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Year 2 > MSK: Part 1 > Flashcards

MSK: Part 1 Flashcards

1
Q

Characteristics of cortical bone

A

Compact

Dense

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2
Q

What are found in the spaces of cortical bone

A

Cells and Blood Vessels

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3
Q

Characteristics of trabecular bone

A
  1. Cancellous (spongy)
  2. Network of bony struts (Trabeculae)
  3. Looks like sponge, many holes with bone marrow
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4
Q

Where do cells of trabecular bones reside

A

Trabceulae

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5
Q

Where are blood vessels of the trabuclar bone found

A

Holes

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6
Q

Woven vs lamellar bone

A

Made quick vs made slow
Disorganised vs organised
No clear structure vs layered

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7
Q

What is the function of th hollow long bone

A

Keeps mass away from neutral axis and minimises deformation

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8
Q

Role of trabecular bone

A

Structural support and minimising mass

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9
Q

Role of wide ends of a long bone

A

Spreads load over weak, frictionless surface

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10
Q

Describe the bone composition

A
  1. 50-70% HYDROXYAPETITE
  2. 20-40% Organic matrix (Type I collagen and non-collagenous proteins)
  3. 5-10% water
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11
Q

Role of minerals

A

Stiffness

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12
Q

Role of collagen

A

Elasticity

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13
Q

What is hydroxyapatite

A

Crystalline form of calcium phosphate

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14
Q

What is the function of the joint

A
  1. Allow movement in 3d
  2. Bear weight
  3. transfer load evenly to MSK system
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15
Q

Where are fibrous joints found

A

teeth sockets

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16
Q

Where are cartilaginous joints found

A

Intervertebral discs

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17
Q

Where are synovial joints found

A

Metacarpophalngeal and knee joints

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18
Q

What separates most articulating joints

A

Fluid-filled cavity

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19
Q

What are the main features of a joint

A
  1. Articular cartilage
  2. Joint capsule
  3. Joint cavity
  4. Synovial fluid
  5. Reinforcing ligaments
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20
Q

What is the inner layer of the joint capsule

A

Synovial membrane

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21
Q

What is the joint cavity

A

Space filled with synovial fluid

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22
Q

What are bursae

A

Found in synovial joints - fluid filled acs

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23
Q

What are meniscis

A

In synovial joints:

Discs of fibrocartilage

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24
Q

What is osteoarthritis

A
  1. Cartilage loss of accompanying periarticular bone response
  2. Inflammation of articular and periarticular structure and alteration in cartilage structure
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25
Q

What structure of the joint is most affected in Non-inflammatory degenerative arthritis

A

ARTICULAR CARTILAGE

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26
Q

What is the most common type of arthritis

A

Non-inflammatory degenerative arthritis

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27
Q

What causes non-inflammatory degenerative arthritis

A

No obvious factor

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28
Q

What conditions can cause SECONDARY OA

A

Haemochromatosis
Obesity
Occupational

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29
Q

What gender is osteoarthritis most common

A

Females

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30
Q

Risk factors for OA

A
  1. Joint HYPERMOTILITY
  2. Insufficient joint repair
  3. Diabetes
  4. Increasing age:
    Due to cumulative effect of traumatic insult
    Decline in neuromuscular junction
  5. Gender (more common in females)
  6. Genetic predisposition
  7. Obesity
  8. Local Trauma
  9. Inflammatory arthritis (Rheumatoid arthritis)
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31
Q

What genetic predisposition causes OA

A
  1. COL2A1 collagen type II gene
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32
Q

How does obesity cause OA

A

Pro-inflammatory state (increased release of IL-1 and TNF)

