MUSCOSKELETAL Flashcards
What are the 2 types of bone at a macro level?
Cortical:
* Compact
* Dense, solid
* Only spaces are for cells and blood vessels
Trabecular:
* Cancellous (spongy)
* Network of bony struts (TRABECULAE)
* Looks like sponge, many holes filled with bone marrow
* Cells reside in trabeculae and blood vessels in holes
What do the minerals and collagen provide to bone respectively?
Minerals - Stiffness
Collagen - Elasticity
Define Osteoarthritis
A non-inflammatory degenerative joint disorder characterised by joint pain and functional limitation.
It commonly affects the synovial joints
Disease of bone and joint cartilage
“wear and tear of the joints”
What is the epidemiology of OA?
One of the leading causes of disability world wide.
Affects 8.5 million people in the UK
More common in women
MOST COMMON type of arthritis
What are some risk factors for Osteoarthritis?
Genetics
Increasing Age - strongest RF
Female - Hip OA 2x more common
High bone density - protective against osteoporosis but RF for OA
Excessive stress for exercise or certain occupations
What gene is related to an increased risk of osteoarthritis?
COL2A1- collagen type 2 gene
What is the pathophysiology of OA?
It appears inflammatory cytokines interrupt normal repair of cartilage damage.
(IL-1) (TNF-alpha) stimulate metalloproteinase production which degrade the collagen and proteoglycans, and inhibits collagen production
As cartilage is lost, the joint space narrows. Bone on bone interaction may occur, leads to stress and over time subchondral sclerosis (via a process called eburnation) seen on x-ray.
Essentially, cartilage is lost and chondroblasts are unable to replace and repair the lost cartilage, this leads to abnormal bone repair.
What happens in a joint affected by osteoarthritis?
Chondrocytes switch from making type 2 collagen to type 1 collagen - leading to Decreased Elasticity
Cartilage flakes into synovial space - joint mice which attracts macrophages and lymphocytes
Subsequent inflammation of articular structures at joint margins called osteophytes - leading to nodes
What are the symptoms of OA?
Joint pain - exacerbated by movement and relieved by rest
Worse as the day goes on
Joint Stiffness
Swelling
OFTEN ASSYMETIRCAL
Joint Locking - inability to straighten joints
What are the clinical signs of OA?
Hands:
Bouchard’s Nodes
Heberden’s Nodes
Thenar Muscle wasting
First CMC Joint affected most
Weak grip
Knees:
Crepitus
Hips:
Antalgic gait
Restricted internal rotation
All affected Joints:
Joint tenderness
What is Heberden’s and Bouchard’s Nodes?
Bouchard’s - Bony swelling at PIP - (tom has this on his deformed finger)
Heberden’s Bony swelling at the DIP
Remember B before H and proximal before distal
What joints are the most commonly affected in OA?
Knees
Hips
Sacro-ileac joints
Cervical spine
Wrist
base of thumb (carpometacarpal)
finger joints (interphalangeal)
What is Crepitus?
Crackling or grating sensation when moving a joint
What is a common differential diagnosis to OA?
Rheumatoid arthritis
This differs from RA due to the absence of systemic features and the pattern of joint involvement.
What are the primary investigations to diagnose OA?
Joint X rays show OA hallmarks: LOSS:
Loss of Joint space
Osteophytes
Subarticular Sclerosis
Subchondral Cysts
What other investigations may be done in OA? (ruling out other diseases)
Bloods - normal in OA
ESR/CRP - inflammatory markers to distinguish between RA or Gout
Negative anti-nuclear antibodies
How can a diagnosis of osteoarthritis be made?
If someone is over 45 and has typical activity related pain with no morning stiffness or stiffness lasting less than 30 minuets
What is the non pharmological management of OA?
Weight loss if overweight to reduce the load on the joint
Physiotherapy to improve strength and function
Occupational therapy to support activities and function
improved diet
anti-inflammatory foods (basically less processed foods: fewer ingredients = less
processed),
Orthotics to support activities and function (e.g., knee braces)
What medical treatments can be used in OA?
Analgesics to control pain and Sx:
1st. Oral paracetamol / topical NSAIDs
2nd. Add oral NSAIDs
3rd . Consider Opiates - Codeine
If these fail:
Inter-articular steroid injections
Joint replacement
When should oral NSAIDs be used with caution for OA?
In an older patient who may be on anticoagulants such as aspirin/DOACs
There may be some drug interactions/side effects using both Tx
Outline what ESR is.
ESR (erythrocyte sedimentation rate)
Rises with inflammation/infection
Increased fibrinogen makes RBCs “stick together” and therefore fall faster
Therefore, if ESR rises, the rate of fall is faster
ESR rises and falls slowly (days to weeks)
Outline what makes up a synovial joint
Bones are covered by articular cartilage. Synovial joints also have a fibrous joint capsule that links them, continuous with the periosteum of the bone
this is lined by synovial membrane which produces synovial fluid. This lubricates the joint as well as clearing debris.
There are also blood vessels and lymphatics attached to the synovial membrane.
Define what rheumatoid arthritis is
Chronic systemic inflammatory disease due to deposition of immune complexes in synovial joints which causes symmetrical, deforming polyarthritis
Can progress to involve larger joint and other organs such as the skin and lungs
Explain why CRP levels are raised in someone with inflammatory joint pain.
Inflammation leads to increased levels of IL-6. CRP is produced by the liver in response to IL-6 and therefore is raised.
Outline some of the epidemology behind Rheumatoid arthritis
- The prevalence of RA is estimated to be 1% in the UK and it is the most common inflammatory arthritis.
- Prevalence is high in smokers
- Age: the peak age of onset is between 5th and 6th decade of life
- Female gender: 2-4x more common in women
What is the aeitology behind Rheumatoid arthritis?
Genetics
Environment
- Smoking
- Other pathogens e.g. bacteria
What genes are implicated in RA?
- HLA-DR1 and DR4are crucial in activating T-cells
- A number of other genes have been implicated, such as PTPN22, which is involved in T-cell activation
What are some risk factors for rheumatoid arthritis?
- Female gender
- Smoking
- Family history
- Infections
- Hormones: increased risk post-menopause, potentially due to a reduction in oestrogen levels
Outline the initial pathophysiology behind RA. 1
Environmental triggers cause modification of self-antigens e.g., arginine is converted to citrulline in type 2 collagen. and vimentin
Due to susceptibility due to genes the immune cells cannot differentiate between self and non-self antigen.
Antigens are picked up by antigen presenting cells and carried to the lymph nodes, where T cells and B cells are activated. Autoantibodies are produced.
