MSK & Rheumatology Flashcards
cortical v trabecular bone?
cortical
- compact
- only spaces for cells and blood vessels
trabecular
- spongy
- many holes filled with bone marrow
woven v lamellar bone
woven
- made quickly
- disorganised
lamellar
- made slowly
- organised
adult bone composition?
50-70% mineral - HYDROXAPATITE (crystaline form of calcium phosphate)
20-40& organic mix - type 1 collagen and non collagenous proteins
5-10% water
MINERAL = STIFF COLLAGEN = ELASTIC
OSTEOARTHRITIS (OA):
Cartilage loss with accompanying periarticular (around the joint) bone response
• Inflammation of articular (actually in contact with bone) and periarticular structure
and alteration in cartilage structure
epidemiology of oesteoarthiritis?
- > 55
- F>M
risk factors of oesteoarthritis
- joint hyper-mobility
- diabetes
- increasing age
- genetic predisposition
- obesity -> pro inflammatory state
- occupation
- local trauma
- inflammatory arthritis
pathophysiology of oesteoarthisits?
Progressive destruction and loss of articular
cartilage with an accompanying periarticular
bone response
- Cartilage is a matrix of collagen fibres,
enclosing a mixture of proteoglycans and water;
it has a smooth surface and is shock-absorbing
- Under normal circumstance, there is a dynamic
balance between cartilage degradation by wear and its production by
chondrocytes
- Early in the development of OA this balance is lost, the cartilage become oedematous
- Subsequently focal erosion of cartilage develops and chondrocytes die
Cartilage ulceration exposes the underlying bone to increased stress,
producing micro-fractures and cysts
- The bone attempts repair but produces abnormal
SCLEROTIC SUBCHONDRAL BONE and overgrowths
at the joint margins which become calcified - known as
OSTEOPHYTES
There is also some secondary inflammation
clinical presentation of oesteoartheritis?
Symptoms are usually gradual in onset and progressive
- Joint pain - made worse by movement and relieved by rest
- Joint stiffness after rest (gelling)
- transit morning stiffness
- nodes and bone swellings at DIPJ
investigations of oesteoarthritis
- CRP can be elevated
- negative RF and ANA
- XRAY (LOSS (loss of joint space, osteophytes, subarticular sclerosis and subchondral cysts)
treatment of oesteoarthritis?
- non medical; exercise, weight loss, alternative therapy
- pharm - paracetamol, opiods and intra-articular corticosteroid injections
- surgery; arthroscopy, arthroplasty
rheumatoid arthritis
A chronic systemic AUTOIMMUNE disorder causing a SYMMETRICAL
POLYARTHRITIS
disease of synovial joints
epidemiology of rheumatoid arthritis?
- 30-50 yrs peak age
- F>M
risk factors for rheumatoid arthritis?
- female -> oestrogen
- genetics -? HLA DR4
- smoking
- family history
- immune system
pathophysiology of rheumatoid arthritis?
RA is primarily a synovial disease and synovitis
(inflammation of the synovial lining) occurs when
chemoattractants produced in the joint recruit
circulating inflammatory cells
- Over-production of TNF-alpha leads to synovitis
and joint destruction - the interaction of
macrophages, T and B lymphocytes drives this overproduction In RA the synovium becomes greatly thickened and becomes infiltrated by
inflammatory cells
Generation of new synovial blood vessels is induced by angiogenic
cytokines and activated endothelial cells produce adhesion molecules which
FORCE LEUCOCYTES into the synovium - where they can trigger
inflammation
- The synovium proliferates and grows
out over the surface of the cartilage
(past the joint margins), producing a
tumour-like mass called ‘pannus’
- This pannus of inflamed synovium
DAMAGES the underlying cartilage
by blocking its normal route for
nutrition and by direct effects of
cytokines on the chondrocytes
- The cartilage becomes thin and the underlying bone exposed
- The pannus DESTROYS the articular cartilage and subchondral bone
resulting in bony erosions
clinical presentation of rheumatoid arthritis?
- usually MCP and PIP
- joints warm and tender
- morning stiffness > 30 mins
- symmetrical
- hand deformities; swan neck
- pain eases with use
- extra-articular; lungs (pleural effusion), heart (pericarditis), eyes (scleritis), neurological (carpal tunnel, cord compression, peripheral sensory neuropathies), kidneys (amyloidosis) and subcutaneous nodules in skin
investigations for rheumatoid arthritis?
- FBC ; low hB, ESR AND CRP raised, RF positive and ANTI CCP positive
- XRAY (soft tissue swelling, joint space narrowing and peri-articular erosions)
- MRI and USS
rheumatoid arthritis tretament?
