MSK & Rheumatology Flashcards
1
Q
Where does osteoarthritis commonly occur?
A
Synovial joint
2
Q
Bones that form the joints are surrounded by …
A
Periosteum
3
Q
What is the purpose of articular cartilage?
A
Absorb shock and allows gliding between thhe bones surrounding the synovial joint
4
Q
Anatomy of a synovial joint
A
5
Q
The knee joint also contains another cartilage called…
A
Meniscus (Fibrocartilage)
6
Q
What occurs during mild osteoarthritis?
A
Have degeneration/damage of the articular cartilage in the presence of joint space narrowing
Common when youage
7
Q
Risk factors of osteoarthritis
A
8
Q
What does mild osteoarthritis progress to?
A
Severe osteoarthritis.
With severe osteoarthritis there is: bone spur formation, loss of articular cartilage, bone/bone joint space narrowing
9
Q
Aetiology - Classification of osteoarthritis
A
Primary (Idiopathic) - no preceeding injury
Secondary - due to congenital abnormality, trauma, inflammatory arthropathy
10
Q
Clinical Presentation of osteoarthritis
A
11
Q
Findings based on clinical examination of osteoarthritis
A
Muscle Wasting
Overweight
Tenderness on joint palpation(+/- osteophytes)
Joint effusion
Crepitations
12
Q
Differential diagnosis of osteoarthritis
A
Calcium pyrophosphate crystal deposition disease
Septic arthritis
Rheumatoid arhtritis
13
Q
Investigations for osteoarthritis
A
MRI is good however X-ray better for initial investigation
14
Q
Management for osteoarthritis
A
15
Q
Pathophisiology of osteoarthritis
A
Progressive Loss of articular cartilage -> friction -> Inflammation -> Pain
16
Q
What is rheumatoid arthritis
A
Systemic rheumatological disorder affecting multiple joints
Autoimmune
Progressive, symmetric joint depression
17
Q
Clinical Presentation of rheumatoid arthritis
A
18
Q
Diff in hand involvement in rheumatoid arthritis vs osteoarthritis
A
The disease can progress you can get other features in the hand:
Swan neck: DIP-Flex + PIP - hyper extension
Boutonniere: DIP - hyperextension, PIP - Flex
Z deformity of thumb: Ulnar deviation
19
Q
Macroscopic view of rheumatoid arthritis
A
Inflammation of the synovium of the synovial membrane (Synovitis) : Pain and swelling
Can also see angiogenesis
Bone/Cartilage Erosion
20
Q
Pathophisiology of rheumatoid arthritis
A
21
Q
Pre rheumatoid arthritis: things that can contribute in the development of rheumatoid arthritis.
A
22
Q
Antibodies found in rheumatoid arthritis
A
Rheumatoid Factor (IgM ~ 75%) : Targets Fc portion of IgG. Forms immune complexes
Anti-citrullinated protein antibidy: targets citrullinated proteins such as fibrin, fillagrin
23
Q
Extraarticular involvement of rheumatoid arthritis
A
Result of cytokines produced within joints : TNF - alpha, IL-1, IL-6
24
Q
Diagnosis of rheumatoid arthritis
A
25
Treatment for rheumatoid arthritis
26
Examples of crystal arthritis
Gout
Pseudogout
27
What is gout
Common form of inflammatory arthritis characterised by recurrent attacks of painful joint pain
Gout attack occurs suddenly often at night. The intial attack usually involves only one joint, most often in the big toe and lasts a few days. Subsequent flares may involve mutliple joints and can last for weeks, with shorter intervals of remission in between
The affected joint is swollen, red and warm to touch
28
Causes of gout
Caused by deposits of monosodium urate crystals in the joints, which can happen when blood levels or uric acid are too high (>6.8mg/L)
High serum urate level may result from decreased urate excretion, increased urate production and/or over consumption of purines.
1. Most common cause is kidney's decreased ability to excrete uric acid: hereditary, kidney diseases, medications (diuretics), alcohol usage, lead poisoning
2. Increased urate production: Lymphoma, leukemia, haemolytic anaemia, psoriasis, radiation therapy, obesity
3. Purine-rich foods: red meat, organ meat, anchovies, sardines, asparagus, beer .. RARELY THE ONLY CAUSE
29
What is uric acid
Waste product from the breakdown of purines
30
What joints are most liely affected by gout and why?