Outline the pathophysiology behind RA - what do the autoantibodies produced by plasma cell as and T cells go on to do? 2
enter the circulation and reach the joints.
Here, T cells secrete cytokines (e.g. Interferon-gamma and IL-17) = recruits macrophages. Macrophages also produce cytokines (TNF, IL-1 and IL-6)
These makes the Synovial cells proliferate, making a Pannus.
pathophysiology behind RA? What is a Pannus, and what can it do? What to cytokines also make T Cells do?
a pannus = (thick synovial membrane made of fibroblasts, myofibroblasts and inflammatory cells). ==> can damage cartilage, soft tissue and bones.
Inflammatory cytokines also cause T-cells to express RANKL which can bind to osteoclasts, = breakdown of bone.
What are two autoantibodies that are found in rheumatoid arthritis?
What can chronic inflammation lead to?
- Rheumatoid factor - IgM antibody that targets altered IgG
- Anti-CCP anti-cyclic citrullinated peptide - targets citrullinated proteins. = forms an immune complexes, that activate complement system,
Chronic inflammation can also cause angiogenesis, allowing more inflammatory cells to arrive.
What other parts of the body can RA affect?
Inflammatory cytokines can also escape the joint space and affect multiple organ systems
Brain
Lungs
Heart
Eyes
Liver
Blood vessels
What are some issues that RA can cause when it spreads to other areas of the body? (Brain, lungs, eyes, liver, blood vessels)
fever in brain, Peripheral neuropathy
Lungs - Plural Effusions/ pulmonary fibrosis
Heart - Increased IHD risk, Pericarditis, MI
Eyes -Episcleritis
Liver - Increase in Hepcidin, which leads to less iron absorption in the blood - Anaemia
Blood - Atherosclerotic Plaque deposition, Vasculitis
Renal - Glomerulonephritis
Oral - Sjogrens Syndrome
Rheumatoid skin nodules
What is a rare complicataion of RA, that is life threatening (consists of a triad)
Felty’s syndrome – rare
Triad of
Seropositive RA
Splenomegaly
Neutropenia
What are some signs of Rheumatoid arthritis?
-
Symmetrical polyarthritis: (on both sides of body)
- Swollen, warm and tender small joints of the hands and feet (MCP, PIP, MTP)
- Progresses to larger joints (shoulder, elbow, knee, ankle)
- Boutonniere deformity:
- Swan-neck deformity:
- Z-thumb deformity:
- Ulnar deviation of the fingers
- Popliteal cyst: synovial sac bulges posteriorly to the knee
- Rheumatoid nodules -
Signs of Rheumatoid arthritis - what is
- Boutonniere deformity:
- Swan-neck deformity:
- Z-thumb deformity: ??
- Boutonniere deformity: PIP flexion and DIP hyperextension
- Swan-neck deformity: PIP hyperextension and DIP flexion
B before S, so in Boutonniere - F before H, and Swan Neck - H before F
- Z-thumb deformity: hyperextension of the thumb IP joint with flexion of the MCP joint.
What are some symptoms of Rheumatoid arthritis?
- Morning stiffness: > 30 mins and improves throughout the day
- Malaise
- Myalgia
- Low-grade fever
What investigations would you do for Rheumatoid arthritis?
Serology -
Rheumatoid factor (RF)
anti-cyclic citrullinated peptide (anti-CCP) antibody
ESP and CRP will be elevated
May show anaemia of chronic disease - Low Hb Count
Joint x-rays -
What would you see on an x ray for rheumatoid arthritis?
can see
X-ray – LESS
Loss of joint space
Erosions (peri-articular)
Soft tissue swelling
Soft bones (osteopenia)
What is the diagnostic criteria for Rheumatoid arthritis? What 4 things does it look at
American college of rheumatology - NEEDS A SCORE OF 6 OR MORE.
Looks at
1. The joints involved (more and smaller joints score higher)
2. Serology
3. Inflammatory markers
4. Duration of symptoms longer or less than 6 weeks
What is the histological appearance of the mobile, subcutaneous nodules seen in Rheumatoid arthritis???
popular exam question
Fibrinoid necrosis in centre
Array of macrophages surrounding that
Lymphocytes surround the macrophages
With this histopathological presentation - will see positive RF
What are some differentials for RA?
- Psoriatic arthritis
- Infectious arthritis
- Gout
- SLE
- Osteoarthritis
What is some first line primary care for Rheumatoid arthritis?
- NSAID: low dose NSAID (e.g. ibuprofen) to cover the period between symptom onset and rheumatology referral
- Refer to specialist care
- Physiotherapy and occupational therapy
What is the first-lie monotherapy for rheumatoid arthritis?
Disease-Modifying Anti-Rheumatic Drugs (DMARDs)
Any one of methotrexate, leflunomide or sulfasalazine.
Hydroxychloroquine can be considered in mild disease, mildest anti rheumatic drug
METHOTREXATE - TAKE ONCE A WEEK, SUPPLEMENTING FOLIC ACID AS WELL
after Disease-Modifying Anti-Rheumatic Drugs (DMARDs), what else can you give in rheumatoid arthritis?
Biologics:
Abatacept - Suppress T Cells
Rituximab - Suppress B Cells
T cell drug ends in T, B cell drug ends in B
Infliximab, or etanercept - Suppress TNF a
Anakinra - Suppress IL-1
What is methotrexate contraindicated in?
Methotrexate
Must give folate supplements as methotrexate inhibits folic acid synthesis
Contraindicated in pregnancy
S/E – can lead to malignancy, most commonly skin
What are some side effects of
Methotrexate
Sulphasalazine
Gout can be precipitated by methotrexate use
Methotrexate can also cause liver damage
Haemolytic anaemia is a side effect of sulphasalazine,
How do you manage acute exacerbations of Rheumatoid arthritis?
Acute exacerbations – Glucocorticoids - steroids (IM methylprednisolone)
How do you monitor RA?
measure ESR and CRP levels
Oultline some differences between RA and Osteoarthritis
osteoarthritis
Morning stiffness <30mins
Affects older people more
Cartilage loss
Degenerative disease
Asymmetrical
Can affects DIP joint
Rheumatoid Arthritis
Morning stiffness >60 mins
Joints hot and red
affects younger people
Symmetrical
Inflamed Synovium
Autoimmune disease
rarely effects DIP joint
What are the two types of crystal arthritis?
Gout
Psuedo gout
What is gout?
A type of crystal arthritis which is associated with chronically high levels of uric acid.
Urate crystals are deposited in the joint causing it to become hot swollen and painful
What are the risk factors for gout?
