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SMP - APP Part 2 > Lectures 15 & 16 - Bones and Joints Pathophysiology I & II > Flashcards

Lectures 15 & 16 - Bones and Joints Pathophysiology I & II Flashcards

1
Q

5 functions of bones?

A
  1. Support: lower limbs, pelvis, spine, neck etc. support body structures
  2. Protection: of some organs
    (e. g. brain, thoracic organs, spinal cord)
  3. Movement: muscles move bones at joints
  4. Storage: calcium (99%) and phosphate (85%)
  5. Hematopoiesis: red bone marrow produces blood cells
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2
Q

What kind of tissue are bone and cartilage?

A

Types of specialized connective tissue: cells surrounded by ECM, in this case the ECM is ossified and encased

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3
Q

What are bones made of?

A

Contain a mixture of compact and spongy bone

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4
Q

Other name for compact bone?

A

Cortical bone

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5
Q

Other name for spongy bone?

A

Trabecular bone

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6
Q

Which type of bone contains bone marrow?

A

Spongy bone

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7
Q

What is found in long bones?

A

Medullary cavity with bone marrow

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8
Q

What is yellow bone marrow?

A

Inactive bone marrow in adults

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9
Q

Which bones grow?

A

Long bones elongate at growth plate during bone growth

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10
Q

3 types of bone cells? Describe each.

A
  1. Osteoblasts: build bone
  2. Osteoclasts: cells from macrophage lineage, break down bone
  3. Osteocytes: osteoblasts surrounded by mineralized bone matrix (less active than osteoblasts)
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11
Q

What are osteons?

A

Units of compact bone

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12
Q

Why does cartilage injury tend to heal more slowly than bone?

A

Because cartilage is not as well vascularized as bone

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13
Q

What provides tensile strength to bone?

A

Organic fibers, mainly type I collagen

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14
Q

What hardens bones?

A

Inorganic materials like calcium hydroxyapatite

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15
Q

Where are osteoblasts located?

A

Toward bone surface

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16
Q

How is bone remodeling regulated?

A

By cytokines, growth factors, and other signal molecules

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17
Q

What is bone resorption?

A

Osteoclasts release breakdown enzymes that degrade the bone matrix and release calcium into blood

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18
Q

What is bone remodeling important for? 4

A
  1. Normal bone health
  2. Blood calcium homeostasis
  3. To maintain bone shape after bone growth or in response to stress/exercise
  4. For bone healing after fracture
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19
Q

What are 2 hormones important for calcium homeostasis?

A
  1. PTH

2. Vitamin D

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20
Q

3 roles of PTH for calcium homeostasis?

A
  1. Release of calcium from bone stores and stimulates bone resorption
  2. Increase renal calcium reabsorption
  3. Increase vitamin D production
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21
Q

Role of vitamin D for calcium homeostasis?

A

Increases calcium absorption from GI

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22
Q

What is articular cartilage made of? 3

A
  1. Chondrocytes
  2. 70% water
  3. ECM: type II collagen, proteoglycans, and other proteins
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23
Q

Role of articular cartilage?

A

Functions as shock absorbed and decreases friction in joints

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24
Q

Name of cartilage in synovial joints? Where is it located?

A

Hyaline cartilage, lines bone at a joint

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25
Q

Does cartilage turn over like bone? What to note?

A

YUP - but not as frequently as with bone and it slows with age

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26
Q

4 components of synovial joints? Describe each.

A
  1. Articular cartilage: thin layer of hyaline cartilage that covers bone ends
  2. Joint/articular capsule: fibrous membrane that holds bones together and is made of dense connective tissue
  3. Synovial membrane: inner lining of capsule at the border of the synovial cavity
  4. Synovial fluid: lubricating fluid secreted by synovial membrane
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27
Q

3 ways of examining bones and joints? Which is best?

A
  1. Observation of bone/joint deformity: fracture, bowing, luxation, or signs of inflammation
  2. Specific exam for each joint including examining patency of structural ligaments, discs, etc. => range of motion, compromise of joint movement
  3. X-ray: best modality for initial bone imaging
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28
Q

4 signs of bone/joint inflammation?

A
  1. Heat
  2. Swelling
  3. Redness
  4. Pain
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29
Q

What is bone luxation?

A

Dislocation

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30
Q

2 bone diseases?

