrogen. Inhibit RANKL production, ensure normal osteoclast activity.

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24
Q

Review slide 25 to see how estrogen has an effect on bone cells

A
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25
Q

What are some other non-estrogen hormone treatments for osteoporosis?

A

Calcitonin inhibits bone resorption by osteoclasts (bone remodelling cells) and promotes bone formation by osteoblasts. Not very effective though. Used when other treatments not tolerated

PTH activates osteoblasts, but needs to be injected daily. Only effective if short term use, otherwise it will cause increased fracture risk (like bisphosphonates)

Sclerostin inhibitors prevent sclerostin from inhibiting osteoblast maturation. So sclerostin inhibitors promote osteoblast function

26
Q

What is osteomalacia?

A

Softening of bones as a result of inadequate mineralization of the organic matrix (caused by vitamin D deficiency)

Known as rickets in kids

27
Q

What are some causes of Vitamin D deficiency?

A

Dietary or inadequate sun exposure due to climate or clothing

INadequate metabolic processing and activation of Vitamin D

Disturbances in phosphate metabolism (kidney unable to retain phosphorus)

28
Q

Should we recommend VItamin D supplements to our patients?

A

Not needed in most people, only those who have an actual Vitamin D deficiency

29
Q

What is the pathology of osteomalacia?

A

Excess nonmineralized osteoid

Bone deformaties

Low serum calcium and phosphorus

30
Q

What are the consequences of rickets (childhood osteomalacia)?

A

Bowlegs (bent lower limbs)

Widened costochondral junction (

Bulging forehead

Delayed dentition (late emergence of teeth)

31
Q

What are some symptoms of osteomalacia?

A

Bone fractures that happen with very little injury

Muscle weakness

Widespread bone pain, especiallly in the hips

If Ca2+ is exceptionally low, neurological symptoms may present:
Abnormal heart rhythms
Numbness around the mouth
Numbness of arms and legs
Spasms of hands or feet

32
Q

What is degenerative joint disease (DJD) or also known as osteoarthritis (OA)?

A

MOst common joint disease (disease of old age)

Osteoarthritis affects larger people more frequently vs. smaller people

Prior injury can predispose patient to osteoarthritis

33
Q

What are the two classes of osteoarthritis?

A

Primary: cause unknown or multi factorial

Secondary: related to another disease

34
Q

What percentage of people over the age of 12 have arthritis?

A

About 20%

35
Q

What is the pathology of osteoarthritis?

A

Damage to joint

Cartilage can become crispy and flake off

BOne grinds against bone (bone damage and erosion)

Pain from inflammation

FIbrosis of supporting tissue

Osteophytes (bony spikes grow and pierce surrounding soft tissue)

36
Q

What is crepitus?

A

It is the presence of sounds coming from a joint (not the same as the popping sounds while moving)

37
Q

What happens in an osteoarthritic hand?

A

Joint space narrowing of radiocarpal, carpometacarpal joint (less cartilage)

38
Q

What happens in an osteoarthritic knee?

A

Asymmetrical breakdown of the cartilage. One side of the knee cartilage is worn down quicker

39
Q

How can osteoarthritis be managed?

A

Exercise (improve range of motion, maintain muscle strength, and reducing weight increase)

PT/OT care and assistive devices

Analgesics, NSAIDs, corticosteroids (used for severe acute inflammation or pain), or hylauronic acid (acts as a lubricant)

Surgery (joint replacement)

40
Q

What is rheumatoid arthritis (RA)?

A

It is a chronic multi system disease primarily involving the joints

It is characterized by chronic symmetrical inflammatory synovitis, joint destruction, muscle atrophy, and bone destruction

Other body parts affected:
Lungs (fibrosis/nodules), eyes (dry), blood vessels (vasculitis), and skin (ulcers)

Fatigue is a major symptom associated with rheumatoid arthritis?

41
Q

What is pannus?

A

It refers to abnormal, hypertrophied synovium, an abnormal tissue that develops in the rheumatic joint

Pannus causes tissue destruction because it releases damaging enzymes, proteins, and acids that break down bone and cartilage

42
Q

Will acetaminophen on its own be helpful in treating rheumatoid arthritis?

A

Mast cells are not the only cells involved, the entire immune system and it cells are contributing to inflammation in the joints

43
Q

What are the stages of rheumatoid arthritis?

A

Healthy joint

Synovitis

Pannus

Fibrous ankylosis

Bony ankylosis

44
Q

What is the mechanism of action of hydroxychloroquine in rheumatoid arthritis?

