MSK: Part 1 Flashcards
1
Q
Characteristics of cortical bone
A
Compact
Dense
2
Q
What are found in the spaces of cortical bone
A
Cells and Blood Vessels
3
Q
Characteristics of trabecular bone
A
- Cancellous (spongy)
- Network of bony struts (Trabeculae)
- Looks like sponge, many holes with bone marrow
4
Q
Where do cells of trabecular bones reside
A
Trabceulae
5
Q
Where are blood vessels of the trabuclar bone found
A
Holes
6
Q
Woven vs lamellar bone
A
Made quick vs made slow
Disorganised vs organised
No clear structure vs layered
7
Q
What is the function of th hollow long bone
A
Keeps mass away from neutral axis and minimises deformation
8
Q
Role of trabecular bone
A
Structural support and minimising mass
9
Q
Role of wide ends of a long bone
A
Spreads load over weak, frictionless surface
10
Q
Describe the bone composition
A
- 50-70% HYDROXYAPETITE
- 20-40% Organic matrix (Type I collagen and non-collagenous proteins)
- 5-10% water
11
Q
Role of minerals
A
Stiffness
12
Q
Role of collagen
A
Elasticity
13
Q
What is hydroxyapatite
A
Crystalline form of calcium phosphate
14
Q
What is the function of the joint
A
- Allow movement in 3d
- Bear weight
- transfer load evenly to MSK system
15
Q
Where are fibrous joints found
A
teeth sockets
16
Q
Where are cartilaginous joints found
A
Intervertebral discs
17
Q
Where are synovial joints found
A
Metacarpophalngeal and knee joints
18
Q
What separates most articulating joints
A
Fluid-filled cavity
19
Q
What are the main features of a joint
A
- Articular cartilage
- Joint capsule
- Joint cavity
- Synovial fluid
- Reinforcing ligaments
20
Q
What is the inner layer of the joint capsule
A
Synovial membrane
21
Q
What is the joint cavity
A
Space filled with synovial fluid
22
Q
What are bursae
A
Found in synovial joints - fluid filled acs
23
Q
What are meniscis
A
In synovial joints:
Discs of fibrocartilage
24
Q
What is osteoarthritis
A
- Cartilage loss of accompanying periarticular bone response
- Inflammation of articular and periarticular structure and alteration in cartilage structure
25
What structure of the joint is most affected in Non-inflammatory degenerative arthritis
ARTICULAR CARTILAGE
26
What is the most common type of arthritis
Non-inflammatory degenerative arthritis
27
What causes non-inflammatory degenerative arthritis
No obvious factor
28
What conditions can cause SECONDARY OA
Haemochromatosis
Obesity
Occupational
29
What gender is osteoarthritis most common
Females
30
Risk factors for OA
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)
31
What genetic predisposition causes OA
1. COL2A1 collagen type II gene
32
How does obesity cause OA
Pro-inflammatory state (increased release of IL-1 and TNF)
33
Where is OA in manual labour found
Small joints of th hand
34
Where is OA in farming found
Hips
35
Where is OA in footballing found
Knees
36
Pathophysiology of OA
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
37
What is cartilage
Matrix of collagen fibres, enclosing a mixture of proteoglycans and water - it has a smooth surface and is shock-absorbing
38
Product of disorganised bone repair
Sclerotic subchondral bone forms and overgrowths as the joint margins become calcified (OSTEOPHYTES)
39
What happens to the exposed underlying bone after cartilage ulceration
Becomes sclerotic (increased vascularity and cyst formation)
40
How do metalloproteinases cause OA
Degradation of collagen and proteoglycan
41
Name two metalloproteinases
Stromelysin
| COllagenase
42
How does IL-1 and TNF-alpha cause OA
Stimulate metalloproteinase production
INHIBIT collagen production
43
How does GF deficiency cause OA
Impairs matrix repair (Insulin-like GF)
44
How does gene susceptibility cause OA
Mutations in type II collagen can cause polyarticular OA
45
Main features of OA
Loss of cartilage
| Disordered bone repair
46
Clinical presentation of OA
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)
6. Muscle wasting of surrounding groups
7. Crepitus - crushing sensation when moving joints as smooth articulating surfaces are disrupted
8. Joint effusions
9. Heberden's nodes (DIP)
10. Bouchard's nodes (PIP)
47
What joints are most commonly effected by OA
1. DIPs (HEBEEDEN'S NODES) and first carpometacarpal joint thumb)
2. First metatarsophalangeal joint of foot
3. Weight-bearing joints (vertebra and hips)
48
