MSK & Rheumatology Flashcards
1
Q
Define osteoarthritis
A
Loss of cartilage, with bone remodelling and inflammation.
2
Q
Define rheumatoid arthritis
A
Autoimmune inflammation of the synovial joints
3
Q
Define osteoporosis
A
Progressive skeletal disease with reduced bone mass and micro-deteriorataion
4
Q
Define osteomalacia
A
Inadequate mineralisation of osteoid framework
5
Q
How does osteoarthritis clinically present?
A
Joint pain exacerbated by exercise.
Joint stiffness after rest (transient in the morning).
Reduced functionality.
Bony swellings (Distal interphalangeal Heberden’s and proximal interphalangeal Bouchard’s) and deformity.
Crepitus
6
Q
How does rheumatoid arthritis clinically present?
A
Insidious onset of pain in the distal small jonts.
Morning stiffness (for more than 30 minutes).
Deformities: Ulnar deviation, swan neck and boutonniere.
7
Q
How does osteoporosis clinically present?
A
Develops asymptomatically.
Bone fragility.
Fracture is often first sign (neck of femur).
Fractures in thoracic vertebrae may lead to kyphosis (widow’s stoop).
8
Q
How does osteomalacia clinically present?
A
Proximal muscle weakness and pain.
Low bone density.
In children; bowed legs and knock knees.
9
Q
Rheumatoid arthritis - note
A
DR: ‘Digital Rheumatoid’
10
Q
Osteomalacia - note
A
‘Rickets’ in children
11
Q
Pathophysiology of osteoarthritis
A
Progressive destruction of the articular cartilage (loss of articular space).
Exposed subchondral bone becomes sclerotic,
increasing vascularity
and subchondral cyst formation -> repair produces cartilaginous growths which become calcified (osteophytes).
12
Q
Pathophysiology of rheumatoid arthritis
A
Infiltration of the synovium by inflammatory cells
- > angiogenic cytokines
- > Formation of new synovial blood vessels
- > Synovium proliferates and grows out over the surface of the cartilage producing a pannus
- > Pannus destroys the cartilage and subchondral bone
- > bony erosions
13
Q
Pathophysiology of osteoporosis
A
Inadequate peak bone mass,
excessive bone resorption
and inadequate formation of new bone during remodelling.
Lack of oestrogen increases bone resorption and decreases bone deposition.
Deficiency of calcium -> Increased bone resorption through PTH.
RANKL binds to RANK, activating osteoclasts.
14
Q
Pathophysiology of osteomalacia
A
Normal bone mineralisation depends on adequate calcium and phosphate.
Vitamin D promotes calcium absorption in the intestines, promotes bone resorption (by increasing osteoclast number).
15
Q
Cause/s of osteoarthritis
A
Usually primary.
Sometimes secondary to particular joints that have been damaged/frequently used.
RF: Females,
FH, obesity, smoking
16
Q
Cause/s of rheumatoid arthritis
A
HLA DR4 and DRB1 confer susceptability.
Triggering antigen not known.
17
Q
Cause/s of osteoporosis
A
Menopause.
Nutritional deficiency, contributes.
Bone density naturally lost from 35.
Steroids can activate osteoclasts.
18
Q
Causes of osteomalacia
A
Profound vitamin D deficiency.
Lack of exposure to sunlight and/or gastiointestinal malabsorption.
19
Q
Epidemiology of osteoarthritis
A
Prevalence increases with age.
More common in women.
Most common form of arthritis.
20
Q
Epidemiology of rheumatoid arthritis
A
1% of population will experience.
More common in women.
Peak incidence in 40s
21
Q
Epidemiology of osteoporosis
A
More common in women, particularly following menopause.
Being thin.
22
Q
Epidemiology of osteomalacia
A
More common in pigmented skin
and the elderly.
23
Q
Diagnostic test for osteoarthritis
A
Examination: Diagnose in >45 yrs,
activity related joint pain,
with either no morning related stiffness
or <30 mins of it Xray: LOSS
24
Q
Diagnostic test for rheumatoid arthritis
A
Anti-CCP: Most specific.