- lifestyle changes
- pain management -> NSAIDs and PARACETAMOL
- corticosteroids (can risk osteoporosis)
- DMARD (inhibits inflammatory cytokines) eg METHOTEXTRATE (GOLD STANDARD)
- biological therapy (TNF alpha blocker eg, INFLUXIMAB) , B cell inhibitors (RITUXIMAB - CD20)
osteoporosis?
A systemic skeletal disease characterised by low bone mass and a micro
architectural deterioration of bone tissue, with a consequent increase in
bone fragility and susceptibility to fracture
bone mineral density (BMD) MORE than 2.5 standard deviations
BELOW the young adult mean value (T score < 2.5)
osteopenia?
Pre-cursor to osteoporosis characterised by low bone density - Defined as BMD between 1-2.5 standard deviations BELOW the young adult mean value (-1< T score < 2.5)
osteomalacia?
Poor bone mineralisation leading to soft bone due to lack of Ca2+
epidemiology of osteoporosis?
- > 50 yrs
- F>M (women lose trabecular with age)
- Caucasian and asians
risk factors for osteoporosis?
- old age
- women
- family history
- smoking
SHATTERED
S - steroid use
H - hyperthyroidism/hyperparathyroidism (increase bone turnover)
A - alcohol and tobacco
T - thin (BMI <22)
T - testosterone decreased
E - early menopause
R - renal or liver failure
E - erosive/inflammatory bone disease
D - dietary calcium decreased
pathophysiology of osteoporosis
Osteoporosis results from increased bone breakdown by osteoclasts and
decreased bone formation by osteoblasts, leading to loss of bone mass
Genetic factors are the SINGLE MOST SIGNIFICANT INFLUENCE on peak
bone mass
Bone strength is determined by bone mineral density, bone size and bone quality (mineralisation)
Oestrogen deficiency - Postmenopausal osteoporosis:
• Results in increased numbers of remodelling units (osteoclasts),
premature arrest of osteoblastic synthetic activity and perforation of
trabeculae with a loss of resistance to fracture
• High bone turnover (resorption greater than formation)
Changes in trabecular architecture with ageing:
• Decrease in trabecular thickness - as we age the strain is felt on bones
from head to tail, in response, we tend to preferentially preserve
VERTICAL TRABECULAE and LOSE HORIZONTAL TRABECULAE
clinical presentation of osteoporosis
- fractures
- colles fracture of wrist
investigations of osteoporosis?
- XRAY
- DEXA SCAN (GOLD STANDARD)
- FBC; ca2+, phosphate
treatment of osteoporosis?
- lifestyle changes
- pharma -> anti-resorptive drugs eg BISPHOSPHONATES (1st line ORAL ALDENIDRONATE), DENOSUMAB (inhibits RANK)
- HRT for menopausal women (RALOXIFENE)
ESR V CRP
ESR
- rises and falls slowly
CRP
-rises and falls rapidly
SLE?
An inflammatory, multisystem autoimmune disorder with arthralgia and rashes
as the most common clinical features, and cerebral and renal disease as the
most serious problems
epidemiology of SLE?
- F>M
- Peak age of onset between 20-40 yrs - typically women of childbearing age
- Commoner in African-Caribbeans and Asians
risk factors of SLE?
Family history - Genetics: • HLA genes have been linked to SLE - Pre-menopausal women MOST AFFECTED - Drugs: • Hydralazine, isoniazid, procainamide and penicillamine - UV light can trigger flares of SLE - Epstein-Barr virus is a potential trigger for SLE
pathophysiology of SLE>
When cells die by apoptosis, the cellular remnants appear on the cell surface
as small blebs that carry self antigens
- These antigens include nuclear constituents such as DNA and histones,
which are normally hidden from the immune system
- In SLE, removal of these blebs by phagocytes is inefficient, so that they are
transferred to the lymphoid tissues, where they can be taken up by antigen-
presenting cells
- These self-antigens from these blebs can then be presented to T cells, which
in turn stimulate B cells to produce AUTOANTIBODIES directed against the
antigens - Can be years before clinical features develop
clinical presentation of SLE?
Most patients suffer fatigue, fever, arthralgia and/or skin problems
- joint involvement - symptoms similar to RA
- skin involvement - butterfly erythema on cheeks, photosensitive rash
- lung involvement - pleural effusions
- heart involvement - pericarditis
- kidney - glomerulonephritis with persistent proteinuria
- CNS - seizures and psychosis
- eyes - Sjornes
- GI - month ulcers
investigations of SLE?