A
  1. Osteoporosis

2. Paget disease of bone

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31
Q

5 types of arthritis?

A
  1. Rheumatoid arthritis
  2. Osteoarthritis
  3. Seronegative spondyloarthropathy
  4. Gout and pseudogout
  5. Infectious arthritis
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32
Q

What is osteoporosis? 2 types? Which is more common?

A

Reduced bone mass and bone strength causing increased risk of fractures due to an imbalance between bone formation and resorption

  1. ***Primary: postmenopausal or senile
  2. Secondary to other conditions
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33
Q

When is peak bone mass achieved? What does this depend on? Implication?

A

Young adulthood

Based on gender (males>females), genetics, physical activity, diet => onset of osteoporosis will be affected by this peak bone mass

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34
Q

When does bone mass start declining? When is peak bone loss?

A

After 40s with each resorption/formation cycle, peak bone loss in 60s onward

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35
Q

Symptoms of osteoporosis?

A

None other than easier to fracture bones (compression fractures and due to falls)

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36
Q

5 contributing factors to osteoporosis?

A
  1. Changes with aging: osteoblasts from elderly have decreased ability to synthesize bone, decreased replicative activity of osteoprogenitor cells, decreased biologic activity of matrix-bound growth factors
  2. Reduced physical activity: bone formation increases with increased stress on bone (e.g. weight bearing exercise increases bone density and immobilized patients and astronauts have decreased bone mass)
  3. Genetic factors: vitamin D receptor type important for peak bone mass acquisition
  4. Environmental: calcium and vitamin D levels, smoking, steroid therapy
  5. Hormone levels: estrogen important for maintaining balanced resorption/formation cycles
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37
Q

Why are women at higher risk than osteoporosis then men?

A

Because of the significant drop in sex hormones at menopause vs a more gradual decline in men

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38
Q

How exactly does decreased estrogen cause osteoporosis at menopause? 2

A
  1. Causes cytokine activation of osteoclast activity > osteoblast activity
  2. RANK: receptor activator of nuclear factor that activates osteoclast differentiation
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39
Q

5 secondary causes of osteoporosis?

A
  1. Osteogenesis imperfecta (dysfunctional type I collagen)
  2. Drugs (e.g. steroids)
  3. Endocrine disorders (e.g. hyperparathyroidism)
  4. Neoplasia
  5. Malnutrition or malabsorption with vitamin deficiency
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40
Q

What are compression fractures?

A

Compression of spine vertebrae due to weight of body

41
Q

Screening and diagnosis for osteoporosis?

A

Dual energy X-ray absorptiometry (DXA) scan determines bone mineral density:

> 2.5 SDs below normal is osteoporosis
1 SDs below normal is osteopenia (low bone mass)

42
Q

Who should be screened for osteoporosis?

A

Post menopausal women > 65 yo or those with multiple risk factors

43
Q

Clinical management of osteoporosis?

A
  1. Life-style changes: exercise, no smoking, calcium/vit D supplementation
  2. Pharmacologic treatment: for pts with fracture history or osteoporosis diagnosed by bone mineral density measurement we can administer bisphosphonates which inhibit bone resorption mediated by osteoclasts, and estrogen
44
Q

How exactly do biphosphonates treat osteoporosis?

A

Stick to bone and inhibit osteoclast activity at bony surface by increasing osteoclast apoptosis via ATP depletion

45
Q

Side effects of biphosphonates to treat osteoporosis? Consequence?

A

Inflammation of the esophagus, so patient needs to be able to sit upright for 30 min after taking meds and patients with issues with esophageal motility should not take them

46
Q

What is Paget’s disease of bone?

A

Overgrowth of bone from abnormal increased rates of bone remodeling limited to specific bone areas => skull, vertebrae, long bones of extremities most common

47
Q

In what patients is Paget’s disease of bone more common?

A
  1. Older patients > 55 yo
  2. Males > females,
  3. Higher in UK and western Europe ancestry
48
Q

Cause of Paget’s disease of bone?

A

Not well understood but we know it is initiated by an increase in osteoclast activity causing an increase in osteoblast activity

Possible genetics and environmental factors (viral?)

49
Q

% elderly affected by Paget’s disease of bone?

A

10%

50
Q

Symptoms of Paget’s disease?