Rheumatoid factor (also AntiNuclear Antibody).
X ray: Loss of joint space
Erosions
Soft tissue swelling
Soft bones (osteopenia)
25
Diagnostic test for osteoporosis
Bone mass density assessment: DEXA.
Clinical.
26
Diagnostic test for osteomalacia
X ray: Defective mineralisation.
27
Treatments for osteoarthritis
Pain relief.
Exercise.
Weight loss.
Assistive devices.
Consider surgery as last resort for debilitating.
Interarticular corticosteroid injection.
28
Treatments for rheumatoid arthritis
DMARDs (sulfasalazine and methotrexate).
NSAIDs.
TNF-a inhibitor (infliximab)
Physiotherapy.
Interarticular corticosteroid injection.
29
Treatments for osteoporosis
Prevent fractures.
Calcium and vitamin D intake.
Bisphosphonates in those who have never had a fracture.
Oestrogen supplement.
30
Treatment for osteomalacia
Oral calciferol.
31
Complication of osteoarthritis
Reduced mobility
32
Complication of rheumatoid arthritis
Social impact
33
Complication of osteoporosis
Fractures
34
Sequelae of rheumatoid arthritis
Depression
35
Define Systemic Lupus Erythematosus
Heterogenous, inflammatory, multisystem autoimmune disease with antinuclear antibodies
36
Define Antiphospholipid syndrome
Autoimmune disorder characterised by arterial and venous thrombosis
and raised levels of antiphospholipid antibodies
37
Define Sjögrens syndrome
Lymphocytic infiltration of exocrine glands
38
Define Polymyositis
Inflammation
and necrosis of skeletal muscle fibres
39
How does Systemic Lupus Erythematosus clinically present?
Vast number of symptoms.
General: Fatigue, malaise, fever, splenomegaly, lympadenopathy, pleuritic chest pain, headache, Raynaud's, mild hair loss myalgia.
Arthralgia: Symmetrical joint and muscle pain.
Mucocutaneous: Discoid lupus, potosensitive rash, butterfly rash
Pulmonary: pleurisy, fibrosing alveolitis, obliterative bronchiolitis
Cardiovascular: pericarditis, hypertension
Renal: nephritis, haematuria, hypertension, glomerulonephritis
Neuro: Anxiety and depression (almost any neuro manifestation).
40
How does Antiphospholipid syndrome clinically present?
Varied clinical features.
Peripheral artery thrombosis,
deep venous thrombosis,
cerebrovascular disease,
pregnancy loss,
MI,
retinal thrombosis,
pulmonary embolism and pulmonary hypertension.
41
How does Sjögrens syndrome clinically present?
Dry eyes,
dry mouth
and enlargement of the parotid glands.
Possibly blepharitis.
42
How does Polymyositis clinically present?
Symmetrical progressive muscle weakness and wasting, affecting the proximal muscles of the shoulder and pelvic girdle.
Difficulty squatting and with stairs, and with raising hands above head.
Can involve dysphagia and dysphonia if pharyngeal and laryngeal muscles are involved.
43
Systemic Lupus Erythematosus - note
It's never lupus.
44
Antiphospholipid syndrome - note
Coagulation problems
Livedo reticularis
Obstetric problems
Thrombocytopenia
45
Pathophysiology of Systemic Lupus Erythematosus
Apoptotic cells and cell fragments are cleared inefficiently by phagocytes
- > transfer to lymphoid tissue
- > taken up by antigen presenting cells
- > self-antigens including nuclear components are presented to T cells
- > T cells stimulate B cells to produce autoantibodies against the antigens.
Clinical manifestations are mediated by antibody formation
and the development and deposition of immune complexes,
complement activation and influx of neutrophils and abnormal cytokine production.
46
Pathophysiology of Antiphospholipid syndrome
Proposed mechanisms for hypercoagulable effect of aPLantibodies include complement activation,
the production of antibodies against coagulation factors,
activation of platelets,
activation of vascular endothelium
and a reaction of antibodies to oxidised low density lipoprotein.