- blood; raised ESR and normal CRP, low Hb, low WCC
- autoantibodies - ANA positive, anti dsDNA (specific but only positive in 60%)
- histology - deposition of IgG
- MRI and CT
treatment of SLE?
IV CYCLOPHOSPHAMIDE + HIGH DOSE PREDNISOLONE
- reduce sunlight exposure, wear sunblock
- symptomatic; NSAIDs, corticosteroids for rashes
- ANTIMALARIAL drugs e.g. CHLOROQUINE OR HYDROXYCHLOROQUINE
help mild skin disease, fatigue and arthralgia that cannot be controlled by
NSAIDs - but watch for retinal toxicity - ORAL METHOTEXTRATE
- RITUXIMAB
antiphsopholipid syndrome?
Syndrome characterised by thrombosis (arterial or venous) and/or recurrent
miscarriages with positive blood tests for antiphospholipid antibodies (aPL)
antiphosphoplipid syndrome epidemiology
F>M
pathophysiology of anti-phospholipid syndrome?
Antiphospholipid antibodies (aPL) play a role in thrombosis by binding to
phospholipid on the surface of cells such as endothelial cells, platelets and
monocytes
- Once bound, this change alters the functioning of those cells leading to
thrombosis and/or miscarriage
- Antiphospholipid antibodies (aPL) cause CLOTs:
• Coagulation defect
• Livedo reticularis - lace-like purplish discolouration of skin
• Obstetric issues i.e. miscarriage
• Thrombocytopenia (low platelets)
clinical presentation of anti-phospholipid syndrome?
- Thrombosis
- Miscarriage
- Ischaemic stroke, TIA, MI - arteries
- Deep vein thrombosis, Budd-chiari syndrome - veins
- Thrombocytopenia
- Valvular heart disease, migraines, epilepsy
investigations of anti-phospholipid syndrome?
Anticardiolipin test:
• Detects IgG or IgM antibodies that bind the negatively charged
phospholipid - cardiolipin
- Lupus anticoagulant test:
• Detects changes in the ability of the blood to clot
- Anti-B2-glycoprotein I test:
• Detects antibodies that bind B2-glycoprotein
treatment of anti-phospholipid syndrome?
Long term WARFARIN to minimise thrombosis
- Pregnant women:
• ORAL ASPIRIN and SC HEPARIN early on in pregnancy
• Reduces chance of miscarriage but pre-eclampsia and poor fetal
growth remain common
- Prophylaxis:
• ASPIRIN or CLOPIDOGREL for people with aPL, especially those with a
high IgG aPL (antiphospholipid antibody)
sjorgrens syndorme?
Chronic inflammatory autoimmune disorder
• Characterised by immunologically mediated destruction of epithelial exocrine
glands, especially the lacrimal (eyes) and salivary glands
epidemiology of sjorgrens syndrome?
F>M
40-50 yrs
family history
pathophysiology of sjorgrens syndrome?
Lymphocytic infiltration and fibrosis of exocrine glands, especially the
lacrimal and salivary glands
clinical presentations of sjorgrens syndrome?
Dry eyes (keratoconjunctivitis sicca) - due to decrease in tear production
- Dry mouth due to decreased saliva production (xerostomia)
- Salivary and parotid gland enlargement
- Dryness of the skin and vagina may be a problem
can have systemic symptoms dysphagia, myasthenia graves, vasculitis
investigations of sjogrens syndrome?
Schirmer tear test:
• Strip of filter paper is placed on the inside of the lower eyelid; wetting of
< 10 mm in 5 mins indicated defective tear production and thus
Sjogrens
- Rose Bengal staining:
• Staining of the eyes shows punctate or filamentary keratitis
FBC
- raised immunoglobulins
- RF positie
- ANA positive
treatment of sjorgrens syndrome?
- artificial tears and saliva replacement
- HYDROXYCLOROQUINE
systematic sclerosis?
• Multisystem disease with involvement of skin and Raynauds phenomenon
epidemiology of systemic sclerosis?
F>M
30-50 yrs
risk factors of systemic sclerosis?
- Exposure to vinyl chloride, silica dust, adulterated rapeseed oil and
trichloroethylene - Drugs such as bleomycin
- Genetic
pathophysiology of systemic sclerosis?
Widespread vascular damage involving small arteries, arterioles and
capillaries is an early feature
- There is initial endothelial cell damage with release of cytokines, including
endothelin-1, which causes vasoconstriction
- Continued vascular damage and increased vascular permeability and the
activation of endothelial cells leads to inflammation
- this causes fibrosis in the lower dermis of skin and internal organs
- The end result is uncontrolled and irreversible proliferation of connective
tissue and thickening of vascular walls with narrowing of the lumen - Damage to small blood vessels also produces widespread obliterative
arterial lesions and subsequent chronic ischaemia
clinical presentation of systemic sclerosis?