Male
Obesity
High purine diet (e.g. meat and seafood)
Alcohol
Diuretics
Existing cardiovascular or kidney disease
Family history
What factors can increase uric acid production?
Malignancy - increased cell turnover
Cytotoxic drugs
Purine rich diet - seafood and alcohol, red meat
Obesity
Psoriasis
Increased production of purines - seen in high fructose corn syrup drink like tango, fanta
What are the decreased secretion of uric acid causes of gout?
CKD
Diuretics e.g., thiazide and loop
Dehydration,
Alcohol intake
Lead toxicity
High fructose intake
Describe the pathophysiology of gout?
Uric acid is formed as a breakdown product if purines
Uric acid has a limited solubility in the blood
If too much urate accumulates, it’ll turn into urate ion and bind to sodium, forming monosodium urate crystals
This forms urate crystals which deposit in areas with slow blood flow the joints and kidney tubules
What are the symptoms of gout?
Rapid onset severe joint pain
Joint stiffness
Commonly swollen red big toe which is painful you cannot put weight on i
What the signs of Gout and where is affected?
What are deposits of uric acid called?
Gout tophi are deposits of uric acid
Ears
Most common site in gout is 1st MTP joint
Base of big toe Podagra - gout of the foot
Wrists
Base of thumb
How would you diagnose gout?
Can be made on just clinical presentation but excluding septic arthritis is key
Joint aspiration and analysis of Synovial fluid will show:
no bacterial growth,
Needle shaped crystals, displaying Negative bifringement under polarised light
undergoing polarised microscopy
Monosodium urate crystals
Measure serum urate levels 4-6 weeks after attack as they can be low at time of attack
What are the x-ray signs of gout?
Joint space maintained
Lytic lesions
Punched out erosions
Sclerotic borders with overhanging edges
What are some non pharmalogical ways to prevent gout
Lifestyle – calorie-restriction, modify diet, weight loss, reduce alcohol, hydration
Foods =Dairy – protective, Also, cherries and vitamin C
What is the first line and second line + 3rd line treatment for gout?
1st line - NSAIDs – naproxen, ibuprofen
2nd line - Colchicine (if NSAIDs contraindicated i.e. peptic ulcer, diabetes, renal disease) - Inhibits WBC migration
3rd line - Steroids
remember that colchicine was also seen in treatment for pericarditis?
What is given to prevent gout?
Lifestyle management and a Xanthine oxidase inhibitor
First-line Allopurinol
What is pseudo gout?
Known as Calcium Pyrophosphate Arthropathy,
it’s the Deposition of Calcium Pyrophosphate crystals in the synovium
Calcium pyrophosphate crystals are deposited in the joint causing joint problems.
Can lead to calcium around the hyaline cartilage - chondrocalcinosis
What are some risk factors for getting psuedo gout
- Increasing age: the greatest known risk factor for pseudogout
- Previous joint trauma
- Hyperparathyroidism
- Haemochromatosis
- Acromegaly
- Wilson’s disease
- Diabetes
-
Hypomagnesaemia
-Hypophosphataemia
Describe the pathophysiology of pseudogout?
What is produced as a result?
Deposition of calcium pyrophosphate triggers synovitis with the knee, shoulder and wrist most commonly being affected
Produces the radiological appearance of chondrocalcinosis (linear calcification parallel to the articular surfaces)
Can be acute or chronic
What are some some signs and symptoms of psuedogout?
Very similar to gout and usually indistinguishable until joint aspiration is performed.
- Signs
- Joint inflammation: pain, erythema and swelling
- Signs can be monoarticular (1 joint) or polyarticular (several joints)
- Symptoms
- Rapid onset severe joint pain: knee, shoulder and wrist are most commonly affected
- Joint stiffness
What investigations should you do for suspected pseudo gout? What is a key one to do in order to rule out a another condition that would be a medical emergency?
Joint aspiration:weakly-positively birefringent rhomboid-shaped crystals under polarised microscopy confirm the diagnosis.
If any bacterial growth, then patient is likely to have septic arthritis - MEDICAL EMERGENCY
Joint X-ray:chondrocalcinosis (calcification of articular cartilage) is seen in 40% of casesand is highly suggestive of pseudogout but is not diagnostic; theabsenceof chondrocalcinosis doesnotexclude pseudogout
FBC – raised WBCs
Pseudogout - positive birefringent crystals
How can you differentiate between gout and pseudo gout ?
Joint aspiration, microscopy
Gout - Negatively birefringent crystals
Pseudogout - positive birefringent crystals
note - most commonly affected joint in gout is 1st MTP of the big toe, most commonly affected joint in pseudogout is the knee joint
What is the management of acute pseudogout?
Acute
- Anti-inflammatory:NSAIDs or colchicine, particularly in polyarticular disease
- Corticosteroid:intra-articularsteroids can be used in monoarticular disease orsystemicsteroids in polyarticular disease
- Cool packs and rest
- Aspiration of the joints - relieves pain
What is the management of chronic pseudogout?
- DMARDs: e.g. methotrexate and hydroxychloroquine may be considered in chronic pseudogout
- Joint replacement: only indicated in chronic, recurrent cases with severe joint degeneration
What is osteoporosis
a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture.
Bones become more porous due to increased breakdown
What is osteopenia? What is it defined by
Osteopenia refers to a less severe reduction in bone density than osteoporosis.
Defined as bone mineral density 1-2.5 standard deviations below young adult mean value
What are the primary causes of Osteopenia?
What are some secondary causes of osteopenia?
Primary – menopause and age, as Oestrogen protects bones
Secondary – to disease or drugs
rememeber as SHATTERED
S – steroid use (prednisolone)
H – hyperthyroidism/hyperparathyroidism
A – alcohol/smoking
T – thin (low BMI)
T – testosterone low
E – early menopause
R– renal or liver failure
E – erosive/inflammatory bone disease e.g. RA, myeloma
D – dietary calcium low
Normal physiology - into what 2 types is bone arranged?
Cortical Bone - around the outside
Spongy/Trabecular bone on the inside
Normal physiology - what is cortical bone made up of?
Cortical Bone - Arranged in Osteons, with osteocytes (old oestoblasts) Also have osteoblasts and oestoclasts.
Have Haversian canal in the middle, blood vessels and nerves
+ lamellae, made of collagen and hydroxyapatite
Normal physiology - what is spongy/trabecullar bone made up of?
made of trabecullae, for structural support
What are some risk factors for patients that can lead to oesteoporosis?