Joints of the extremities
Due to uric acid crystals forming more easily in cooler temperatures
31
What are tophi
Crystals deposited under skin
Not usually painful
-Can limit joint motions
-Can become inflammed/ruptured
32
People with gout are at an increased risk of developing ..
osteoarthritis
can also lead in the development of kidney stones
33
Risk factors of gout
Men (middle aged), women (menopause)
Diet
Obesity
High bp, diabetes, metabolic syndrome, heart and kidney diseases
Family History
Surgery/trauma
34
Diagnosis of gout
Urate crystals in synovial joint fluid
High serum urate levels alone not conclusive
35
Treatment for gout
Anti-inflammatory drugs (NSAIDS, corticosteroids, colchicine)
Dissolve tophi by lowering serum urate to <5 to 6 mg/dL:
+ block urate production with xanthine oxidase inhibitors (allopurinol, febuxostat)
+ increase urate excretion (probenecid, losartan)
36
Appeaence of monosodium urate crystals
Appear as yellow shaped needles with negative birefrigence
37
What is pseudogout
Form of arthritis causing pain and inflammation in affected joints
There is acute onset joint pain, swelling and erythema
38
Causes of pseudogout
Buildup of calcium pyrophosphate dehydrate crystals within the cartilage and synovium of a joint
CPPD crystals appear as blue rhomboid shapes with weakly postive birefringence
39
Areas affected by gout vs pseudogout
Gout: Smaller joints e.g big toe called pedagra
Pseudogout: Larger joints
40
Risk Factors of pseudogout
41
Investigations for pseudogout
Joint aspiration
Xray: cartilage calcification
Blood test:
-Ca & PTH
-Iron studies
-Mg
-ACP
42
Management for pseudogout
43
Gout vs Pseudogout table
44
What is osteoporosis
when there is a higher breakdown of bone in comparison to the formation of new bone which results in porous bones, meaning a decrease in bone density to the point of potential fracture.
45
Structure of bone
46
How often does bone remodelling take place
spongy bone replaced every 3-4 years
compact bone replaced every 10 years
47
What is bone remodelling dependent on
Dependent on serum Ca2+ levels:
PTH, Calcitonin, Vit D
48
What causes osteoporosis
when osteoclasts break down bone faster than the osteoblasts can rebuild, it results in the lowering of the bone mass and eventually in osteoporosis.
49
Osteoporosis vs. osteomalacia
Osteoporosis: normal mineralisation, normal cells
Osteomalacia: lack of mineralisation
50
Abnormal findings of osteoporosis
1. fewer trabeculae in the spongy bone
2. thinning of the cortical bone
3. widening of the Haversian canals
These bone changes increase the risk of fracture, and they are known as fragility or pathologic fractures
51
Bones at risk of fragility fractures
vertebrae
shoulder blades
ribs
= as they consist mainly of spongy bone
52
Factors that increase bone mass loss, increase risk of osteoporosis
53
Types of osteoporosis
Postmenopausal: decreased oestrogen levels lead to increased bone resorption.
Senile: believed that osteoblasts just gradually lose the ability to form bone, while the osteoclasts keep doing their thing unabated.
54
Symptoms of osteoporosis
People with osteoporosis don’t usually have symptoms until a fracture occurs.
The most common type of fractures are vertebral fractures (compression fracture). Occurs when one or more bones in the spine weaken and shatter.
Vertebral fractures cause back pain, height loss, and a hunched posture.
Femoral neck fractures and distal radius fractures can also occur, and they’re often associated with postmenopausal osteoporosis.
55
Diagnosis of osteoporosis
Dual-energy x-ray absorptiometry (DEXA) scan
56
Treatment for osteoporosis
57
What is osteopenia
Osteopenia and osteoporosis are two very similar conditions, but one is more severe than the other. Both conditions are decreased bone density, but osteopenia is to a lesser degree than osteoporosis.
58
What is vasculitis?
Inflammation of the blood vessels resulting in damaged vessels
59
What are the complications of vasculitis?
Tissue ischaemia
Aneurysms
60
How is primary vasculitis classified?
Size of blood vessels affected
Large/Medium/Small
61
What does large cell vasculitis affect?