A

Majority of patients have no symptoms, but those who do have pain at the site of bone overgrowth and an increase in bone size => more prone to fractures and rare development of cancer

51
Q

Diagnosis of Paget’s disease? 2

A
  1. Radiographic features sufficient
  2. Elevated blood alkaline phosphatase of bone origin, which is produced with bone formation aka with increased osteoblast activity => can be used to monitor disease progression and is a marker of bone turnover
52
Q

Histology for Paget’s disease?

A

Puzzle piece sign

53
Q

Treatment for Paget’s disease?

A

Biphosphonates

54
Q

What are 4 seronegative spondyloarthropathies? What do they all have in common?

A
  1. Ankylosing spondylitis
  2. Immune mediated arthropathies from previous exposure/infection
  3. Reactive arthritis (GI or chlamydia infection => Reiter’s syndrome)
  4. Arthritis associated with other conditions (psoriasis, inflammatory bowel disease)

All immune-mediated

55
Q

Other name for infectious arthritis?

A

Septic arthritis

56
Q

What causes infectious arthritis? 2

A
  1. Hematogenous spread of bacterial pathogen to joint (e.g. Borrelia burgdorferi (Lyme’s disease), gonococci in STI)
  2. Direct spread from penetrating injury
57
Q

What is gout?

A

Uric acid crystal deposition arthropathy

58
Q

What gives seronegative spondyloarthropathies their name?

A

In the blood, they do are not positive for rheumatoid factor

59
Q

What is rheumatoid arthritis?

A

Autoimmune disorder of joints that leads to synovitis and progressive destruction of cartilage/joints

60
Q

3 risk factors for rheumatoid arthritis?

A
  1. Higher prevalence in women
  2. 40s-70s
  3. Smoking
61
Q

What are 8 extra-articular manifestations of RA?

A
  1. Rheumatoid subcutaneous soft tissue nodules
  2. Neuropathy
  3. Eye involvement
  4. Vasculitis
  5. Interstitial lung disease
  6. Chronic fatigue symptoms
  7. Elevated blood markers of inflammation
  8. Heart manifestations
62
Q

What is the pathophysiology of RA?

A
  1. Autoimmune response to unknown arthritic antigen in genetically susceptible individual causing lymphocyte activation and inflammatory mediator release
  2. Gradual overactivation of innate immune response due to the activation of enzyme that converts arginine to citrulline => citrullination of joint protein causes activation of immune response with anti-citrullinated protein antibodies

=> CAUSING:

  1. Development of inflammatory synovium that invades joint cartilage and bone
  2. Pannus formation: synovial tissue with inflammatory cells, connective tissue cells, and scar-like connective tissue => causes EARLY protease-mediated and inflammatory bone destruction
  3. Angiogenesis to nourish the proliferating tissue and further increases fluid and immune cell deposition in the joint
63
Q

2 interleukins involved in RA inflammation?

A
  1. IL-1

2. TNF

64
Q

Which joints are affected first in RA? Then what?

A

Small joints in hands, feet in a symmetric manner

Then, large joints

Axial skeleton involvement may progress in some pts (especially the neck)

65
Q

What is polyarthritis?

A

RA when more than 3 joints are affected

66
Q

7 symptoms of RA? What to note?

A
  1. Joint paint
  2. Joint stiffness
  3. Joint swelling
  4. Joint deformity
  5. Fatigue
  6. Low-grade fever
  7. Generalized muscoloskeletal pain

NOTE: gradual onset with possible periods of disease and remission

67
Q

What worsens joint symptoms of RA?

A

Inactivity (worse in the morning)

68
Q

What is RA with remission called?

A

Palindromic rheumatism

69
Q

How to diagnose RA? 5

A
  1. Clinical features
  2. X-ray: joint swelling, joint space narrowing, joint malalignment, bone erosion
  3. Joint exam
  4. Serology
  5. Synovial fluid exam
70
Q

What 2 findings with a synovial fluid exam indicate RA?

A
  1. Effusion

2. Elevated leukocyte count

71
Q

What 3 serology findings indicate RA?

A
  1. Rheumatoid factor + => may not be present, may also be present in other conditions
  2. ACPA = anti-citrullinated peptide antibodies
  3. Other non-specific inflammatory factors also tested (ESR, CRP, ANA)
72
Q

What does ESR stand for?