SHATTERED
Steroid (prednisolone use) – SSRIs, GnRH analogues
(goserelin)
Hyperthyroidism, hypercalciuria and hyperparathyroidism + Cushing’s
Alcohol and tobacco
Thin – BMI < 18.5, T1DM
Testosterone ↓ - ↑ bone turnover, hypogonadism turner’s/Klinefelter
Early menopause – ↑ bone turnover, premature ovarian failure
Renal or liver failure
Erosive/inflammatory bone disease – RA/myeloma
Dietary calcium ↓ or malabsorption, T1DM
Strength training can increase bone mass, so protective
Name some diseases that can increase the risk of getting oesteoporosis.
Joint disease e.g. RA, SLE
Hyperthyroidism and hyperparathyroidism – increased bone turnover
High cortisol – Cushing’s (increases bone resorption and induces osteoblast apoptosis)
Low oestrogen/testosterone e.g. hypogonadism, anorexia, menopause
Renal disease – decreased vitamin D
Previous fracture
Anorexia
Pathophysiology of OP - How can old age and oestrogen affect bone turnover?
As we age, the activity of osteoclasts increases and is not matched by osteoblasts.As such bone mass decreases.
Oestrogen is key to the activity of bone cells with receptors found on osteoblasts, osteocytes, and osteoclasts. The mechanisms are still being understood, but it appears osteoclasts survive longer in the absence of oestrogen, and there is arrest of osteoblastic synthetic architecture.
What are some microscopic findings of a bone from a patient with osteoporosis
Fewer trabeculae
Thinning of cortical bone
Widening of Haversian canals
Cells and mineralisation remain normal, unlike osteomalacia
What are some symptoms of oesteoporosis? What are the most common sites of fractures for someone with oesteoporosis?
Asymptomatic condition with the exception of fractures
Common fragility fractures include vertebral crush fracture and those of the distal wrist (Colles’ fracture) and proximal femur.
may also see Thorasic Kyphosis (hunching over)
What screening tool can you use in osteoporosis?
FRAX = fracture risk assessment tool
Predicts the risk of a fragility fracture over the next 10 years. Usually the first step of assessment and is done on patients at risk of osteoporosis
BMI, co-morbidities, smoking, alcohol and family history +/- bone mineral density
- It gives results as a percentage 10 year probability of a:
- Major osteoporotic fracture
- Hip fracture
What is the gold standard investigation you would do for suspected osteoporosis?
DEXA Scan (dual-energy xray absorptiometry)
Measures bone mineral density by measuring how much radiation is absorbed by the bones
Scanning Hip is best
Gives T score (main one) - number of standard deviations below the mean for a healthy young adult their bone density is.
and Z score - represent the number of standard deviations the patients bone density falls below the mean for their age.
What T scoring on a DEXA scan would be indicative of
Better than reference
No evidence of oesteoporosis
Osteopenia (offer lifestyle advice)
Osteoporosis
T-score
>0 BMD = is better than the reference.
0 to -1 = BMD is in the top 84%: no evidence of osteoporosis.
-1 to -2.5 = Osteopenia. Risk of later osteoporotic fracture. Offer lifestyle advice.
-2.5 or worse = Osteoporosis. Offer lifestyle advice and treatment Repeat DEXA in 2yrs.
What are some lifestyle management/light treatment for mild osteoporosis/osteopenia?
Activty and exercise
Weight control
Reduce alcohol/stop smoking
NICE recommend calcium supplementation with vitamin D - eg Calcihew-D3
vitamin D supplementation.
What is the treatment for someone at high risk of a fracture? (specific drug name)
Bisphosphonates- they interfere with osteoclast activity reducing their activity.
Alendronate 70mg once weekly
How do bisphosphonates work?
Bisphosphonates inhibit an enzyme in the cholesterol synthesis pathway – Farnesyl Pyrophosphate Synthase - Targets the HMG-CoA pathway (the same pathway as statins)
Blocks osteoclasts from breaking down bone, by inhibiting RANKL signalling
How should you take bisphosphonates?
Take once a week in the morning and at least 30 minutes before any food
the patient should remain upright for at least half an hour after taking
What are the side effects of bisphosphonates?
Oesophagitis/Reflux and oesophageal erosions.
GI distress
Renal Toxicity
Hypocalcaemia
Oesophageal ulcers
Osteonecrosis (death of bone tissue) of the jaw and external auditory canal
What are some other treatment options for osteoporosis?
Hormone replacement therapy should be considered in women that go through menopause early.
Raloxifene - Selective oestrogen receptor
Teriparatide - recombinant PTH, increases bone formation
How does Denosumab work
monoclonal anitbody to RANKL -
Define what fibromyalgia is
Non-specific muscular disorder with unknown cause (aka chronic persistent pain). No signs of inflammation
What are some risk factors for fibromyalgia - what is the some things seen in common presentations
Female - 10x more common
Middle aged
Low household income
Divorced
Often associated with
IBS
Chronic headache
Depression
Chronic fatigue syndrome
outline some clinical symptoms regarding pain seen in fibromyalgia
Widespread muscle pain of >3 months
Pain
Pain worse with stress, cold weather activity
Morning stiffness <1 hour
Non-restorative sleep
Headache/diffuse abdominal pain
outline some clinical symptoms regarding neurocognition seen in fibromyalgia
Neurocognitive features
Poor sleep
Fatigue
Mood disorder
Poor concentration
Memory
normal physiology - how is pain felt from the body carried by neurons up to the brain?
- When you injure yourself, this stimulus is carried as an electrical signal , to cell body of sensory neuron in dorsal root ganglion.
- ===> causes Substance P is released from the axon terminal at the dorsal root horn
- Inhibitory neurons Whose job it is release serotonin and noradrenaline to dampen pain response
- If action potential of Substance P > than that of Serotonin/NA = pain signal relayed by second order neuron up to brain
Outline some of the pathophysiology that is thought to cause fibromyalgia.
Problems with pain signals
Low serotonin – inhibits pain signals
Raised substance P and nerve growth factor – increased pain signals
What the two key clinical presentations seen in fibromyalgia?
- Allodynia - pain in response to non-painful stimulus
- Hyperaesthesia - exaggerated perception of pain to mildly painful stimulus
How would you diagnose fibromyalgia?
Diagnosis of fibromyalgiais based on clinical features:
- Chronic pain that has been present for at least 3 months
- Widespread pain - involved left and right sides, above and below waist, and the axial skeleton.
- Palpate tender point sites - severe pain in 3 to 6 different areas of your body, or you have milder pain in 7 or more different areas
- No other reason for symptoms has been found
What are some differentials for fibromyalgia?