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33
Q

Where is OA in manual labour found

A

Small joints of th hand

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34
Q

Where is OA in farming found

A

Hips

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35
Q

Where is OA in footballing found

A

Knees

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36
Q

Pathophysiology of OA

A
  1. Progressive destruction and loss of articular cartilage with an accompanying periarticular bone responses
  2. Balance between collagen degradation and its production is lost and increased synthesis of extracellular matrix the cartilage becomes oedematous
  3. Focal erosion of cartilage develops and chondrocytes die - attempted repair from adjacent cartilage
  4. Process of repair is disorganised leading to failure of synthesis of extracellular matrix so that the surface is fibrillated and fissured
  5. Cartilage ulceration exposes underlying bones to increased stress producing micro-fractures and cysts + secondary inflammation
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37
Q

What is cartilage

A

Matrix of collagen fibres, enclosing a mixture of proteoglycans and water - it has a smooth surface and is shock-absorbing

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38
Q

Product of disorganised bone repair

A

Sclerotic subchondral bone forms and overgrowths as the joint margins become calcified (OSTEOPHYTES)

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39
Q

What happens to the exposed underlying bone after cartilage ulceration

A

Becomes sclerotic (increased vascularity and cyst formation)

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40
Q

How do metalloproteinases cause OA

A

Degradation of collagen and proteoglycan

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41
Q

Name two metalloproteinases

A

Stromelysin

COllagenase

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42
Q

How does IL-1 and TNF-alpha cause OA

A

Stimulate metalloproteinase production

INHIBIT collagen production

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43
Q

How does GF deficiency cause OA

A

Impairs matrix repair (Insulin-like GF)

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44
Q

How does gene susceptibility cause OA

A

Mutations in type II collagen can cause polyarticular OA

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45
Q

Main features of OA

A

Loss of cartilage

Disordered bone repair

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46
Q

Clinical presentation of OA

A
  1. Mechanical pain in movement
  2. Symptoms are gradual
  3. Joint pain (worsened by movement and relieved on rest)
  4. Joint stiffness after rest
    5 Only transient stiffness (30 mins)
  5. Muscle wasting of surrounding groups
  6. Crepitus - crushing sensation when moving joints as smooth articulating surfaces are disrupted
  7. Joint effusions
  8. Heberden’s nodes (DIP)
  9. Bouchard’s nodes (PIP)
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47
Q

What joints are most commonly effected by OA

A
  1. DIPs (HEBEEDEN’S NODES) and first carpometacarpal joint thumb)
  2. First metatarsophalangeal joint of foot
  3. Weight-bearing joints (vertebra and hips)
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48
Q

Where are Bouchard’s nodes found

A

PIPs (B is before H so Bouchard’s are more proximal to Heberden’s)

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49
Q

Differential diagnosis of OA

A
  1. Rheumatoid arthritis
  2. Chronic tophaceaous gout
  3. Psoriatic arthritis affecting DIPs
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50
Q

How is OA differentiate from rheumatoid

A

Pattern of joint movement
No systemic features
Early morning stiffness is in rheumatoid

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51
Q

Diagnostics for OA

A

X-rays
FBC
MRI
Aspiration of synovial fluid

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52
Q

What would X-ray show in OA

A 
1. LOSS
L - Loss of joint space
O - Osteophytes
S - Subarticular sclerosis
S - Subchondral cysts
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53
Q

What would FBC show for OA

A
  1. CRP

2. Rheumatoid factor and Antinuclear antibodies are NEGATIVE

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54
Q

What would an MRI show in OA

A

Early cartilage injury and subchondral bone marrow changes

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55
Q

What would aspiration of synovial fluid show in OA

A

Viscous fluid with few leucocytes

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56
Q

upon physical examination of OA what would we see

A

Deformity

Bone enlargement of joints

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57
Q

Non-medical treatment of OA

A
  1. Excercise to improve local muscle strength, improve mobility of weight bearing joints, general aerobic fitness (regardless of age, severity or comorbidity)
  2. Lose weight
  3. Local heat and ice packs
  4. Joint supports/insoles for joint stability and footwear with shock-absorbing properties for lower limb OA
  5. Acupuncture, physiotherapy and occupational therapy
58
Q