- Raynaud’s phenomenon
- digital pits or ulcers
- swelling of the hands and feet
- fatigue
dry cough
decreased exercise tolerance
weight loss
investigations of systemic sclerosis?
- FBC -> low Ebb
- autoantibodies - ACAs and ANA postive
- imaging
- urinalysis
treatment of systematic sclerosis?
- no cure
- help with symptoms; oral vasodilators CCB, PPPI, ACE inhibitors (prevent renal crisis)
polymyositis?
rare muscle disorder of unknown aetiology in which there
is inflammation and necrosis of skeletal muscle fibres
When the skin is involved it is called dermatomyositis (DM)
epidemiology and risk factors of polymyositis
- F>M
- risk factors virus eg COXSACKIE and genetic predisposition of sjorgrens
clinical presentation of polymyositis and dermatomyositis
Polymyositis (PM):
• There is symmetrical progressive muscle weakness and wasting
affecting the proximal muscles of the shoulder and pelvic girdle
• Patients have difficulty squatting, going upstairs, rising from a chair
and raising their hands above their head
• Pain and tenderness are uncommon
• Involvement of pharyngeal, laryngeal and respiratory muscles can lead
to dysphagia, dysphonia (difficulty speaking) and respiratory failure
Dermatomyositis (DM):
• Characteristic skin changes; heliotrope (purple) discolouration of the
eyelids and scaly erythematous plaques over the knuckles (Gottron’s
papules)
• Arthralgia, dysphagia resulting from oesophageal muscle involvement
and Raynauds phenomenon
• DM is associated with an increased incidence of underlying malignancy
investigations of polymyositis
- GOLD STANDARD - muscle biopsy
- muscle enzymes; Serum creatine kinase, aminotransferases, lactate dehydrogenase
(LDH) and aldolase are ALL RAISED - ESR not raised
- ANA positive and can have RF positive
treatment of polymyositis?
- bed rest
- ORAL PREDNISOLONE
- ORAL METHOTEXTRATE for relapse
reynauds phenomenon?
Consists of intermittent spasm in the arteries supplying the fingers and toes
usually precipitated by cold and relieved by heat
- no underlying cause of disease but underlying cause in phenomenon
epidemiology of raynauds phenomenon?
F>M
pathophysiology of raynauds phenomenon
Peripheral digit ischaemia due to sudden vasospasm, precipitated by cold or
emotion and relieved by heat
- Usually bilateral and fingers are affected more commonly than toes
clinical presentation of raynauds phenomenon
Vasoconstriction (causing ischaemia) causes skin pallor followed by
cyanosis (deoxygenation) due to sluggish blood flow, then redness due to
hyperaemia - white, blue then red
- numbness and burning sensation
treatment for raynauds phenomenon
- avoid cold
- stop smoking
- vasodilators eg, NIFEDIPINE
SERONEGATIVE SPONDYLOARTHROPATHIES/SPONDYLOARTHRITIS (SpA):
Group of overlapping conditions that all share certain clinical features:
- Axial inflammation - spine and sacroiliac joints
- Asymmetrical peripheral arthritis
- Absence of rheumatoid factor hence ‘seronegative’
- STRONG ASSOCIATION with HLA-B27 - but aetiological relevance is unclear
HLA B27
Class I surface antigen - present on all cells, except RBCs
- Encoded by Major Histocompatibility Complex (MHC) on chromosome 6
- Most common in the northern hemisphere - 9% in UK, very rare in sub-
Saharan Africa - Main theory is ‘molecular mimicry’ whereby an infection triggers an
immune response and the infectious agent has peptides very similar to
the HLA-B27 molecules so there is an auto-immune response triggered
against HLA-B27
seronegative spondyloarthropathies (SpA) mnemonic?
SPINEACHE:
Sausage digit (dactylitis)
- Psoriasis
- Inflammatory back pain
- NSAID good response
- Enthesitis (particularly in heel - plantar fasciitis)
- Arthritis
- Crohn’s/Colitis/elevated CRP (can be normal in AS)
- HLA-B27
- Eye (uveitis)
ankylosing spondylitis?
Chronic inflammatory disorder of the spine, ribs and sacroiliac joints
• Ankylosis = abnormal stiffening and immobility of joint due to new bone
formation
analysing spondylitis, epidemiology?
M>F
<30 yrs
HLA B27
risk factors of ankylosing spondylitis?