Hypothyroidism
SLE
B12 deficiency
Polymyalgia rheumatica (PMR)
Inflammatory arthritis
What investigations would you do in suspected fibromyalgia to rule out other conditions can could cause the symptoms seen?
TFTs – rule out hypothyroidism
ANAs and dsDNA – to exclude SLE
ESR and CRP – to exclude Polymyalgia rheumatica (PMR)
Calcium and electrolytes – to exclude high calcium
Vitamin D – to rule out low vitamin D
Examine patient and CRP – to rule out inflammatory arthritis
What are some non pharmalogical measures for fibromyalgia?
MDT approach advise there is not one specific treatment that will defo work
Regular exercise for CV fitness eg fast walking, biking, swimming, or water aerobics can help by reducing pain and fatigue.
- Relaxation techniques and good sleep hygiene can also help.
- Physiotherapy and rehabilitation
- CBT
What are some pharmacological measures to help manage fibromyalgia
- Amitriptyline - tricyclic antidepressant
- Serotonin-norepinephrinereuptake inhibitors (SNRIs) e.g. duloxetine
Anticonvulsants like pregabalin and gabapentinwhich slow nerve impulses
Steroids or NSAIDS are not recommended because
there is no inflammation (if it does respond, reconsider your diagnosis!)
What is Sjogren’s Syndrome?
Autoimmune destruction of exocrine glands, especially the lacrimal (tear) and salivary glands.
What are the two types of Sjogren’s syndrome?
Primary SS: where the condition occurs in isolation - known as SICCA SYNDROME
Secondary SS; where the condition occurs with SLE or rheumatoid arthritis
Normal physiology - oultline how forgein pathogens are picked up and recongnised by the body, leading to inflammation.
Forgein pathogens are picked up and engulfed by antigen presenting cells eg Dendritic cells and macrophages
An antigen from the forge in pathogen is presented on a Major Histocompatibility complex II to a CD4+ (helper)
This activates the T Cell - which goes onto release proinflammatory cytokines, leading to recruitment of neutrophils, macrophages, B cells.
What are some factors that are associated with Sjogren’s Syndrome?
Genetic ;
Associated with HLA-D8,
HLA-DQ A1
HLA-BQ B1
Environmental
Infections of salivary and lacrimal glands
What is the pathophysiology of Sjogren’s Syndrome?
immune cells pick up bits of exocrine glands
Lymphocytic infiltration (anti-SS-A and anti-SS-B) and fibrosis of exocrine glands, especially the lacrimal and salivary glands
Create anti-SS-A and anti-SS-B antibodies
Anti-SSA autoantibodies (anti–Sjögren’s-syndrome-related antigen A autoantibodies, are also called anti-Ro, or anti SSA/Ro,
What are some symptoms of Sjogren’s Syndrome?
THINK ABOUT WHAT IS AFFECTED IN SS!
Lacrimal gland involvement - Keratoconjunctivitis (inflammation and ulceration of cornea and conjunctiva)
Blurring of vision, Itching, Redness, Burning
Salivary gland involvement – xerostomia (dry mouth)
Difficulty tasting and swallowing
Cracks and fissure
Nose and respiratory passages – ulceration and peroration of nasal septum 🡪 crusting and bleeding
Larynx – difficult speaking
Dryness of the skin and vagina
What investigations would you do for Sjorgrens Syndrome?
Sialometry – measures saliva flow
Lip biopsy
Bloods =Anti-Ro antibodies, and Presence of anti-SS-A and anti-SS-B antibodies. Positive ANA and positive RF
Schirmer’s tear Test – place filter paper at the base of eyes, induce tears. Tears should travel at least 20mm, but will travel >10mm in SS
(anti–Sjögren’s-syndrome-related antigen A autoantibodies, are also known as anti-Ro,)
What is the management for Sjorgens Syndrome?
Sicca =
Artificial tears
Frequent drinks/artificial saliva
Sugar-free pastilles
Vaginal lubricants
NSAIDs and hydroxychloroquine for arthralgia and fatigue
What is a key complication of Sjorgens Syndrome?
Risk of B-Cell Lymphoma with Sjögren’s as the lymph nodes are often hyperplastic 🡪 emergence of dominant B-cell clone responsible for a marginal zone lymphoma
What is vasculitis?
Inflammatory disorder of the blood vessel walls, which can affect any organ by causing destruction (aneurysm/rupture) or stenosis of a vessel
Can be classified by size.
What is the general Pathophysiological consequences of vasculitis?
Artery walls weaken
Walls get stiffer from fibrin deposition
Lumen of vessel narrows
Aneurysms can often occur
Outline the pathophysiology of Giant cell arteritis, and what it leads to.
It is a granulomatous vasculitis. Arteries become inflamed and thickened and there is a narrowed vascular lumen and can obstruct blood flow.
Cerebral arteries are particularly affected.:
Superficial temporal: headache and scalp tenderness
Mandibular: Jaw claudication
Ophthalmic artery: visual loss due to retinal ischaemia
What are the primary investigations of GCA?
1st line:
INCREASED ESR - ELEVATED IN 83% OF CASES
ANCA Negative
Temporal Artery biopsy - diagnostic
Fundoscopy
Picture - diagnostic criteria
What would you see under a microscope in a biopsy from a patient with Giant cell arteritis?
- A positive biopsy = presence of multinucleated giant cells (granulomas)
-may see Intimal thickening and a narrowed vascular lumen
occur in Patchy skip lesions and therefore a large chunk must be taken
multinucleated giant cells under microscopy - think of the name!
What are the differences and some similarities between Giant cell Arteritis and Takayasu arteritis?
Giant cell:
affects people >50
often affects branches of the carotid artery
Takayasu arteritis
Typically affects Asian women <40 years
often causes fibrosis and narrowing of the aortic arch
You will still see giant cell in internal elastic lamina, and raised ESR.
Management is the same
What happens polyarteritis nodosa?
Immune cells attack ALL LAYERS of the vessel wall (transmural) , mistaking it for Hepatitis B virus
Adventitia, media, intima all die, leaving fibrinoid necrosis
What are some clinical manifestations seen in poor sods with polyarteritis nodosa?
Severe systemic Sx:
Fever, malaise, myalgia
Followed by severe organ infarction:
Mononeuritis Multiplex - symptoms of peripheral neuropathy
GI bleeds, abdo pain
CDK/AKI - leading to hypertension
Skin nodules + haemorrhage
What is the diagnostic investigation for polyarteritis nodosa? What would you see?