Pharmacological treatment of OA

A
  1. Paracetamol prescribed before NSAIDs (IBUPROFEN)
  2. Weak opioids alongside paracetamol (DIHYDROCODEINE)
  3. Intra-articular corticosteroids reduce joint effusion
59
Q

What corticosteroid is not used

A

Systemic

60
Q

When do you not administer corticosteroids

A

if joint is going to be replaces (has immunosuppression properties)

61
Q

Surgical interventions for OA

A
  1. Arthroscopy
  2. Arthroplasty
  3. Osteotomy
  4. Fusion
62
Q

What is arthroscopy

A

Scope inserted into joint to assess damage and remove loose bodies (cartilage fragments causing knee lock)

63
Q

What is arthroplasty

A
  1. Knee/hip replacement
64
Q

Indications of arthroplasty

A
  1. Uncontrolled pain at night

2. Significant limitation of function

65
Q

How long does a prosthetic joint last for

A

10-15 years and need a replacement

66
Q

What is an osetotomy

A

Cut bone to change shape/length

67
Q

What is fusion

A
  1. Usually of ankle and foot to prevent painful grinding of bones
  2. Loss of motility
68
Q

What is rheumatoid arthritis

A

Autoimmune disorder causing SYMMETRICAL DEFORMING POLYARTHRITIS

69
Q

Does RA have inflammation

A

Yes

70
Q

Risk factors for RA

A
  1. Women
  2. Smoking
  3. Before menopause more common
  4. Family history
  5. Genetic factors
  6. Immune system
71
Q

What genetic factors cause RA

A
  1. HLAs DR4 and DRB1 confer susceptibility to RA
72
Q

What factors of the immune system contribute to RA

A

T cells : INF, IL-2 + IL-4
Macrophages: IL-1, 8 and TNF-alpha
Mast Cells: Histamine + TNF-alpha
Fibroblasts: IL-6

73
Q

What maintains the chronic inflammation of RA

A

Local production of rheumatoid factor by B cells and formation of IMMUNE COMPLEXES with complement activate

74
Q

What is rheumatoid factor

A

Autoantibodies directed against Fc portion of immunoglobulin

75
Q

What does RA effect

A

Synovial joints

76
Q

What is synovitis

A

Inflammation of synovial lining

77
Q

When does synovitis occur in RA

A

When chemoattractants produced in the joint recruit circulating inflammatory cells

78
Q

What chemoattractant causes synovitis and joint destruction

A

TNF-alpha

79
Q

What drives overproduction of TNF-alpha

A

Interaction between macrophages, T and B cells

80
Q

What happens to the synovium in RA

A

Becomes greatly thickened and infiltrated in inflammatory cells

81
Q

Describe what happens in RA after synovium thickens

A
  1. Generation of new synovial blood vessels by angiogenic cytokines
  2. Activated endothelial cells produce adhesion molecules which force leucocytes into synovium = inflammation
  3. SYnovium proliferates and grows out over surface of the cartilage (past joint margins) producing a pannus
  4. Pannus of inflamed synovium damages underlying cartilage blocking route for nutrition and effects of cytokines by chondrocytes
  5. Cartilage thins and underlying bone exposed
  6. Pannus destroys articular cartilage and subchondral bone = bony erosions
82
Q

What parts of the body are effected by RA

A
  1. Slowly progressive, SYMMETRICAL swollen, painful and stiff
  2. DIPs are SPARED
  3. MTP of feet
  4. Wrist, elbows, shoulders, knees and ankles
83
Q

Clinical presentation of RA

A
  1. Joints warm and tender
  2. Symptoms worse in morning and in cold
  3. Morning stiffness lasting more than 30 mins
  4. SYMMETRICAL peripheral polyarthritis
  5. Joints swollen, tender and WARM
  6. Movement limitation and muscle wasting
  7. Fatigue, sleep disturbed and pain + stiffness are significantly worse in morning
  8. Shoulder and elbows swollen and stiff
  9. Feet pain in MTP joints, foot broadens and hammer toe deformity leads to ulcers and callouses
  10. Synovitis and effusion in knees
  11. Tenosynovitis (inflammation of knees)
84
Q