47
Pathophysiology of Sjögrens syndrome
Not fully known.
Possibly inflammation of the glands prompts autoimmune response.
48
Pathophysiology of Polymyositis
Mediated by cytotoxic T cells.
Involves autoimmune factors.
49
Cause/s of Systemic Lupus Erythematosus
Unknown.
Likely multifactorial.
Strong genetic association.
Ultraviolet light causes onset of rash.
Higher incidence premenopausal -> oestrogen has an effect.
50
Cause/s of Antiphospholipid syndrome
Unknown.
Some genetic association.
51
Cause/s of Sjögrens syndrome
Can be idiopathic (primary)
or associated with another autoimmune condition (secondary),
often rheumatoid arthritis.
52
Causes of Polymyositis
Unknown.
53
Epidemiology of Systemic Lupus Erythematosus
More common in premenopausal females.
54
Epidemiology of Antiphospholipid syndrome
Higher prevalence in black people.
Occurs most commonly in women of fertile age.
55
Epidemiology of Sjögrens syndrome
Classicallly disease of middle aged women.
56
Epidemiology of Polymyositis
Presents between 30 and 60 (small peak at 15).
Twice as common in females.
57
Diagnostic test for Systemic Lupus Erythematosus
FBC, ESR and antinuclear factor.
58
Diagnostic test for Antiphospholipid syndrome
Screen for aPL antibodies.
59
Diagnostic test for Sjögrens syndrome
Serum antibodies.
Schirmer's test: Whether the eye can self hydrate.
60
Diagnostic test for Polymyositis
Muscle biopsy.
61
Treatments for Systemic Lupus Erythematosus
Avoid sunlight and smoking.
NSAIDs and coritcosteroid for arthralgia.
Immunosuppressives for severe symptoms.
Rituximab.
62
Treatments for Antiphospholipid syndrome
Healthy lifestyle.
Acute management of thrombosis: Heparin
63
Treatment for Sjögrens syndrome
Artificial tear and saliva replacement.
64
Treatment for Polymyositis
Oral prednisalone.
65
Complications of Systemic Lupus Erythematosus
Depends on organ involvement
66
Complications of Antiphospholipid syndrome
Stroke. MI
67
Complications of Sjögrens syndrome
Infection of eyes or mouth.
68
Complications of Polymyositis
Interstitial lung disease,
dysphagia,
infection.
69
Sequelae of Systemic Lupus Erythematosus
Characterised by relapse and remission.
70
Define Raynaud's phenomenon
Paroxysmal vasospastic
--> vasodilatory events in peripheral arteries.
71
How does Raynaud's phenomenon clinically present?
Usually following cold: Pallor of distal portion of one or more digits
- > Numbness/pain and cyanosis of the digit
- > Hyperaemic; red and warm
72
Pathophysiology of Raynaud's phenomenon
Abnormalities in the blood vessel wall,
neural control mechanisms
and intravascular circulating factors are thought to combine.
73
Cause of Raynaud's phenomenon
Primary (Raynaud's disease): Genetic cause, usually.
Secondary: Depends on underlying disease.
74
Epidemiology of Raynaud's phenomenon
Primary: Usually young women.
Smoking and hand vibration (tools) associated.
75
Diagnostic test for Raynaud's phenomenon
Examination of affected region.
76
Treatments for Raynaud's phenomenon
Primary: smoking cessation,
calcium channel blockers if symptomatic .
Secondary: Treatment of the underlying cause.
77
Sequelae of Raynaud's phenomenon
About 13% of patients -> Scleroderma.
78
Define Ankylosing spondylitis
Inflammatory disorder of the spine
79
Define psoriatic arthritis
Inflammatory arthritis associated with psoriasis
80
Define reactive arthritis
Inflammatory arthritis that usually follows a GI or GU infection
81
Types of reactive arthritis
Post-enteric
Post-venereal
82
How does Ankylosing spondylitis clinically present?
Increasing pain and prolonged morning stiffness in the lower back and buttocks.