CT angiogram:
Beads on a string - micro aneurysms
Biopsy - of kidney - Shows necrotising vasculitis due to HTN
What is seen in Buerger’s disease? (yet another form of medium vessel vasculitis ffs)
Clots in vessels supplying fingers and toes
Biggest risk factor is tobacco products
Outline the pathophysiology behind Granulomatosis w/polyangiitis? (Also known as Wegener’s granulomatosis)
B-cells mistakenly target bodies own neutrophils, and make ‘cytoplasmic anti-neutrophilic cytoplasmic antibodies’ or cANCAs. Typically IgG,
c-ANCA targets and bind to a specific neutrophil granule/ major antigen called proteinase 3 which is embedded in the membrane of some neutrophils.
When this happens, neutrophil resleases oxygen free radicals, indirectly damage the nearby endothelial cells, causing vasculitis
What are some symptoms some with Granulomatosis w/polyangiitis may experience? (kidneys, misc)
Kidneys - rapidly progressing glomerulonephritis
- Decreased urine production due to glomeruli death
- Proteinuria
- Haematuria
- Increase in BP
- Vasculitic rash (palpable purpura): due to skin involvement
- Hoarse voice: laryngeal involvement
- Scleritis/ uveitis/ conjunctivitis: small vessels of eyes affected
- Mononeuritis multiplex
- Sensory neuropathy
What is the difference between
p-ANCA
and
c-ANCA
c-ANCA are primarily, but not exclusively, directed against proteinase 3
p-ANCA are most commonly directed against myeloperoxidase but with a much wider group of potential intracellular targets
p-ANCA seen in Churg Strauss syndrome
What is seen in Paget’s Disease of bone
Loads and loads of bone remodelling -
Excessive bone resorption and growth
Will lead to deformities and potential fractures
Normal physiology - want stimulates osteoclasts to carry out bone resorption?
How is osteoclast activity stopped
Osteoblasts release RANKL, that binds to receptors on osteoclasts, activating them
Osteoblasts also release a substance call Osteoprotegerin, which blocks RANKL receptors on osteoclasts, so RANKL can’t bind to them and therefore prevents too much bone resorption
What can trigger Paget’s disease of bone
- Can be triggered by infections e.g. measles virus
Outline the 3 phases of Paget’s disease of bone.
1st phase - Lytic Phase - Osteoclasts have 100 nuclei which aggressively demineralise bone
2nd phase - Mixed blast and lytic phase - Bone resorption and formation, collagen put down in haphazard way
3rd phase - Sclerotic phase - formation overtakes resorption - disorganized and weak bone
- Osteoblastic activity slows down leading to dormant phase - ‘burned out state’
What things can Paget’s disease of bone lead to?
Misshapen bone, that can impinge on nerves = pain
Overgrowth of bone, can lead to Hearing and vision loss
Can lead to osteosarcoma - Paget Sarcoma
Can lead to bony deformities, like
Kyphosis
Bow legs
pelvic asymmetry
Arthritis, joint inflammation, Easy fractures
What is the management for Pagets disease of bone?
- ain relief
- NSAIDs
- Anti-resorptive medication - Biphosphonates e.g. alendronic acid
- Along with calcium and vit D supplementation
- Surgery -
- Correct bone deformities
- Decompress impinged nerve
- Decrease fracture risk
What is HLA-B27? What is it’s function?
is a class I surface antigen - Meaning it is on all cells, except red blood cells
It’s job is an antigen presenting cell
What are the shared clinical features of spondyloarthropathies?
Rheumatoid factor negative - Seronegative
Strong association with HLA-B27
Pathology in the spine
Asymmetrical inflammation of an entire joints
Sausage fingers
Extra-articular manifestations
When should you suspect spondyloarthropathies?
S- Sausage digit
P- Psoriasis - itchy flaky red skin
I- inflammatory back pain
N- NSAIDs illicit a good response
E- Enthesitis inflammation where tendon meets joint Acheilies, elbow, pelvis
A- Arthritis asymmetrical
C- Crohn’s/colitis/CRP
H- HLA-B27
E- eye uveitis
Patients with AS can have a normal CRP
SPINE ACHE
What is ankylosing spondylitis?
A chronic progressive inflammatory arthropathy. It mainly affects the spine and cause progressive stiffness and pain.
Ankylosis= abnormal stiffening and immobility of a joint due to the fusion of a bone
Normal physiology - what are the two types of joints in the spine?
Facet Joints - Synovial, - guide and limit range of motion in spine
Intervertebral discs - Made of Type I and II collagen - forms a joint between each vertebrae, main function is shock absorption
Outline the pathophysiological process behind Ankylosing Spondylitis.
Inflammation destroys the intervertebral joints, facet joints and sacroiliac joints
Fibroblasts replace the destroyed joints with fibrin 🡪 formation of tough fibrin band around joints which limits range of motion
Ossification occurs (fibrous tissue turns to bone) and makes spine immobile
Syndesmophytes – new bone formation and vertical growth from anterior vertebral corners
What are some clinical signs you may see in a patient presenting with ankylosing spondylitis?
- Enthesitis - inflammation at point of insertion of tendons and ligaments in bones
- Dactylitis - inflammation of entire digit
What investigations would you do for someone with ankylosing spondylitis?
- CRP and ESR - elevated
- Genetic testing - HLA-B27?
- Early stages - MRI of spine if x-ray is normal - can show early changes which show up as bone marrow oedema (red arrows) as well as erosions, sclerosis and ankylosis
What would you see on x-ray of Ankylosing spondylitis, at later stages of the disease?
Bamboo spine
calcification of all the ligaments of the spine
squaring of the vertebral bodies
subchondral sclerosis
Syndesmophytes - bony outgrowths from the spinal ligaments as they attach to adjacent vertebral bodies
fusion of joints (facet / sacroiliac / costovertebral)
What is the bedside clinical test you can do in Ankylosing spondylitis?
Schober’s test
- Have the patient stand, locate L5 vertebrae
- Mark a point 10cm above and 5cm below point of L5
- Get patient to bend over forwards as far as they can, measure the distance between the two points
- Distance of less than 20cm = indicates reduced lumbar movement and will support a diagnosis of AS
Give the order of management for Ankylosing spondyltis.
Physio and hydrotherapy
Long term high dose NSAIDs e.g. ibuprofen or naproxen
DMARDs e.g. methotrexate – treat peripheral arthritis but not the disease
Biologics– Anti-TNF e.g. etanercept or monoclonal antibodies against TNF e.g. infliximab,
Monoclonal antibodies targeting IL-7 - e.g. secukinumab
What are the complications of ankylosing spondylitis?