What hand deformities are seen in RA

A
  1. Ulnar deviation (swelling of MCP and PIPs)
  2. Swan neck (Z-thumb)
  3. Boutonniere deformity
85
Q

How does Ra effect the lungs

A
  1. Pleura effusions
  2. Fibrosing alveoli’s
  3. Pneumoconiosis (miners)
  4. Interstitial lung disease
  5. Bronchiectasis
86
Q

How does Ra effect the heart

A
  1. Pericarditis
  2. Raynauds
  3. Pericardial effusion
87
Q

How does Ra effect the eyes

A
  1. Dry eyes
  2. Episcleritis (redness of eyes)
  3. Scleritis (severe pain - can’t look at bright lights)
88
Q

Neurological effects by RA

A
  1. Peripheral sensory neuropathies
  2. Compression/entrapment neuropathies
  3. Cord compression
89
Q

What is entrapment neuropathies

A

Soft tissue swelling due to inflammation at site where rigid structures contain nerves (wrist and elbow - carpal tunnel syndrome)

90
Q

What is cord compression

A

Due to instability of cervical spine, we get sensory loss, weakness and disturbed bladder function

91
Q

How does Ra effect the kidneys

A
  1. Amyloidosis (proteinuria and renal impairment)
  2. Nephrotic syndrome
  3. CKD
92
Q

How does RA effect the skin

A

Subcutaneous nodules

93
Q

How is RA diagnosed

A
  1. Normochromic normocytic anaemia
  2. ESR and raised CRP = inflammation
  3. Positive Rheumatoid factor
  4. Positive Anti-cyclic citrullinated peptide
  5. X-ray
  6. MRI and ultrasound
94
Q

What is Positive Anti-CCP

A
  1. Marker of the disease
  2. Presents earlier in the disease and inflammatory arthritis and indicates likelihood of progression to RA

Positive = worst prognosis

95
Q

What is X-ray used for in RA

A
  1. Soft tissue swelling in early disease
  2. Joint space narrowing in late disease
  3. PERI-ARTICULAR EROSIONS
96
Q

What is MRI and ultrasound used for in RA

A
  1. Erosions at joint margins and bones

If effusion present then aspiration of joint - will be cloudy due to high White cells

97
Q

How is RA treated

A
  1. No cure
  2. Smoking cessation to reduce risk of CV disease
  3. Reduce weight
  4. Exercise
  5. Surgery (synovectomy to reduce bulk of inflamed tissue + prevent damage)
  6. Analgesics
  7. Corticosteroids
  8. Biological therapy
98
Q

How is pain in RA managed

A
  1. NSAIDs - IBUPROFEN and COX inhibitors (ASPIRIN) for pain + stiffness
  2. Paracetamol with DIHYDROCODEINE
99
Q

What corticosteroids are prescribed for RA

A
  1. ORAL PREDNISOLONE

2. drug while DMARDs kick in - IM METHYLPREDNISOLONE

100
Q

How are corticosteroids delivered

A

Intra-articular injection (short-lived but rapid effect)

101
Q

Role of corticosteroids

A

Suppress disease activity but risk of long-term toxicity

102
Q

Side-effects of corticosteroids

A

Causes osteoporosis (most common cause of osteoporosis) and increases risk of fracture

103
Q

What are DMARds

A

Inhibit inflammatory cytokines - suppress immune system and carry risk of infection

104
Q

Why are DMARDs used

A

Early to reduce inflammation and slow development of joint erosions and irreversible damage