- HLA B27
- Klebsiella, salmonella, shingella
pathophysiology of ankylosing spondylitis
Lymphocyte and plasma infiltration occurs with local
erosion of bone at the attachments of the intervertebral
and other ligaments (enthesitis - inflammation where
tendons/ligaments insert into bone), which heals with
new bone (SYNDESMOPHYTE) formation
- Syndesmophyte:
• New bone formation and vertical growth from
anterior vertebral corners
clinical presentation of ankylosing spondylitis
- back pain - worse at night
- morning pain relieved by exercise
- loss of spinal movement (loss of lumbar lordosis and increased kyphosis)
- asymmetrical joint pain
- enthesitis -> inflammation on tendon eg, Achilles tendon
investigations of ankylosing spondylitis?
- ESR and CRP raised -> CRP can be normal
- XRAY; erosions and sclerosis of joint margins, bony spurs and fusions of sacroiliac joints
treatment of ankylosing spondylitis?
- morning exercise
- NSAIDs
- METHOTEXTRATE
- INFLIXIMAB
- steroid infections
psoriatic arthritis, risk factors?
family history
can occur without psoriasis
clinical presentation of psoriatic Arthritis
5 patterns;
- asymmetrical oligoarthritis
- symmetrical seronegative poly arthritis
- distal interpharangeal arthritis
- arthritis mutilans -> bone shortening of small bones in hands and feet
investigations of psoriatic arthritis?
- bloods and ESR may be normal
- XRAY - bone erosions
treatment of psoriatic arthritis?
- NSAIDs
- METHOTEXTRATE
- GOLIMUMAB
reactive arthritis?
• Sterile inflammation of the synovial membrane (synovitis), tendons and fascia
triggered by an infection at a distant site, usually gastro-intestinal or genital
• Typically affects the lower-limb
epidemiology of reactive arthritis?
M>F
main causes of reactive arthritis?
GI infections
sexually acquired
pathophysiology of reactive arthritis?
Bacterial antigens or bacterial DNA have been found in the inflamed
synovium of affected joints - suggesting that his persistent antigenic
material is driving the inflammatory response
clinical presentation of reactive arthritis?
acute, ASYMMETRICAL, lower-limb arthritis
- Occurring a few days to a couple of weeks after the infection
- The arthritis may be the presenting complaint if the infection is mild or
asymptomatic
CANR SEE (uveitis), CANT WEE, CANR CLIMB TREE (enthesitis)
investigations of reactive arthritis?
- ESR and CRP raised
- stool culture
- aspirate synovial fluid
treatment of reactive arthritis?
- NSAID
- corticosteroid injections
- antibiotics
- METHOTREXATE
- GOLIMUMAB
systemic vasculitis?
Is a histological term describing inflammation of the vessel wall
Inflammation and necrosis of blood vessel walls with subsequent impaired blood
flow resulting in:
- Vessel wall destruction - aneurysm, rupture and stenosis:
• Resulting in perforation and haemorrhage into tissues
- Endothelial injury:
• Resulting in thrombosis + ischaemia/infarction of dependent tissues
classification of systemic vasculitis?
LARGE
- aorta and major vessels
eg, giant cell arthritis
MEDIUM
- medium and small sized arteries and arterioles
eg, classical polyarthetis nodosa
SMALL
- small arterioles, arterioles, venules and capillaries
ef, ANCA associated and ANCA negative
large vessel vasculitis?
Polymyalgia rheumatica (PMR) and Giant Cell (temporal) Arteritis (GCA) are
systemic illnesses affecting patients older than 50 yrs
• Both are associated with the finding of GCA on temporal artery biopsy
• These are two SEPARATE CONDITIONS but normally co-exist
polymyalgia rheumatica, epidemiology?
- > 50
- F>M
- SLE
- polymyostits/dermatomyositis
clinical presentation of polymyalgia rheumatic?
- sudden onset pain and stiffness of shoulders and neck
- worse in morning >30 mins
- fatigue, fever, weigh loss
investigations of polymyalgia rheumatica?
- ESR and CRP raised
- ANCA negative
- temporal artery biopsy
treatment of polymyalgia rheumatica?
- corticosteroids + PPI
giant cell arthritis?
Inflammatory granulomatous arteritis of large CEREBRAL ARTERIES as well as
other large vessels e.g aorta, which occurs in association with PMR
giant cell arthritis, epidemiology?
F>M
>50
SLE, RA, scleroderma
pathophysiology of giant cell arteritis?
Arteries become inflamed, thickened and can obstruct blood flow
- Cerebral arteries affected in particular e.g. temporal artery
- Opthalmic artery can also be affected potentially resulting in permanent or
temporary vision loss
clinical presentation of giant cell arthritis?