Aorta and its branches
62
Example of large cell vascultis
Giant cell arteritis
63
What is giant cell arteritis
Granulomatous arteritis of the aorta and the large vessels
Location: temporal branch of carotid artery
64
Clinical Features of giant cell arteritis
severe unilateral headache around temporal region
visual changes: amaurosis fugax
if facial artery is affected: jaw claudication. Lingual artery: tongue claudication
Association with polymyalgia rheumatica
Classic Presentation is an elderly female with new headache, new neck pain with a potential superficial temporal artery
65
Histopathological changes of giant cell arteritis
Presence of giant cells
Pan arthritis inflammation of all the vessel layers
Presence of CD4 & CD8 lymphocytes, macrophages
=all of thesecells are present in smoother muscle layers of the vessel
Skip lesions
No fibrinoid necrosis
66
Investigations for giant cell arteritis
Increase ESR
Increase CRP
Ultrasound doppler: Halo sign, stenosis
67
Diagnosis of giant cell arteritis
Temporal artery biopsy
Immune cell infiltration in smooth muscle layer
Evidence of pan arthritis
68
Management of giant cell arteritis
High dose steroids
Calcium and Vit D
Bisphosphanate
69
Classification of Spondyloarthropathies
* Ankylosing spondylitis
* Psoriatic arthritis
* Reactive arthritis
* Enteric arthritis
70
What is ankylosing spondycitis
chronic inflammatory disease of intervertebral & facet joints that affects the vertebral joints and makes the spine really stiff, but can also cause inflammation in other parts of the body like the eyes and blood vessels.
Associated with HLA-B27 gene
71
Ankylosing spondylitis is also called
Bechterew disease
72
What are spondyloarthropathies
Spondyloarthropathies are all autoimmune diseases that affect the joints, and they’re seronegative (rheumatoid factor not found in the blood)
73
Cause of ankylosing spondylitis
autoimmune process attacking type I and type II collagen in the joints.
Over time, the inflammation destroys the intervertebral joints, the facet joints, and the sacroiliac joints, and fibroblasts replace the destroyed joint with fibrin
ossification results in small bony outgrowths will form at the joint edges, called syndesmophytes in the beginning
74
Other part of the body affected by ankylosing spondylitis due to inflammation
Eye: anterior uveitis
Aortic valve: aortic regurgitation
tendons (like the achilles tendon) :enthesitis
75
Symptoms of ankylosing spondylitis
weight loss, fevers, and fatigue.
If ankylosing spondylitis affects the sacroiliac joints it typically causes buttock pain, and if it affects the cervical or thoracic region it can cause neck or back pain and stiffness.
Because the ribs and vertebrae are involved in breathing, stiffness can cause shortness of breath.
76
Diagnosis of ankylosing spondylitis
77
Treatment for ankylosing spondylitis
Inflammation and pain:
Treated with non-steroidal anti-inflammatory drugs like ibuprofen.
The pain can also be relieved by exercise or physical therapy.
In more severe cases, disease modifying anti-rheumatic drugs, or DMARDs, like sulfasalazine and methotrexate can be helpful.
Newer therapies called biologics can also be useful, because they block the actions of cytokines like tumor necrosis factor alpha and the interleukins.
Surgery can repair damaged hip and knee joints, but spinal surgery is typically considered risky and is rarely performed.
78
What is psoriatic arthritis?
psoriatic arthritis is a type of joint inflammation that happens in individuals with psoriasis.
It is chronic and progressive
Associated with the HLA-B27 gene T-cell mediated attack of joints
79
Cause of psoriatic arthritis
80
Symptoms of psoriatic arthritis
81
Types of psoriatic arthritis
82
Diagnosis of psoriatic arthritis
83
Treatment for psoriatic arthritis
84
What is reactive arthritis
Reactive arthritis, formerly known as Reiter’s syndrome, is inflammation of a joint which usually develops after an infection, and that infection is typically a sexually transmitted disease or gastroenteritis
85
Tissues affected by reactive arthritis
Starts 2-3 weeks after infection
86
What are the symtpoms of reactive arthritis
87
Diagnosis of reactive arthritis
History of previous infection
Clinical exam
Positive for HLA-B27
88
Treatment for reactive arthritis
antibodies for infection
NSAIDs
89
What is septic arthritis
Septic arthritis, also called infectious arthritis, refers to any joint inflammation caused by a microbe - and usually it results from a bacterial infection of the joint
90
Types of infective arthritis
Septic arthritis
Osteomyelitis
91
Clinical Presentation of septic arthritis
92
What do people presenting with an inflamed joint require?