Vertebral fractures
Osteoporosis
Aortitis
Restrictive lung disease
Heart block
What is psoriatic Arthritis?
An inflammatory arthritis associated with psoriasis characterised by red scaly patches
Within the group of SERONEGATIVE spondyloarthropathies and has a link to HLAB27
Also known as peripheral arthritis, compared to AS which is formerly known as axial arthritis
What is the pathophysiology of psoriatic arthritis?
Has strong genetic component, pathogenesis is not fully understood, activation ofCD8+ T cellsis thought to play a critical role.
These are thought to trigger prolfieration of keratinocytes, fibroblasts, and osteoblasts and osteoclasts
What are some signs of psortiatic arthirits?
-
Joint tenderness, warmth and reduced range of motion
- Typically affects DIP joints, rather than MCP/PIP joints in rheumatoid arthritis
- Dactylitis: swelling of an entire digit
- Enthesitis: inflammation of the plantar fascia and Achilles’ tendon (back of foot)
- Psoriasis: psoriatic lesions, scalp and nail symptoms - (pitting of nails, onycholisis - separation of nail from nail bed)
What are is most severe form of psoriatic arthritis? What is seen here?
Arthritis mutilans - - Most severe and least common form
- Deforming and destructive subtype
- Occurs in the digits
Skin around the bones, folds in on itself as the bones get shorter (telescopic finger)
What are some investigations for psoriatic arthritis? How can you tell it apart from Rheumatoid arthritis?
Bloods
HLA-B27 positive
Raised ESR
RF and anti-CCP absent - whereas they would be positive in Rheumatoid arthritis.
X-ray – erosive changes (pencil in cup deformity)
What criteria can be used for diagnosing psoriatic arthritis? What kind of things does it look at?
CASPAR
CASPAR criteria: diagnosis of psoriatic arthritis can be made if the patient scores > 2 points on the following:
History of Psoriasis
Psoriatic nail changes
RF negative
History of Dactylitis
What is the management for psoriatic arthritis? What disease is the management similar to?
Similar to RA
NSAIDs
Early intervention with DMARDs
Methotrexate, sulfasalazine
DMARDs often help disease
Anti TNF drugs (biologics)
Etanercept, adalimumab, infliximab - Block TNF-a
IL 12/23 blockers – ustekinumab
What is reactive arthritis?
An arthritis that is triggered following an infection (probs by molecular mimicry)
Also known as Reiter syndrome
Its a type of Seronegative spondyloarthropathy - RF is absent
Outline the pathophysiology that is thought to be behind reactive arthritis
Thought that the lipopolysaccharide (Endotoxin) on the gram negative bacteria produces a particularly strong response from immune system.
This response also results in antibodies or inflammation that also affect the joints.
In reactive arthritis, there are no actual joint infections (as seen in septic arthritis). The infection is at another site!
What is the key presentation of reactive arthritis?
Acute, asymmetrical monoarthritis typically in lower leg (knee).
Can also present with triad of: Urethritis, arthritis and conjunctivitis
Can’t see, pee or climb a tree THIS TRIAD IS KNOWN AS REITER’S SYNDDROME
What are some other signs and symptoms of reactive arthritis?
Iritis - swelling and irritation of eye
Keratoderma blennorrhagia - painless, red, raised plaques and pustules
Circinate balanitis - dermatitis of the head of the penis
-Mouth ulcers
- Pericarditis
What are the investigations for reactive arthritis?
- ESR and CRP - elevated
- Infectious serology ask about history of infection
- Genetic testing for HLA-B27
- If diarrhoea - culture stool
Aspirate joints to rule out septic arthritis/Gout - should be sterile in RA
Sexual health review
What is the management of Reactive arthritis?
Management
Treat cause of infection – antibiotics
NSAIDs ± steroid joint injections
Consider use of methotrexate and sulfasalazine as steroid sparing agents if >6 months
- Recurrent/ persistent reactive arthritis
- DMARDs e.g. methotrexate or sulfasalazine
- Anti-TNF
What is septic arthritis? What are the two ways in which it can occur?
Septic arthritis is defined as the infection of 1 or more joints caused by pathogenic inoculation of microbes.
It occurs either by direct inoculation or via haematogenous spread.
It is a medical emergency!- CAN AFFECT ANY JOINT, MOST COMMONLY KNEE
What are the signs and symptoms of septic arthritis?
Normally only one joint is affected. Most commonly the knee.
Hot tender and swollen joint
Limited range of movement
Difficulty weight bearing
Fever
What investigations would you do for septic arthirits? What is gold standard?
- FBC: leukocytosis
- CRP and ESR: elevated due to inflammation and used for monitoring response to treatment
- Blood cultures: should be performed onallpatients before commencing antibiotics
Joint aspiration (arthrocentesis): definitive investigation ideally prior to commencing antibiotics; synovial fluid should be sent to the lab for microscopy and culture
What is the management for Septic arthritis?
- IV antibiotics
- Empirical therapy: flucloxacillin is first-line
- Penicillin allergy: clindamycin
- Suspected or confirmed MRSA: vancomycin
- Gonococcal arthritis or gram-negative infection: cefotaxime or ceftriaxone
-
Joint drainage
- Aspiration
- Arthroscopic drainage
- Open drainage
What is osteomyelitis?
Inflammation of the bone marrow (infection localised to bone) caused by an infecting organism, most commonly Staphylococcus aureus.
What are ways osteomyelitis can occur?
What is more common in adults, and what is the most common way in children?
Non-haematogenous spread - occurs due to breakdown/removal of soft tissue/skin (aka protective barriers), or contiguous spread aka from a skin infection, or in , trauma, skin ulcers, surgery
Haematogenous spread - Pathogen spreads through blood - eg intravascular catheter (Hickman Line), haemodialysis, Endocarditis, IV drug use
haematogenous is more common in children, Local is more common in adults
What bacteria can cause osteomyelitis?
- Staphylococcus aureus:A gram-positive cocci. Includes MRSA - MOST COMMON
- Pseudomonas aeruginosa:A gram-negative rod. More commonly seen in IV drug users.
- Salmonellaspp.:Gram-negative rods. Most commonly seen in patients with sickle cell anaemia.
What are some risk factors for getting osteomyelitis?
Diabetes mellitus - vascular compromise due to high blood sugar
Trauma – bone exposed to outside environment (open fractures)
Surgery
Peripheral vascular disease
Malnutrition
Inflammatory arthritis
Debilitating disease
Immunosuppression – HIV or immunosuppressive drugs
Sickle cell disease
Prosthetic material
RISK FACTORS FOR OSTEOMYELITIS ARE THE SAME AS THOSE FOR SEPTIC ARTHRITIS
What is the acute phase of osteomyelitis?