Severe headaches (temporal pulsating)
- Tenderness of scalp (combing hair can be painful) or temple
- Claudication of the jaw (pain in jaw) when eating
- SUDDEN PAINLESS VISION LOSS - EMERGENCY - Arteritic anterior
ischaemic optic neuropathy - optic disc is very pale/swollen
investigations of giant cell arthritis?
- age, headache, temporal artery tenderness, ESR and CRP raised and abnormal artery biopsy
- ANCA negative
GOLD STANDARD -> TEMPORAL ARTERY BIOSPY
treatment of giant cell arthritis?
- high dose PREDNISOLONE + PPI
poly-arthritis nodosa, epidemiology?
- M>F
- Hep B
pathophysiology of poly-arthritis nodosa?
Necrotising vasculitis that causes aneurysms and thrombosis in medium
sized arteries, leading to infarction in affected organs
- Has severe systemic symptoms
clinical presentation of poly-arthritis nodosa?
Fever, malaise, weight loss and myalgia
- neurological -> numbness, tingling
- abdo -> pain and GI haemorrhage
- renal -> haematuria, proteinuria
- cardio -> MI
- skin -> gangrene
investigations of poly-arthritis nodosa?
- anaemia
- WCC raised
- ESR raised
- ANCA negative
- biopsy f kidney
- angiography
treatment of poly - arthritis nodosa?
- control of bp - RAMIPRIL
- corticosteroids
types of crystal arthropathies?
Monosodium urate crystals:
• Needle-shaped (long and thin) urate crystals
• Negatively bifringent under polarised light
- Calcium pyrophosphate crystals:
• Small rhomboid brick-shaped pyrophosphate crystals
• Positively bifringent under polarised light
gout?
A inflammatory arthritis that is associated with hyperuricaemia (high levels of uric
acid) and intra-articular monosodium urate crystals
epidemiology of gout?
M>F
increasing age
risk factor of gout?
risk factors
High alcohol intake (highest risk for beer then spirits then wine)
- Purine rich foods - red meat e.g. liver and seafood
- High fructose intake (sugary drinks, cakes, sweets and fruit sugars) -
reduces uric acid excretion
- High saturated fat diet
- Drugs such as low-dose aspirin
- Ischaemic heart disease
aetiology of gout?
renal causes; defective URAT 1 transporter in kidneys
increased production of uric acid from polycythemia vera
family history
pathophysiology of gout?
two steps of purine metabolism,
HYPOXANTHINE is converted to XANTHINE
and then xanthine is converted to URIC
ACID under the action of the enzyme XANTHINE OXIDASE
URIC ACID is excreted via kidneys but if there is excess uric acid, it is converted into monosodium crate crystals
gout clinical presentations?
- pain and swelling and redness of MTP joint - BIG TOE
- chronic tophi
investigations of gout?
- GOLD STANDARD -> joint fluid aspiration and microscopy -> negatively bifringent
- raised uric acid
- signed of renal impairment
treatment for gout?
- lifestyle changes (dairy foods are GOOD)
- NSAIDS - if not tolerated COLCHICHINE (v. toxic)
- PREDNISOLONE
prevention
- ALLOPURINOL (inhibits xanthine oxidase)
pseduogout?
Deposition of Calcium Pyrophosphate crystals on joint surface
epidemiology and risk factors of pseudo gout?
elderly women
risk factors
- diabetes
- oesteoartheritis
- joint trauma
- metabolic diseases -> hyperparathyroidism
pathophysiology of pseudo gout
Deposition of calcium pyrophosphate in articular cartilage and periarticular
tissue producing the radiological appearance of chonedrocalcinosis (linear
calcification parallel to the articular surfaces)
clinical presentations of pseudo gout?
Shedding of crystals into a joint produces acute synovitis that resembles
ACUTE GOUT but is more common in elderly women and usually affects the
knee or wrist
- The attacks are very painful
- Acute hot swollen wrist or knee (fever)
investigations for pseudo gout?
Joint fluid aspiration & microscopy - Positively bifringent crystals
XRAY - chonedrocalcinosis
Bloods - WCC raised
treatment of pseudo gout?
- NSAIDs - if not tolerated COLCHICINE
- PREDNISOLONE
- aspiration
Paget disease of bone?
disorder of bone turnover
epidemiology of Paget disorder of bone?
- > 40
F>M
family history
aetiology of paget disease?
Aetiology is unknown
- May result from latent viral infection (canine distemper virus, measles or
respiratory syncytial virus) in osteoclasts in genetically susceptible
individuals
pathophysiology of paget disease?