History
Examination
93
Causative agent for septic arthritis
94
Pathogensis of septic arhtiris
Skin infection such as Staphylococcus aureus can disseminate into joint causing septic arthritis
osteomyelitis can also locally invade the joint causing septic arthritis
Lower/upper respiratory tract infections from group A streptococcus
STI
Procedures
Surgery
95
Septic arthritis is considered to be a ...
surgical emergency >24hrs -> irreversible damage
96
Investigations for septic arthritis
X-Ray:
shows sublaxation/dislocation
shows joint space widening
97
Steps taken after intial investigation in patient with septic arthritis
98
What is osteomyelitis
Inflammation of the bone or bone marrow, and it typically results from an infection.
99
In osteomyelitis, microorganisms, such as bacteria, reach the bone to cause an infection in a few different ways. How
Bacteria particularly affect certain high-risk individuals like those with a weak immune system, and those with poor blood circulation due to uncontrolled diabetes.
1.Bacteria reaches the bone through the bloodstream: contaminated needles to inject drugs or in individuals undergoing hemodialysis that may be contaminated by a bacteria or even through the dental extraction of an infected tooth.
2.Trauma
3.Surgery
4.Contiguous spread
CAN ALSO BE A COMBINATION
100
Through the bloodstream, the microorganisms may reach specific places in the body, and this mostly depends on the age of the person ..
In older adults, for example, the microorganisms may reach the vertebrae and cause vertebral osteomyelitis. This usually affects two adjacent vertebrae and the interintervertebral disk between them.
In children, the metaphysis of long bones like the femur is commonly affected.
101
Pathophisiology of osteomyelitis
Chronic osteomyeltis lasts months-year -> Affeted bone becomes necrotic and separates
102
Occasionally, in both acute and chronic osteomyelitis the inflammation may involve the ...
Perisoteum
103
Infection of osteomyelitis can spread to:
104
Microorganisms that cause osteomyelitis
105
Symptoms of osteomyelitis
106
Diagnosis of osteomyelitis
107
Treatment for osteomyelitis
108
What is systemic lupus erythematosus
Autoimmune disease mediated by antibodies and immiune complexes
It is a multi-system disorder that most commonly affects women during reproductive years
109
Pathophisiology of SLE
110
Constitutional symptoms of SLE
111
Investigations for SLE
+Antinuclear Antibody (ANA):
Anti dsDNA, anti histone, anti SM , anti Ro, anti nRNP
Extractable nuclear antigens (ENA)
Anti cardiolipin
Anti RF
112
Serum markers associated with disease flare ups (s
SLE)
Decrease in complement 3 & 4
Increase Anti dsDNA
113
SLE + DRUG
114
Complications of SLE
115
Risk Factors for SLE
116
Treatment for SLE
117
What is fibromyalgia
Chronic condition characterised by widespread pain and hypersensitivity to pressure
118
Epidemiology of fibromyalgia
8% of population affected
2: 1 Female to male
Most commonly diagnosed between 35-45 years
119
Signs and symptoms of fibromyalgia
120
Cause of fibromyalgia
Exact cause/mechanism is unknown
Thought to have central sensitisation: More sensitive to pain and therefore lower threshold for pain.
Hyperexcitation of pain sensing neurons and under activity of inhibitory pathways
Physical/enotional stress is often a trigger: Link with IBS/TMS/Chronic fatigue
121
Risk Factors for fibromyalgia
Poor sleep
Smoking
Obesity
Sedentary lifestyle
122
Diagnosis for fibromyalgia
unremarkable test results
widespread pain index/symptom severity score
up to 66% may have symptoms explained by other conditions:
-SLE (Lupus)
-Non coeliac gluten sensitivty
-Polymyalgia rheumatica
-Hypothyroidism
-Nerve compression syndrome
123
Subtypes of fibromyalgia
1. Extreme sensitivity to pain without pyschiatric association
2. Fibromyalgia with pain related depression
3. depression with fibromyalgia syndrome
4. Fibromyalgia due to somatisation
124
Treatment for fibromyalgia
No cure or treatment - symptom management
1. Non-pharmacological:
Exercise: reduces pain and fatigue, aerobic yoga
CBT
Reduce Stress
Sleep hygiene: avoid caffeine, large meals, screen environment
2. Pharmacological
Anti depressants:
-SNRI: Duloxetine, milnacipran
-TCA: Amitriptyline
Anti convulsants
-Pregabalin
125
What is Sjogren Syndrome ?