Improves with exercise.
Progressive loss of spinal movement.
Characteristic abnormalities: Loss of lumbar lordosis,
increased kyphosis
and limitation of lumbar spine mobility.
83
How does psoriatic arthritis clinically present?
Ranges from mild synovitis to severe progressive erosive arthropathy, usually preceded by the rash.
Skin disease can be as minor as an occult rash.
Nail changes are characteristic.
84
How does reactive arthritis clinically present?
2-4 weeks following a GI or GU infection.
Acute onset, with malaise, fatigue and fever.
Low back pain common.
Asymmetrical, oligoarthritis (no more than 6 joints).
Can't see, can't pee, can't climb a tree (Conjunctivitis urethritis, arthritis).
85
Seronegative spondyloarthopathies (this encompasses Ankylosing spondylitis, psoriatic and reactive arthritis) - note
Seronegative spondyloarthopathies share five main traits:
Predilection for axial inflammation,
Asymmetrical peripheral arthritis,
Absence of rheumatoid factor,
Inflammation of the enthesis
and a Strong association with HLA-B27
86
Pathophysiology of Ankylosing spondylitis
Ankylosis occurs by forming syndesmophytes following inflammation.
This leads to the fusion of the vertebrae.
The cause of the inflammation is not known, but thought to involve CD8 T cells.
87
Pathophysiology of psoriatic arthritis
Exact mechanisms unknown.
88
Pathophysiology of reactive arthritis
Persistent bacterial antigen in the inflamed synovium of affected joints is thought to drive the inflammation.
89
Cause of Ankylosing spondylitis
Unknown.
Strong genetic association.
90
Cause of psoriatic arthritis
Autoimmune mediated, with defined HLA associations (HLA-B27, -B17, -CW6, -DR4, -DR7).
91
Cause of post-enteric reactive arthritis
Usually infection by Campylobacter, Salmonella and Shigella.
92
Cause of pose-venereal reactive arthritis
Usually infection by Chlamydia trachomatisor with HIV.
93
Epidemiology of Ankylosing spondylitis
Usually young males.
More common and severe in males.
94
Epidemiology of psoriatic arthritis
20% of patients with psoriasis.
95
Epidemiology of reactive arthritis
Typically affects young males.
96
Diagnostic test for Ankylosing spondylitis
X ray: normal, or show erosion and sclerosis of the margins of the sacroiliac joints -> ankylosis.
Bamboo spine from rehealing of the enthesitis.
97
Diagnostic test for psoriatic arthritis
Xray: Pencil in cup deformity.
98
Diagnostic test for reactive arthritis
Once arthritis discovered, cultures show negative;
take serum antibodies.
99
Treatments for Ankylosing spondylitis
NSAIDs, TNF-alpha inhibitors (infliximab).
Surgery: Can correct spinal deformities to repair damage.
Possibly hip/shoulder replacement.
100
Treatments for psoriatic arthritis
Drugs: NSAIDs, DMARDs, TNF-alpha inhibitor (infliximab)
Surgical: Can correct deformed joints
101
Treatments for reactive arthritis
Aspirate synovial effusions.
Physiotherapy.
NSAIDs, Corticosteroids.
Antibiotics for causative organism.
102
Complications of Ankylosing spondylitis
Small chance of spinal fusion
-> severe kyphosis.
103
Complication of psoriatic arthritis
Joint destruction,
psycho social damage.
104
Complication of reactive arthritis
Minority may develop destructive enthesitis or spondylitis.
105
Sequelae of reactive arthritis
High recurrence by new infection or stress.
106
Define gout
Deposition of monosodium urate monohydrate crystals wthin joints.
107
Define pseudogout
Deposition of calcium pyrophosphate crystals within joints.
108
How does gout clinically present?
A joint becomes swollen, tender and erythmatous.
Florid synovitis,
extreme tenderness,
with overlying erythema.
Usually affects the metatarsalphalangeal joint of the big toe.
109
How does pseudogout clinically present?
Often asymptomatic.
Joints become swollen tender and erythmatous (as above).