There is increased osteoclastic bone resorption followed by formation of
WEAKER NEW BONE, increased local bone blood flow and fibrous tissue
- Ultimately, formation exceeds resorption but the new woven bone is
WEAKER than normal bone - this leads to deformity and increased fracture
risk - Disease doesn’t spread but can become symptomatic at previously silent
sites
clinical presentation of paget disease?
- most are asymptomatic
- joint pain
- deformaties
- neurological complications; nerve compressions, partial paralysis of lower limbs
- cardiac failure
investigations of paget disease?
- serum alkaline phosphatase increased and calcium + phosphate normal
- XRAY
- bone scans
treatment of paget disease?
- BISPHOSPHONATE - inhibits bone resorption by decreasing osteoclast activity
osteomalacia?
There is a normal amount of bone but its mineral content is LOW (there is excess
uncalcified osteoid and cartilage) - defective mineralisation
aetiology of osteomalacia?
Most common cause of osteomalacia is hypophosphataemia due to
hyperparathyroidism (excess release of parathyroid hormone results in the
decreased absorption of phosphate in the kidneys resulting in more
excretion in the urine - in response to decreased Ca2+ absorption) secondary
to vitamin D deficiency
Vitamin D deficiency:
• Due to malabsorption, since vitamin D is fat soluble so GI disease can
result in malabsorption e.g. in Coeliac or Crohn’s
• Poor diet - not enough oily fish or egg yolks
• Lack of sunlight:
- Those with pigmented skin, using sunscreen, concealing clothing
- The elderly and institutionalised e.g. nursing home
Renal disease:
• Renal failure means there is inadequate conversion of 25-hydroxy
vitamin D to 1,24-hydroxy vitamin D
- Drug induced:
• Anticonvulsant may induce liver enzymes leading to increased
breakdown of 25-hydroxy vitamin D
• Rifampicin - antibiotic - Liver disease:
• Leading to reduce hydroxylation of vitamin D to 25-hydroxy vitamin D
e.g. cirrhosis
clinical presentation of oestemalacia?
- muscle weakness 0 waddling gait
- widespread bone pain
- knock knees, bowed legs (rickets)
investigations for osteomalacia?
- FBC; low ca2+ and phosphate
- elevated PTH
- low 25-hydroxy vitamin D
GOLD STANDARD - biospy
treatment of osteomalacia?
VIT D replacement
acute disc disease?
Prolapse of the intervertebral disc results in acute back pain (LUMBAGO)
epidemiology of acute disc disease?
- 20-40 yrs
clinical presentations of acute disc disease?
Sudden onset of severe back pain - often following a strenuous activity
- Pain is often clearly related to position and is aggravated by movement
- Muscle spasm leads to a sideways tilt when standing
- The radiation of the pain and the clinical findings depend on the disc
affected - the LOWER THREE DISCS being the MOST COMMONLY
AFFECTED
diagnosis of acute disc disease
XRAY and MRI
treatment of acute disc disease?
- bed rest
- analgesics
- physio
- surgery if SEVERE
osteosarcoma?
Most common primary bone malignancy in children
• Usual peak onset 15-19 yrs
• Associated with Paget’s disease in adult life
- common in knee
- painless
- XRAY
Ewing’s sarcoma
• Thought to arise from mesenchymal stem cells
• Very rare
• Average age of onset is 15 yrs
• Presents with a mass/swelling in long bones eg arm and legs
- painful swelling, weight loss, fever
fibromyalgia?
Fibro = soft tissue & myalgia = muscle pain
- Widespread musculoskeletal pain AFTER other diseases have been
excluded - Symptoms present for at least 3 months and other causes have been
excluded - Pain at 11 of 18 tender point sites on digital palpation (with enough pressure
so that the thumb blanches)
epidemiology of fibromyalgia?
- female
- middle age
associations
- depression, chronic headache, IBS, chronic fatigue syndrome
clinical presentations of fibromyalgia?
- pain! - lower neck, base of skill, upper edge of breast, shoulders elbow, buttock, hip bone and knee
- fatigue
- non restorative sleep
investigations of fibromyalgia?
- thyroid function test
- ANA
- ESR and CRP
- vit D and ca2+
- pain at 11/18 sites
treatment of fibromyalgia?
- low dose antidepressants eg ORAL AMITRIPTYLINE
Red flags for possible SERIOUS SPINAL PATHOLOGY:
Age of onset LESS than 20 or GREATER than 55 yrs
- Violent trauma e.g. fall from height or road traffic accident (RTA)
- Constant, progressive, non-mechanical pain
- Thoracic pain
- Systemic steroids, drug abuse or HIV
- Systemically unwell, weight loss
- Persisting severe restriction of lumbar flexion
- Widespread neurology
- Structural deformity
*do spinal X-RAY**
lumbar spondylosis
Main lesion occurs in an intervertebral disc
capsule encloses a fibrous outer zone and a gel-like inner zone
changes to the disc -> bulging or swelling causes bone to become sclerotic
common in L5/S1 and L4/L5
facet joint syndrome?