Autoimmune disorder
-Typically occuirng in women
-Immune cells attack exocrine glands. Primarily lacrimal & salivary glands
126
Pathophisiology of Sjogren Syndrome
127
Cause of Sjogren Syndomre
Exact cause is unknown
Thought to be a combination of genetic (Anti-SS-A & Anti-SS-B) and environmental factors
128
Classification of Sjogren syndrome
Primary (Occurs alone)-> Sicca syndrome
Secondary (occurs with other autoimmune diseases) -> e.g rheumatoid arthritis
129
Symptoms of sjogren's syndrome
130
Diagnosis of Sjogren's syndrome
131
Treatment for Sjogren's syndrome
Suppress the immune response: Corticosteroids
Increase the exocrine secretions: Pilocarpine
132
What is anti-neutrophilic cytoplasmic antibody associated vasculitis
Vasculitis that affects small blood vessels.
There are three diseases and are all characterised by the presence of the ANCA antibodies
This includes granulamatosis with polyangitis
133
Complication of Wegener’s granulomatosis (granulomatosis with polyangiitis)
ANCA nephritis
134
What is Wegener’s granulomatosis (granulomatosis with polyangiitis)
ANCA positive against proteinase 3
An anti-neutrophilic cytoplasmic antibody associated vasculitis. Most common
Small vessel vascultis characterised by the inflammation of the small blood vessels with infiltrationof immune cells forming granulomas
135
Where does inflammation occur in Wegener's granulomatosis
Blood vessels of:
Upper respiratory tract
Lower respiratory tract
Kidney
=Wegener's triad
136
Histopathological findings of Wegener's granulomatosis
Granuloma formation
Pauci immune necrotising vasculitis
137
Clinical Features of Wegener's granulomatosis
138
Investigations for Wegener's syndrome
139
Diagnosis for Wegener's syndrome
Skin biopsy: Leukocytoclastic vasculitis (No compplemet or immunoglobulin)
Renal biopsy: Rapidly progressing glomerulonephritis. Crescents. Pauci immune glomerulonephritis
140
Management of Wegener's syndrome
141
What is antiphospholipid syndrome
An autoimmune disease where antiphospholipid antibodies attack phospholipids in cell membrane or proteins bound to phosphlipid
More common in young females
142
Classification of antiphospholipid syndrome
Primary: Occurs by itself
Secondary: occurs with other autoimmune diseases (esp. SLE)
143
Cause of APS
Cause is unknown
Known genetic (HLA-DR7 Gene) and environmental factors
Environmantal trigger msut be present
144
Pathology of APS
145
Complications of APS
146
Diagnosis of APS
147
Treatment for APS
148
What are the types of idiopathic inflammatory myopathies
Polymyositis
Dermatomyositis
149
What are idiopathic inflammatory myopathies
Autoimmune conditions involving proximal muscle weakness and muscle inflammation
-Polymyositis does not involve the skin
-Dermatomyositis does involve the skin
150
Incidence & Onset of idiopathic inflammatory myopathies
Incidence: approx 2 per 100,000 per year
Female - Male Ratio = 2:1
Onset 40-50
151
Causes of idiopathic inflammatory myopathies
1. Genetics
HLA 8.1, PTPN22, STAT4, TRAF6
2. Environmental trigger
Uv rdiation, previous infections, prior lung disease
152
Polymyositis vs dermatomyositis pathogenesis
153
Polymyositis vs dermatomyositis clinical features
Myalgia
Dysphagia
Symmetrical proximal muscle weakness (most common)
154
Associated conditions with idiopathic inflammatory myopathies
Instertitial lung disease
Raynaud's phenomenon
Polyarthritis
SLE
155
Features specific to dermatomyoitis
Heliotrope rash
Gottron's Papules
Shawl sign: rash on shoulders, back elbows and knees
V sign: rash on neck and upper chest
Holster sign: rash on lateral thighs
Periungual erythema
Calcinosis Cutis
156
Diagnosis polymyositis vs dermatomyositis
Diagnostic Criteria:
1. Symmetric proximal muscle weakness
2. Elevated enzymes
3. EMG abnormalities
4. Muscle biopsy findings
5. Cutaneous findings = only for dermatomyositis
157
Treatment for polymyositis & dermatomyosits
158
What is scleroderma
Scleroderma refers to systemic sclerosis, a rare autoimmune disorder in which normal tissue is replaced with thick, dense connective tissue. It affects the skin, blood vessels and internal organs
159
Types of scleroderma
Limited cutaneous systemic scleroderma (CREST syndrome)
Diffuse cutaneous systemic scleroderma
160
Causes of scleroderma
Affects women 3x more often than men
Pathology not understood
-Genetic predisposition
-Triggered by external factors: viral infection, exposure, medication
161
What organs does scleroderma primarily involve
Skin
-First appears on fingers (sclerodactyly): swollen and doughy
-Later: tight, shiny, smooth and stiff
Lung
Heart
Kidney
GI tract
162
Symptoms of scleroderma
With diffuse scleroderma organ damage occurs earlier
163
Diagnosis of scleroderma
164
Treatment for scleroderma
165
Treatment for scleroderma
166
What is polyarteritis Nodosa (PAN)
Necrotising vasculitis involving medium-sized vessels
ANCA negative
Association with Hep B
Systemic involvement:
-Kidneys most commonly involved organ
-Spares the lungs
167
Signs and symptoms of PAN
Myalgias
Renal Infarts
Mononeuritis multiplex
Fever
Rash:
-Purpuric rash
-Subcutaneous nodules
-Bullous/vesticular lesions
-Livedo reticularis
168
Investigations for PAN
Hepatitis serology
FBC
EUC
Angiogram microaneurysms
169
Treatment for PAN
Glucocorticoids
Cutaneous polyarteritis Nodosa -> Skin limited Disease
170
What is Pagat's disease ?
Metabolic disease of increased bone destruction and remodelling
171
Pathology of Pagat's Disease
Basic pathology is overactove osteoclastic activity
Accelerated bone re-absorption is accompanied by disordered bone formation, resulting in excess bone formation, altered in shape and size
172
Aetiology of Pagat's Disease
Probably triggered by paramyxovirus
173
Treatment for Pagat's disease
Oral (risedronate) or an IV (zoledronate) bisphosphonate
174
Complications of Pagat's disease
General: risk of osteosarcoma, high output congestive cardiac failure
Skull: entrapment of cranial nerves leading to deafness, visual loss, headache. Cord compression, hydrocephalus
Face: cosmetic issues, dental abnormalities
Spine: spinal cord compression, radiculopathy, cauda equina syndrome, spinal stenosis
Femur: osteoarthritis at the knee and hip
175
Differential diagnosis for Pagat's disease
Malignancy
Osteoporotic fractures in spine
176
Investigations for Pagat's disease
Elevated ALP: reflects extent of disease:
-With treatment, ALP should normalise
Plain radiography of affected part: lytic, sclerotic disorganised bone
Bone scan: focal areas of increased uptake reflect extent of disease
177
What is polymyalgia rheumatic (PMR)
Pain and stiffness of proximal extremities in the absence of muscle weakness
Commonly associated with temporal arteritis
178
Polymyalgia rheumatic signs and symptoms
Fever
Weight Loss
Malaise
Pain and stiffness of proximal muscles symmetrically
-neck
-shoulders and hips
Gelling
Muscle tenderness nut NO weakness or atrophy
179
Diagnosis of PMR
Age >50 years old at onset
Proximally and bilaterally distributed aching and morning stiffness (lasting at least 30mins or more) persisting for at least two weeks. Stiffness should involve at least two of the following three areas: neck or torso, shoulders or proximal regions of the arms, hips or proximal aspects of the thigh
ESR >=40mm/hour
180
Treatment for PMR
Low dose corticosteroids such as prednisone
181
What is mechanical lower back pain