A

Erythrocyte sedimentation rate

73
Q

What does CRP stand for?

A

C-reactive protein

74
Q

What does ANA stand for? What is this?

A

Anti-nuclear antibody = autoantibody against cell nucleus

75
Q

What is rheumatoid factor?

A

Anti-self IgM antibody against Fc of self IgG

76
Q

What are high RF values concordant with?

A

More severe RA with extra articular disease

77
Q

Clinical management of RA? 4

A
  1. NSAIDs: analgesia and anti-inflammatory
  2. Steroids: anti-inflammatory
  3. DMARDs = disease modifying anti-rheumatic drugs: prevent joint destruction (joint damage occurs early, so early therapy highly recommended)
  4. Cytotoxic drugs and other anti-immune medication
78
Q

Main risk of RA?

A

Reduced life expectancy due to complications related to BVs, other organs or treatment

79
Q

2 DMARDs to treat RA?

A
  1. TNF alpha inhibitors (Humira, Remicade)

2. IL-1 receptor antagonists

80
Q

5 side effects of DMARDs to treat RA?

A
  1. Myelosuppression
  2. Infection risk
  3. Liver toxicity
  4. GI effects
  5. Renal effects
81
Q

What is osteoarthritis?

A

Degenerative joint disease with progressive erosion of articular cartilage in joint

82
Q

What is the most common joint disease? What to note?

A

OA

NOTE: major cause of disability in US

83
Q

In what patients is OA most common?

A

Older individuals

84
Q

2 types of OA? Describe each.

A
  1. Primary OA: occurs with no predisposing cause, associated with aging, lifestyle (obesity, activity, etc.)
  2. Secondary OA: following specific injury to joint, congenital joint deformity
85
Q

Describe the pathophysiology of OA. 4

A
  1. Mechanical wear, which increases with age and excess stress on joints (obesity, joint injury), affects weight-bearing large joints (knees, hips, spine etc.) and causes mechanotransduction: increased chondrocytes response to stress => cellular signaling
  2. Damage to cartilage by trauma (single or continued over time) due to age, obesity, disease, defective cartilage, repetitive activities (athletes, occupation), genetics, female gender, previous injury
  3. Decreased cartilage strength with increased water content, decreased proteoglycans, decreased collagen synthesis and increased collagen destruction due to increased activity of proteases and IL-1
  4. Exposure of underlying bone after cartilage destruction => friction on bone and microfractures
86
Q

What is the key cytokine in OA?

A

IL-1

87
Q

6 symptoms of OA?

A
  1. Joint pain that is worse with activity and relieved by rest
  2. Joint short term stiffness with inactivity may occur (not as long as with RA)
  3. Limitation in joint movement
  4. Joint crackling/popping (crepitus)
  5. Non-symmetric joint involvement (mono or polyarthritic)
  6. Osteophytes: bone spurs, bony projection on joint margin
88
Q

Most common 5 joints affected by OA?

A
  1. Hands
  2. Feet
  3. Knee
  4. Hip
  5. Spine
89
Q

What is important to note about the treatment for OA?

A

Treatment is joint specific

90
Q

3 types of treatments for OA? Describe each.

A
  1. Non-pharmacologic: weight loss, rest, physical therapy/exercise program to strengthen supporting muscles and improve range of motion, bracing for some joints, etc
  2. Pharmacologic:
    - Analgesic for pain control
    - Anti-inflammatory
    - Intra-articular steroid injection
  3. Surgical: arthroscopic joint lavage, repair, joint replacement
91
Q

Can DMARDs be used to treat OA?

A

NOPE

92
Q

Normal viscosity of synovial fluid?

A

Very high

93
Q

Normal color of synovial fluid?

A

Clear

94
Q

Color of synovial fluid with inflammatory arthritis?

A

Yellow to opalescent

95
Q

Viscosity of synovial fluid with inflammatory arthritis?

A

Low

96
Q

Viscosity of synovial fluid with noninflammatory arthritis?

A

High

97
Q

Color of synovial fluid with noninflammatory arthritis?

A

Yellow

98
Q

List the 3 types of arthritis by number of WBCs in synovial fluid.

A
  1. Septic arthritis
  2. Inflammatory arthritis
  3. Noninflammatory arthritis
99
Q

Do either OA or RA have a rapid onset?

A

NOPE - both progressive

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