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1st Year Med > Bone Disorders (OA/RA/OP) > Flashcards

Bone Disorders (OA/RA/OP) Flashcards

1
Q

what are the characteristics of a joint in osteoarthtitis?

A

thickened capsule, cyst formation and sclerosis in subchondral bone, shelving ‘fibrillated’ cartilage, osteophytic lymphing, synovial hypertrophy, altered bone contour

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2
Q

what cartilage is primarily affected by OA, and how so?

A

articular cartilage
causes increased swelling, colour change, cartilage fibrillation, cartilage erosion down to subchondral bone

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3
Q

what are the 3 types of cartilage?

A

hyaline (articular)
elastic (nose/ear)
fibrocartilage (meniscus/pubic ramus)

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4
Q

what 2 things is cartilage made up of?

A

cells (chrondocytes)
extracellular matrix (collagen/water)

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5
Q

describe the 3 layers of cartilage

A

superficial, middle and deep zone, all have different compositions of collagen and chondrocytes, calcified cartilage within

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6
Q

describe the function of the cartilage features

A

chondrocytes - synthesise and maintain ECM
ECM - collagen type 2 embedded in proteoglycan gel, protects chondrocytes from loading forces

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7
Q

what biological changes are seen in OA?

A

decreases in water content, proteoglycan synthesis, collagen cross linking and hyalauronic acid
trauma damage

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8
Q

what are the primary and secondary types of OA?

A

primary - degenerative

secondary - trauma, hip dysplasia, infection, diabetes

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9
Q

what may an x-ray find in OA?

A

LOSS
L - loss of joint space
O - osteophytes
S - subchondral sclerosis
S - subchondral cysts

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10
Q

what non-surgical treatments are administered for OA?

A

medications, physiotherapy, walking aids, joint injections

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11
Q

what are the surgical treatments administered for OA?

A

arthroscopy, cartilage transplantation, bone re-alignment, joint replacement

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12
Q

what are the principles of joint replacement surgery?

A

remove worn cartilage and replace with synthetic material
objective - pain relief, increase motion range, improve daily life activities

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13
Q

What is autoimmunity?

A

loss of immunological tolerance to self

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14
Q

describe the basics of RA

A

widespread joint pain, stiffness and swelling leading to joint destruction

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15
Q

what are some of the systemic symptoms of RA?

A

fevers, weight loss, extra-articular features (inflammation in other joints)

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16
Q

name the 6 phases of RA development

A

genetic risk factors
environmental risk factors
autoimmunity
symptoms
undifferenciated arthritis
RA

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17
Q

where are most genes causing RA found?

A

in adaptive immunity pathways (B-cell, T-cell, cytokines)

18
Q

what environmental risk factor aggrevates the shared epitope (HLA-DRB1 allele)

A

smoking

19
Q

explain the physiological changes occuring in the autoimmunity stage of RA development

A

autoantibodies present (rheumatoid factor and CCP)
increased cytokines and chemokines
altered cholestorol metabolism

20
Q

explain the changes in the symptom phase of RA development causing the symptoms

A

monocytes/macrophages activated
and cytokine and chemokines release causing damage, meaning more self-antigens and epitope spread
local tissue environment takes over (osteoclasts)
inflammation becomes established

21
Q

what is the standard treatment for RA?

A

DMARDs (disease-modifying anti-rheumatic drugs) e.g methatrexate
NSAIDs
corticosteroids

22
Q

what are biologic agents?

A

drugs (e.g monoclonal antibodies) which have been developed rationally by targetting processes important in disease pathogenesis (e.g T-cells)

23
Q

what are the differences in using biologic drugs compared to conventional drugs?

A

biologics differ in size, manufacturing complexity, and in the way they interact with cells and other proteins in the body

24
Q

define OA

A

chronic degenerative change of damaged articular cartilage

25
Q

what are the clinical features of OA?

A

pain (worse on weight bearing)
night waking
stiffness (often in morning)
walking aid reliance
loss of function

26
Q

what is the clinical term for a joint replacement?

A

arthroplasty

27
Q

what are the risks of an arthroplasty?

A

blood clots, infection, stiffness, ongoing pain, dislocation, leg length discrepancy, neurovascular damage, anaesthetic risk

28
Q

what are the risk factors for OA?

A

age, sex (more likely in females), trauma (intra-articular fracture), microtrauma (repetitive high impact activities), genetics, congenital abnormality
obesity

29
Q

what is the function of articular cartilage?

A

smooth lubricated surface for articulation
facilitate load transmission and lower impact movement

30
Q

name the alternate medications used for articular cartilage repair

A

glucosamine and chondroitin sulfate

31
Q

define osteoporosis (OP)

A

systemic skeletal disease characterised by low bone density and microarchitectual deterioration of bone tissue with a consequent increase in bone fragility

32
Q

what is a fragility fracture?

A

fracture sustained by a fall from standing or less

33
Q

what are the non-modifiable risk factors for OP?

A

age (65+ F, 75+ M)
gender (F)
race (caucasian)
previous fracture
early (untreated) menopause
family history

34
Q

what are the modifiable risk factors for OP?

A

bone mineral density
alcohol (3.5+ units daily)
low BMI (<20)
smoking
physical inactivity

35
Q

name any OP related conditions

A

diabetes
inflammatory rheumatic diseases
GI conditions
endocrine conditions
chronic liver/kidney disease
neuro - alzeimers/MS

36
Q

compare FRAX and Q-fracture screening

A

FRAX (fracture risk assessment) - includes bone mass density (BMD)
doesn’t include several important variables
Q-fracture - includes other factors but not BMD

37
Q

explain the DXA scan

A

dual energy x-ray absorptiometry
measures bone mineral density at spine and hip
gives a T-score (for OP)

38
Q

explain the T-score system of DXA screening

A

+1 to -1: normal range
-1 to -2.5: osteopenia (slightly below normal)
-2.5 and below: OP

39
Q

describe how bisphosphonates work as a therapy for OP

A

inhibits osteoclasts
high affinity for bone mineral

40
Q

explain how denosumab acts as a therapy for OP

A

monoclonal antibody against receptor activator for RANK ligand (required for osteoclast function)

41
Q

what are the 2 general treatment strategies for OP?

A

antiresorptive - reduces bone turnover
anabolic - stimulates bone formation

1st Year Med (52 decks)

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