105
Q

How long does it take for DMARDs to work

A

6 weeks

106
Q

Why do we monitor DMARD use with blood tests

A

All DMARDs have serious side effects

107
Q

Name the gold standard drug for DMARDs

A

METHOTREXATE

108
Q

When is METHOTREXATE contraindicated

A

Pregnancy

109
Q

Side-effects of methotrexate

A
  1. Nausea
  2. Mouth ulcers
  3. Diarrhoea
  4. Abnormal LFTs
  5. Neutropenia
  6. Thrombocytopenia
  7. Renal impairment
110
Q

Alternative DMARDs to METHOTREXATE

A

SULFASALAZINE

LEFLUNOMIDE

111
Q

When is SULFASALAZINE given

A

Mild/moderate disease

112
Q

When is SUlfasalazine given

A

Young and women

113
Q

Side-effects of SULFASALAZINE

A
  1. Nausea
  2. Skin rashes
  3. Mouth Ulcers
  4. Neutropenia
  5. thrombocytopenia
  6. abnormal LFTs
114
Q

How does Leflunomide work

A
  1. Blocks T cell proliferation
115
Q

Side-effects of Leflunomide

A
  1. Diarrhoea
  2. Neutropenia
  3. Thrombocytopenia
  4. Alopecia
  5. Hypertension
116
Q

What biological therapy is used for RA

A
  1. TNF-alpha blockers:

Halts erosion formation

117
Q

What are TNF-alpha blockers given alongside with

A

METHOTREXATE

118
Q

Name a TNF-alpha blocker

A

Infliximab

119
Q

Side-Effects of imfliximab

A

Demyelination

Autoimmune syndromes

120
Q

What is Imfliximab

A

Monoclonal antibodies

121
Q

How is Imfliximab delivered into the body

A

IV

122
Q

What is Etanercept

A

Receptor fusion protein

123
Q

Side-effects of TNF-alpha blocker Etanerept blockers

A

Infections

Hypersensitivity reaction

124
Q

Other than IMfliximab and Etanercept what other TNF-alpha blocker is used for RA

A

ADALIMUMAB

125
Q

What is ADALIMUMAB

A

Monoclonal antibodies

126
Q

Side-effects of ADALIMUMAB

A

Hypersensitivity reaction

Heart failure

127
Q

What are B-cell inhibitors

A

They stop production of rheumatoid factors

128
Q

How does Rituximab function

A

Monoclonal antibod that targets CD20 on B cells

129
Q

Side-effect of RITUXIMAB

A 
Hypo/hypertension
skin rash
nausea
pruritus
back pain
130
Q

When is Rituximab given

A

When anti-TNF agents fails

131
Q

Name two interleukin blockers

A

TOCILIZUMAB

ANAKINRA

132
Q

What is TOCILIZUMAB

A

Monoclonal antibody that binds to IL-6 cytokine before target receptor

133
Q

What are the most common joint inflammation cytokines present

A

IL1

IL6

134
Q

Along what medication is TOCILIZUMAB given with

A

METHOTREXATE

135
Q

What interleukin blocker antagonises IL-1

A

ANAKINRA

136
Q

Name a T-cell activation blocker

A

ABATACEPT

137
Q

Role of ABATACEPT

A

Blocks T cell activation which means macrophages and B cells can’t be activated thus reducing inflammation

138
Q

RHEUMATOID vs OSTEOARTHRITIS

A
  1. Begins at any time vs begins later
  2. Rapid onset vs Slow (over years)
  3. Joints are painful, swollen and stiff vs Joints ache and may be tender but no swelling
  4. Effects small and large joints on both sides of the body vs one side of the body
  5. Morning stiffness lasts longer than 30 mins vs morning stiffness lasts less than 30 mins
  6. Frequent fatigue vs whole body symptoms
139
Q

X-ray results for RA

A

Juxta-articular osteoporosis
Soft Tissue Swelling
Joint Deformity
Loss of Joint Space

140
Q

GI effects of RA

A
  1. FELTY’S SYNDROME: Seropositive RA + Splenomegaly + Neutropenia

Year 2 (155 decks)

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