Where are Bouchard's nodes found
PIPs (B is before H so Bouchard's are more proximal to Heberden's)
49
Differential diagnosis of OA
1. Rheumatoid arthritis
2. Chronic tophaceaous gout
3. Psoriatic arthritis affecting DIPs
50
How is OA differentiate from rheumatoid
Pattern of joint movement
No systemic features
Early morning stiffness is in rheumatoid
51
Diagnostics for OA
X-rays
FBC
MRI
Aspiration of synovial fluid
52
What would X-ray show in OA
```
1. LOSS
L - Loss of joint space
O - Osteophytes
S - Subarticular sclerosis
S - Subchondral cysts
```
53
What would FBC show for OA
1. CRP
| 2. Rheumatoid factor and Antinuclear antibodies are NEGATIVE
54
What would an MRI show in OA
Early cartilage injury and subchondral bone marrow changes
55
What would aspiration of synovial fluid show in OA
Viscous fluid with few leucocytes
56
upon physical examination of OA what would we see
Deformity
| Bone enlargement of joints
57
Non-medical treatment of OA
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
Pharmacological treatment of OA
1. Paracetamol prescribed before NSAIDs (IBUPROFEN)
2. Weak opioids alongside paracetamol (DIHYDROCODEINE)
3. Intra-articular corticosteroids reduce joint effusion
59
What corticosteroid is not used
Systemic
60
When do you not administer corticosteroids
if joint is going to be replaces (has immunosuppression properties)
61
Surgical interventions for OA
1. Arthroscopy
2. Arthroplasty
3. Osteotomy
4. Fusion
62
What is arthroscopy
Scope inserted into joint to assess damage and remove loose bodies (cartilage fragments causing knee lock)
63
What is arthroplasty
1. Knee/hip replacement
64
Indications of arthroplasty
1. Uncontrolled pain at night
| 2. Significant limitation of function
65
How long does a prosthetic joint last for
10-15 years and need a replacement
66
What is an osetotomy
Cut bone to change shape/length
67
What is fusion
1. Usually of ankle and foot to prevent painful grinding of bones
2. Loss of motility
68
What is rheumatoid arthritis
Autoimmune disorder causing SYMMETRICAL DEFORMING POLYARTHRITIS
69
Does RA have inflammation
Yes
70
Risk factors for RA
1. Women
2. Smoking
3. Before menopause more common
4. Family history
5. Genetic factors
6. Immune system
71
What genetic factors cause RA
1. HLAs DR4 and DRB1 confer susceptibility to RA
72
What factors of the immune system contribute to RA
T cells : INF, IL-2 + IL-4
Macrophages: IL-1, 8 and TNF-alpha
Mast Cells: Histamine + TNF-alpha
Fibroblasts: IL-6
73
What maintains the chronic inflammation of RA
Local production of rheumatoid factor by B cells and formation of IMMUNE COMPLEXES with complement activate
74
What is rheumatoid factor
Autoantibodies directed against Fc portion of immunoglobulin
75
What does RA effect
Synovial joints
76
What is synovitis
Inflammation of synovial lining
77
When does synovitis occur in RA
When chemoattractants produced in the joint recruit circulating inflammatory cells
78
What chemoattractant causes synovitis and joint destruction
TNF-alpha
79
What drives overproduction of TNF-alpha
Interaction between macrophages, T and B cells
80
What happens to the synovium in RA
Becomes greatly thickened and infiltrated in inflammatory cells
81
Describe what happens in RA after synovium thickens
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
What parts of the body are effected by RA
1. Slowly progressive, SYMMETRICAL swollen, painful and stiff
2. DIPs are SPARED
3. MTP of feet
4. Wrist, elbows, shoulders, knees and ankles
83
Clinical presentation of RA
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
What hand deformities are seen in RA
1. Ulnar deviation (swelling of MCP and PIPs)
2. Swan neck (Z-thumb)
3. Boutonniere deformity
85
How does Ra effect the lungs
1. Pleura effusions
2. Fibrosing alveoli's
3. Pneumoconiosis (miners)
4. Interstitial lung disease
5. Bronchiectasis
86
How does Ra effect the heart
1. Pericarditis
2. Raynauds
3. Pericardial effusion
87
How does Ra effect the eyes
1. Dry eyes
2. Episcleritis (redness of eyes)
3. Scleritis (severe pain - can't look at bright lights)
88
Neurological effects by RA
1. Peripheral sensory neuropathies
2. Compression/entrapment neuropathies
4. Cord compression
89
What is entrapment neuropathies
Soft tissue swelling due to inflammation at site where rigid structures contain nerves (wrist and elbow - carpal tunnel syndrome)