Usually affects knee or wrist.
In chronic condition, destructive changes as in OA.
110
Gout - note
'One of the most painful acute conditions human beings can experience'.
111
Pseudogout - note
Calcium pyrophospate dihydrate crystal deposition disease.
112
Pathophysiology of gout
Monosodium urate (derived from purine breakdown) precipitates and forms deposits in joints.
Crystals formed are very painful.
Can form tophi; asymmetrical chalky appearance, firm nodules.
113
Pathophysiology of pseudogout
Excess of pyrophosphate and calcium in the blood
-> crystal deposition in synovium.
114
Causes of gout
Hyperuricaemia.
Often idiopathic Impaired excretion: CKD, diuretics, hypertension
Increased uric acid production (rarer): PPS overactivity, increased turnover.
115
Causes of pseudogout
Unknown.
Precipitated by dehydration, steroids, hyperparathyroidism.
In younger patients, associated with; haemochromatosis and wilson's disease.
116
Epidemiology of gout
Much more common in males.
RF: Meat, seafood, alcohol, diuretics
117
Epidemiology of pseudogout
Usually affects elderly women.
118
Diagnostic test for gout
Joint fluid microscopy: MSU negatively birifringent needle crystals or
Examination: tophi confirm diagnosis.
119
Diagnostic test for pseudogout
Joint fluid microscopy: rhomboid positively birifringent crystals.
120
Treatment for gout
Acute: ice pack,
rest,
elevation.
NSAIDs (diclofenac), colchicine (if NSAIDs aren't tolerated).
Long term: Allopurinol.
121
Treatment for pseudogout
Joint aspiration with NSAIDs or colchicine.
Possibly corticosteroids.
122
Complications of gout
Nephrolithiasis,
infection.
123
Complications of pseudogout
Pain.
124
Sequelae of gout
Recurrence, usually within first year.
125
Define Paget's disease of bone
Increased bone turnover
-> enlarged misshapen bones
126
Define Degenerative disc disease
Pathological process of degeneration of intervertebral discs.
127
Define Fibromyalgia
Chronic widespread pain and sensitivity to pressure.
128
Define Mechanical back pain
Back pain as a result of physical wear and tear.
129
How does Paget's disease of bone clinically present?
Commonly asymptomatic.
When presents; often bone pain and/or deformity.
Localised to one or a few bones.
Bone fragility -> Pathological fractures
130
How does Degenerative disc disease clinically present?
Chronic low back pain,
sometimes radiating to the hips,
or the buttocks.
131
How does Fibromyalgia clinically present?
Chronic, widespread pain associated with unrefreshing sleep and tiredness.
Often occurs with inflammatory and osteo arthritices.
Symptoms generally worse in the cold, and under stress.
132
How does Mechanical back pain clinically present?
Back pain in lumbosacral.
History of bowel / bladder dysfunction suggestive of cauda equina.
133
Paget's disease of bone - note
There is also a Paget's of breast,
and Juvenile Paget's.
134
Pathophysiology of Paget's disease of bone
Lytic phase: Increased bone resorption with abnormal osteoclast activity
- > Rapid increase in bone formation by osteoblasts
- > New bone is mechanically weaker, more vascularised and poorly organised (pathological fractures)
135
Pathophysiology of Degenerative disc disease
Degenerative fibrocartilage and clusters of chondrocytes present.
Fibrocartilage replaces the gelatinous mucoid material of the nucleus pulposus as the disc chagnes with age.
Possibly splits in the anulus fibrosus allow nucleus pulposus to herniate out.
There may be shrinkage of the nucleus pulposus that produces prolapse or folding of the anulus fibrosus with secondary osteophyte formation at the margins of the adjacent vertebral body.
Pathology: Protrusion, spondylolysis, and/or spinal stenosis.
136
Pathophysiology of Fibromyalgia
Unknown.
Theories include; peripheral and central hypersensitivity,
altered pain perception,
somatisation.
137
Pathophysiology and cause of Mechanical back pain
Nerve root: Nerve root impingement due to herniated discs.