Lower back pain that is triggered by movement and improved with rest
182
Causes of mechanical lower back pain
1. Lumbar spine strain/sprain (70%)
2. Degeneration of discs/facets
-discogenic worsens with flexion + coughing / sneezing
-facet pain worsen with extension
3. Disc herniation (nucleus pulposus)
4. Spinal stenosis - osteophyte formation, ligament hypertrophy
5. Spondylolysis
183
Red flags for mechanical lower back pain
1. Saddle Anesthesia
2. Urinary Incontinence/Retention
3. Neurological deficit
4. Systemic Manifestations
-Weight Loss
-Fever
-Night Sweats
5.History of malignancy
6.Immunosupression
7.IV Drug user
8.Osteoporosis
9.Trauma
10.Visible Injury
11.Non-mechanical suggestion
-waking from sleep
-no improvement with rest
184
Conditions to rule out with mechanical lower back pain
1. Cauda Equina Syndrome
2. Spinal Cord compression
3. Abscess
4. Ruptured AAA
5. Acute Pancreatitis
185
Diagnosis of mechanical lower back pain
History + Physical Exam mostly
***Physical:***
1.Inspection - deformities/abnormal curvature
2.Palpation - Focal Tenderness
*-Movement:*
active + passive
pain on flexion + leg radiation -> suggestive of disc herniation
pain on extension -> suggestive of facet involvement or spinal stenosis
young + reduced range of motion -> consider ankylosing spondylitis
*--Provocative tests:*
1. Disc herniation : striaght leg raise + femoral stretch
2. Sacroiliac joint involvement- thigh thrust, distraction, gaenslen's test, pelvic compression, faber
3. Neurological Exam
4. Hip Asessment
Lab values - FBC, CRP, ESR
Imaging
-Red Flag patients/refractory: to conservative management
-Vertebral x-ray: Fractures
-MRI
-CT- Generally as part of trauma workup
186
Treatment for mechanical lower back pain
3rd line:
Radiofrequency ablation
Injection therapy
Surgical Intervention
187
What is osteomalacia
Bone softening caused by a faulty process of bone mineralisation or deficiency/impaired metabolism of Vit D, phospahte, calcium
Rickets = children
Osteomalacia = adults
188
Causes of Vit D deficiency
189
Symptoms of rickets/osteomalacia
190
Diagnosis of rickets/osteomalacia
191
Treatment for rickets/osteomalacia
192
Examples of connective tissue disorders
* Marfan’s
* Ehlers Danlos
193
What is Marfan Syndrome
Marfan syndrome is a genetic disorder that results in defective connective tissue, which can affect a person’s skeleton, heart, blood vessels, eyes, and lungs.
Inheritance is autosomal dominant
Mutation in FBN1:
-Fewer fibrillin microfibrils
-More TGF-Beta
194
Complications of Marfan Syndrome
Lens dislocation
Aortic rupture
Pneumothorax
195
Signs and symptoms of Marfan Syndrome
Skin: Stretch marks
Lungs: Bulla -> Pneumothorax
Eyes: Retinal detachment & lens dislocation
Cardiovascular:
-Aorta dilates: Aortic valve insufficiency
-Cystic medial necrosis: tunica media degenerates
-Mitral Valve Prolapse
196
Features of Marfan Syndrome
not always present
more/less severe
usually not noticeable at birth -> show up with age
present at birth -> early - onset (neonatal) Marfan Syndrome
197
Diagnosis of Marfan Syndrome
If has clinical features:
-aortic disease
-dislocated lens
-family history
-FBN1 Mutations
198
Treatment for Marfan Syndrome
199
What is Ehlers-Danlos syndrome
In Ehlers-Danlos syndrome, defective collagen leads to stretchy skin, easy bruising, and joints that are super flexible.
200
Symptoms of Ehlers-Danlos syndrome
Overly flexible joints
Easy bruising
Elastic Skin
201
Diagnosis of Ehlers-Danlos syndrome
Characteristic symptoms
examining joints and skin
DNA studies that identify mutation
202
Treatment for Ehlers Danlos syndrome
Supportive care
-Physiotherapy to supporting bones and joints
--orthopedic instruments
203
Connective Tissue Disorder table