Bacteria reach the bone and start to proliferate. This alerts immune cells and they try and fight off the infection.
The immune cells release chemicals that cause local bone destruction and usually this can often resolve, with oestoblasts and clasts repairing lesion over weeks
Outline the pathophysiology behind chronic osteomyelitis.
the affected bone sometimes becomes necrotic and separates from the healthy part of the bone - called a sequestrum
osteoblasts that originate from the periosteum may form new bone that wraps the sequestrum in place, this is called an involucrum.
How can the periosteum be affected in osteomyelitis? What can it lead to?
The periosteum is loosely attached to the compact bone, so infection can make two layers can separate - allow an abscess to form between them.
The abscesstracks along the periosteum, lifting it up - away from the compact bone
Infection could now spread to nearby joint, or maybe even to muscle, skin, vessels —-Thrombophlebitis
Describe the pathophysiology of SLE?
Environmental triggers e.g., UV light causes cell death
Genetic factors mean there is a reduced clearance of this cellular debris, so it accumilates
Genetics also cause immune system to not recognise debris (particularly DNA/Histone/Nuclear etc) as self so they attack, forming antibody-antigen complexes which get deposited in different tissues
These go on to activating the complement pathway (type III hypersensitivity)
In SLE, what other things can patients with SLE make antibodies to? What is this known as?
other cells like red and white blood cells, and molecules like various phospholipids, which can mark them for phagocytosis and destruction
This is considered a type II hypersensitivity reaction
What are the symptoms of SLE?
Fatigue
Weight loss
Joint and muscle pain
Fever
Photosensitive malar rash. Get’s worse with sunlight and is butterfly shaped across the cheeks
Hair loss
Mouth ulcers
Shortness of breath
What sort of things are included in the diagnostic criteria for SLE?
Diagnosis – must have >4
MD SOAP BRAIN
Malar rash
Serositis - pleuritis, pericarditis (inflammation of serous membrane)
Oral ulcers
Arthritis
Photosensitivity
Bloods - all low anaemia, leukopenia, thrombocytopenia
Renal disease - Proteinuria
Anti- nuclear antibody positive, anti-dsDNA (double stranded DNA)
seizures,
Describe the pathophysiology of APS
Antiphospholipid antibodies can cause thrombosis by binding to the phospholipid on the surface of cells such as endothelial cells, platelets and monocytes.
Once they bind to these cells it can result in thrombosis formation and/or miscarriage. They tend to affect cerebral and renal vessels
What things do Antiphospholipid antibodies cause?
C- Coagulation defects
L- livedo reticularis - lace-like purplish discolouration of skin
O- Obstetric issues e.g., miscarriage
T- Thrombocytopenia (low platelets)
CLOT
picture - livedo reticularis
What are some arterial and venous complications of anti phospholipid syndrome
Arterial :
Stroke
MI
Renal thrombosis
Venous:
DVT
PE
What are some pregnancy related complications of APL? What a specific cardiac complication of APL?
Recurrent miscarriage
Still birth
Preeclampsia
Libmann-Sacks endocarditis: is a type of non-bacterial endocarditis where there are growths (vegetations) on the valves of the heart. The mitral valve is most commonly affected. It is associated with SLE and antiphospholipid syndrome.
Outline the pathophysiology behind Dermatomyostits and Polymyositis.
Molecular mimicry (often of a tumour protein) by Muscles cells, and also capillary endothelial cells in the skin.
What are the skin features of polymyositis and dermatomyositis?
Polymyositis occurs without skin features
Gottron lesions - scaly patches on backs of fingers also seen on elbows/knees
Photosensitive rash on back shoulders and neck
Lilac-purple (heliotrope) rash on face and eyelids
Periorbital oedema
Subcutaneous calcinosis
What is scleroderma and Sclerodactyly?
- Scleroderma refers to the hardening of the skin. It gives the appearance of shiny tight skin without normal folds
-Sclerodactyly describes skin changes in the hand where the skin tightens around the joints and restricts movement
What is Telangiectasia?
Telangiectasia are dilated small blood vessels in the skin. They are tiny veins that have dilated. They have a fine, thready appearance.
What is Marfan Syndrome? What gene is affected and what does it lead to,
Autosomal dominant condition affecting the FB1 gene which results in abnormal fibrillin production and therefore a reduced connective tissue strength
What are some clinical features of Marfans Syndrome?
tall stature with arm span to height ratio > 1.05
high-arched palate
arachnodactyly - (fingers are long, slender, and curved, like spider)
pectus excavatum -(breastbone is sunken into chest)
pes planus - (flat footed)
scoliosis of > 20 degrees
heart:
dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic regurgitation
mitral valve prolapse (75%),
lungs: repeated pneumothoraces
What is Osteosarcoma? Where will it metastises, what ages doees it affect and what will xrays show of it?
Most common primary bone cancer.
Associated with Paget’s Disease
Affects 15-19 yr olds
Will metastasis to the lung
XR shows “Sunburst” appearing bone, as well as Codman’s triangle
Bone cancers - What is Codman’s triangle? Name some conditions that you’d see it in
Codman triangle is a radiological sign.
It is the name given to a periosteal reaction that occurs when bone lesions grow so aggressively that they lift the periosteum off the bone and do not allow the periosteum to lay down new bone.
3 main causes for it: osteosarcoma. Ewing’s sarcoma. subperiosteal abscess.
What is Ewing’s Sarcoma?
Arises from mesenchymal stem cells
affects 15 yr olds
Very rare
can feature Codman’s triangle on xray
Outline some differences between osteoarthritis and rheumatoid arthritis
Rheumatoid - most common systemic (whole-body) autoimmune disease
Caused by autoimmune, - so inflammation of joints is primary
Can damage other organs, not just joints
Will often affect multiple joints, symmetrically
RA also causes flu-like symptoms, such as fever and malaise (a general unwell feeling).
Usually affects MCP and PIP joints in hand, not DIP.
Earlier onset
Morning stiffness for more than 30 mins
Osteoarthritis - most common arthritis
Caused by wearing down of articular cartilage between bones, any inflammatory is secondary
Is limited to just effecting the joints
Does not cause systemic, flu like symptoms
Typically later onset than RA
Pain in 1st Carpo-metacrapal
morning stiffness passes in less than 30 minutes
usually affects DIP
What is the diagnosis for Ehlers Danlos Syndrome?
Clinical Patient
Beighton Score
Examine Px to exclude Marfan features (long arm span etc)