Could also be cauda equina syndrome.
Causes a sharp, well-localised pain, can be associated with paresthesia
MSK pain: myofascial pain syndromes and fibromyalgia
Other: Osteomyelitis, sacroiliitis and malignancy.
138
Cause of Paget's disease of bone
Genetic component: autosomal dominance in some cases.
Unclear what causes attacks.
Possibly mechanical stress.
139
Cause of Degenerative disc disease
Disease of aging;
increased fragility of the cartilage of the disc can lead to the onset of pathology.
140
Cause of Fibromyalgia
Unknown.
Some genetic association.
141
Epidemiology of Paget's disease of bone
1-2% of white adults over 55.
UK has highest incidence in the world. S
lightly more common in males.
142
Epidemiology of Degenerative disc disease
More common in the elderly.
143
Epidemiology of Fibromyalgia
More common in women.
Middle age.
144
Epidemiology of Mechanical back pain
2/3 affected at some point.
145
Diagnostic test for Paget's disease of bone
Xrays: Deformity
Bloods: Bone specific alkaline phosphatase raised
146
Diagnostic test for Degenerative disc disease
CT and/or MRI
147
Diagnostic test for Fibromyalgia
Clinical, 9 pairs of sites to assess for tenderness
148
Diagnostic test for Mechanical back pain
CT and/or MRI
149
Treatment for Paget's disease of bone
Bisphosphates inhibit bone resorption by reducing osteoclast activity.
150
Treatment for Degenerative disc disease
Physical therapy,
NSAIDs,
epidural steroids.
If no effect; surgery to relieve pain.
151
Treatment for Fibromyalgia
Drugs: Analgesic ladder (strong opioids not advised).
Psychosocial: exercise and strength training.
152
Treatment for Mechanical back pain
NSAIDs,
analgesics,
and muscle relaxants.
153
Complications of Degenerative disc disease
Sciatica,
ankylosis.
154
Sequelae of mechanical back pain
Recurrence.
155
Define septic arthritis
Infection producing inflammation in a joint.
156
Define osteomyelitis
Infection of the bone marrow.
157
Types of septic arthritis
Acute
Chronic
158
How does septic arthritis clinically present?
Single swollen joint with pain on movement, usually the knee.
Joint swollen, warm, tender.
159
How does osteomyelitis clinically present?
Fever, local pain and erythema.
In chronic: sinus formation.
160
Septic arthritis - note
Medical emergency: can destroy a joint in 24hrs.
161
Pathophysiology of septic arthritis
Infection of the joint can cause damaging inflammation, and loss of function.
162
Pathophysiology of osteomyelitis
Results in inflammatory destruction of bone.
When dead bone detaches from healthy, it forms a sequestrum.
Large sequestrum that remains in situ acts as a focus for infection.
New bone can form around this and often causes deformity.
163
Cause of septic arthritis
Direct injury or blood-borne infection.
Prosthetic joints are more susceptible.
Mostly Staphylococcus aureus.
Gram negative are more common in the elderly.
164
Cause of osteomyelitis
Local infection (usually following trauma)
or due to metastatic haematogenous spread.
Usually Staphylococcus,
but sometimes Haemophilus influenza and Salmonella.
165
Epidemiology of septic arthritis
Increases with age.
Immunocompromised.
166
Epidemiology of osteomyelitis
Increasing due to increase of predisposing conditions such as diabetes.
167
Diagnostic test for septic arthritis
Bloods: ESR and CRP elevated.
Synovial fluid exam: culture.
168
Diagnostic test for osteomyelitis
CT, MRI or bone scan.
169
Treatment for septic arthritis
Immediate empirical antibiotics (flucloxacillin usually).
Splinting.
Aspiration to drain the joint.
170
Treatment for osteomyelitis
Flucloxacillin and fusidic acid IV.
171
Complications of septic arthritis
Delay in treatment can cause joint destruction
and long-term disability.
172
Complications of osteomyelitis
Bone abscess,
bacteraemia,
growth arrest,
chronic infection.