A

It raises lysosomal pH in antigen presenting cells (ATC), thereby reducing antigen processing efficiency

A reduction in processing efficiency effectively reduces autoimmune attack by reducing presentation of antigen to other immune/inflammatory cells

45
Q

What is the effect of sulfasalazine in rheumatoid arthritis?

A

Inflammatory cell function

Inhibition of folate dependant enzymes (DNA replication)

Inhibition of synovial revascularization

Increase in free radical scavenging activity

46
Q

What is the effect of minocyline in rheumatoid arthritis?

A

Reduces IL-10, suppresses Band T cells (immune system deregulation)

Reduces nitric oxide synthase (an enzyme that breaks down cartilage)

Synergistic effects with NSAIDs

47
Q

What is the effect of methotrexate in rheumatoid arthritis?

A

Inhibits purine and pyrimidine synthesis (inhibition of DNA replication)

Reduces a bunch of interleukins and TNF-alpha (pro-inflammatory cytokines)

48
Q

What is the difference between osteoarthritis and rheumatoid arthritis in joint stiffness?

A

In rheumatoid arthritis, the joints are very stifff and remain like this for more than 1 hour after waking

In osteoarthritis, the joints are only transiently stiff for seconds to minutes after waking. Pain gets worse throughout the the day and depending on activity level. Stiffness also occurs after resting and can also last seconds to minutes

49
Q

What is Ankylosing Spondylitis?

A

Ankylosing spondylitis is a form of chronic inflammation of the spine and sacroiliac joints

Causes pain and stiffness in and around the spine

Affect young men disproportionately (HL-B27 is present in 90% of cases)

Ligaments are more affected than bones

Can also cause inflammation or injury to other joint and organs like the eyes, heart, lung, and kidneys

50
Q

What is the pathogenesis of ankylosing spondylitis?

A

Initial inflammation may be a result of an activation of the body’s immune system (could be due to a bacterial or microbial infection

51
Q

What is psoriatic arthritis?

A

IN 30% of psoriasis patients, they will also develop multi-joint arthritis

52
Q

What are DMARDs?

A

Disease-modifying anti-rheumatic drugs

These drugs can have oral formulation or parenteral

53
Q

What are some treatment options for joint pain in psoriatic arthritis?

A

NSAIDs

Disease-modifying antirheumatic drugs (DMARDs)

Immunosupressants (reduce autoimmune inflammation)

TNF-alpha inhibitors (reduce joint swelling, pain, and stiffness)

54
Q

What are some newer drugs approved for use in rheumatoid arthritis?

A

Apremilast (reduces TNF-alpha, IL-23, and interior

Increased anti-inflammatory mediators such at IL-1999

55
Q

What is sepsis arthritis?

A

The joints are infected with pyrogens bacteria

Bacterial inflections usually derive from a hematogenous route of spread (ex. Gonorrhea, Stepolococci, pneumonococci).

Two minor sources of infection of the synovial capsule is direct inoculation directly onto the joint (trauma), and contiguous spread (from nearby tissues)

Usually involves one large joint. Synovial membranes become edematous and congested, the joint wills with pus

56
Q

What is the pathogenesis of osteomyelitis (septic arthritis)?

A

PAthogens are seeded into the bone

Infection established

Acute inflammatory response

57
Q

What are the different types of DMARDs?

A

Conventional DMARDs: methotrexate, sulfasazine, hydroxychloroquine, and leflunomide

Biological DMARDs (biologics): TNF inhibitors, B cell depleting agent, T cell modulator, IL6 inhibitors, and IL-17 inhibitors

Targeted synthetic DMARDs: JAK inhibitors

58
Q

What are some sources of joint infections?

A

Hematogenous (through the blood stream): most common

Direct inoculation (bacteria introduced directly into the joint): trauma or bad injection technique

59
Q

What are the consequences of an untreated joint infection?

A

Joint destruction

60
Q

What is osteomyelitis?

A

It is the infection the bone itself

61
Q

What is the pathogenesis of osteomyelitis?

A

Pathogens can become seeded into the bone

Local edema can put pressure on vascular supply, effectively trapping the dead areas (sequestrum)

In response to the inflammatory process, reactive bone is laid (like of like stye formation in osteoarthritis)

The walled off infection may serve as a source off pathogens for a future infection. Need IV antibiotics to treat this type of infection

PHAR 123* (11 decks)

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