90
What is cord compression
Due to instability of cervical spine, we get sensory loss, weakness and disturbed bladder function
91
How does Ra effect the kidneys
1. Amyloidosis (proteinuria and renal impairment)
2. Nephrotic syndrome
3. CKD
92
How does RA effect the skin
Subcutaneous nodules
93
How is RA diagnosed
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
What is Positive Anti-CCP
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
What is X-ray used for in RA
1. Soft tissue swelling in early disease
2. Joint space narrowing in late disease
3. PERI-ARTICULAR EROSIONS
96
What is MRI and ultrasound used for in RA
1. Erosions at joint margins and bones
If effusion present then aspiration of joint - will be cloudy due to high White cells
97
How is RA treated
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
How is pain in RA managed
1. NSAIDs - IBUPROFEN and COX inhibitors (ASPIRIN) for pain + stiffness
2. Paracetamol with DIHYDROCODEINE
99
What corticosteroids are prescribed for RA
1. ORAL PREDNISOLONE
| 2. drug while DMARDs kick in - IM METHYLPREDNISOLONE
100
How are corticosteroids delivered
Intra-articular injection (short-lived but rapid effect)
101
Role of corticosteroids
Suppress disease activity but risk of long-term toxicity
102
Side-effects of corticosteroids
Causes osteoporosis (most common cause of osteoporosis) and increases risk of fracture
103
What are DMARds
Inhibit inflammatory cytokines - suppress immune system and carry risk of infection
104
Why are DMARDs used
Early to reduce inflammation and slow development of joint erosions and irreversible damage
105
How long does it take for DMARDs to work
6 weeks
106
Why do we monitor DMARD use with blood tests
All DMARDs have serious side effects
107
Name the gold standard drug for DMARDs
METHOTREXATE
108
When is METHOTREXATE contraindicated
Pregnancy
109
Side-effects of methotrexate
1. Nausea
2. Mouth ulcers
3. Diarrhoea
4. Abnormal LFTs
5. Neutropenia
6. Thrombocytopenia
7. Renal impairment
110
Alternative DMARDs to METHOTREXATE
SULFASALAZINE
| LEFLUNOMIDE
111
When is SULFASALAZINE given
Mild/moderate disease
112
When is SUlfasalazine given
Young and women
113
Side-effects of SULFASALAZINE
1. Nausea
2. Skin rashes
3. Mouth Ulcers
4. Neutropenia
5. thrombocytopenia
6. abnormal LFTs
114
How does Leflunomide work
1. Blocks T cell proliferation
115
Side-effects of Leflunomide
1. Diarrhoea
2. Neutropenia
3. Thrombocytopenia
4. Alopecia
5. Hypertension
116
What biological therapy is used for RA
1. TNF-alpha blockers:
| Halts erosion formation
117
What are TNF-alpha blockers given alongside with
METHOTREXATE
118
Name a TNF-alpha blocker
Infliximab
119
Side-Effects of imfliximab
Demyelination
| Autoimmune syndromes
120
What is Imfliximab
Monoclonal antibodies
121
How is Imfliximab delivered into the body
IV
122
What is Etanercept
Receptor fusion protein
123
Side-effects of TNF-alpha blocker Etanerept blockers
Infections
| Hypersensitivity reaction
124
Other than IMfliximab and Etanercept what other TNF-alpha blocker is used for RA
ADALIMUMAB
125
What is ADALIMUMAB
Monoclonal antibodies
126
Side-effects of ADALIMUMAB
Hypersensitivity reaction
| Heart failure
127
What are B-cell inhibitors
They stop production of rheumatoid factors
128
How does Rituximab function
Monoclonal antibod that targets CD20 on B cells
129
Side-effect of RITUXIMAB
```
Hypo/hypertension
skin rash
nausea
pruritus
back pain
```
130
When is Rituximab given
When anti-TNF agents fails
131
Name two interleukin blockers
TOCILIZUMAB
| ANAKINRA
132
What is TOCILIZUMAB
Monoclonal antibody that binds to IL-6 cytokine before target receptor
133
What are the most common joint inflammation cytokines present
IL1
| IL6
134
Along what medication is TOCILIZUMAB given with
METHOTREXATE
135
What interleukin blocker antagonises IL-1
ANAKINRA
136
Name a T-cell activation blocker
ABATACEPT
137
Role of ABATACEPT
Blocks T cell activation which means macrophages and B cells can't be activated thus reducing inflammation
138
RHEUMATOID vs OSTEOARTHRITIS
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
X-ray results for RA
Juxta-articular osteoporosis
Soft Tissue Swelling
Joint Deformity
Loss of Joint Space
140
GI effects of RA
1. FELTY'S SYNDROME: Seropositive RA + Splenomegaly + Neutropenia