Lumbar spondylosis also causes secondary osteoarthritis of the
misaligned facet joints
Pain is typically worse on bending backwards and when straightening
from flexion - it is lumbar in site, unilateral or bilateral and radiates to the
buttock
seen in MRI and treatment is corticosteroid injections
thoracic outlet syndrome?
Pain or tingling down arms or blanching of fingers related to posture of arm
- May also present as wasting of hands
- Due to compression of the brachial plexus or subclavian artery/vein in the
neck
from poor posture and working on key board
hand arm vibration syndrome?
Raynaud’s phenomenon of industrial origin
- Caused by excessive exposure to hand-transmitted vibration
septic arthritis?
Acutely inflamed joint which can destroy a joint in under 24 hour
- knee joint most common
epidemiology of septic arthritis?
- increased with age
- STAPHYLOCOCCUS AUREUS - MOST COMMON CAUSE!
• Streptococci
• Neisseria gonorrhoea
• Haemophilus influenzae in children
risk factor of septic arthritis?
Pre-existing joint disease - especially RA (chronically inflamed joints are at
more risk of infection than normal joints)
- Diabetes melllitus
- Immunosuppression e.g. HIV
- Chronic renal failure
- Recent joint surgery
- Prosthetic joints - prosthetic joint infection (see below)
- IV drug abus
- Those over 80 yrs and infants
- Recent intra-articular steroid injection
- Direct/penetrating trauma
clinical presentation of septic arthritis?
In the young and previously fit:
• Agonisingly painful, red, swollen, hot joint
- In the elderly and immunosuppressed and in RA the articular signs may be
muted - less dramatic
- fever
investigations for septic arthritis?
- joint aspiration *BEFORE ANTIBIOTICS
- bloods
- X-RAY
treatment of septic arthritis?
STOP methotrexate and anti-TNF alpha
Double prednisolone dose - ONLY IF ALREADY ON LONG TERM
PREDNISOLONE
prevent stiffness and muscle wasting
- If in doubt start IV antibiotics AFTER JOINT ASPIRATION!:
• IV FLUCLOXACILLIN - most gram-NEGATIVES e.g. E.coli
• IV ERYTHROMYCIN/CLINDAMYCIN if allergic to penicillin
• IV CEFOTAXIME for gram-NEGATIVES or gonococcal
• IV VANCOMYCIN for MRSA
• In immunocompromised give IV FLUCLOXACILLIN + GENTAMICIN
-
oesteomyelitis?
Osteon-myelo-itis = bone-marrow-inflammation
• Infection localised to bone
epidemiology of osteomyelitis?
Osteomyelitis predominantly occurs in children
Adolescents and adults tend to get osteomyelitis due to infection secondary
to direct trauma
- Elderly get it due to risk factors
main causes of osteomyelitis?
Staphylococcus Aureus is the most common organism - 90% of acute
osteomyelitis
• Coagulase negative staphylococci e.g. Staphylococcus Epidermidis
• Haemophilus influenzae
• Salmonella - can occur as a complication of sickle cell anaemia
• Pseudomonas aeruginosa and Serratia marcesans in IVDU
risks factors of osteomyelitis?
Diabetes mellitus - Peripheral vascular disease - Malnutrition - Inflammatory arthritis - Debilitating disease Decreased immunity e.g. HIV or immunosuppressive drugs - Sickle cell disease - Prosthetic material - Immunosuppressive drugs - Trauma
pathophysiology of osteomyelitis?
Pathogen has to get into bone and there many routes each of varying
difficulty:
• Direct inoculation of infection into the bone either via trauma of surgery
(easy)
• Contiguous spread of infection into bone without breaking the skin (medium):
Haematogenous seeding (hard):
- E.g. infection from skin spreading to the blood then to the bone e.g.
Staphylococcus aureus from cannula on skin to blood
(bacteraemia) then into bone
Inflammatory exudate (in response to bacteria) in the marrow leads to
increased intramedullary pressure, with extension of exudate into the
bone cortex
• This causes rupture through the periosteum and interruption of
periosteal blood supply resulting in necrosis
• This leaves pieces of separated dead bone known as sequestra
• New bone form here called involucrum
clinical presentation of osteomyelitis?
- Dull pain at site of osteomyelitis that may be aggravated by movement
- Fever, sweats, rigors and malaise
- tenderness
ddx -> Charcot joint
investigations of osteomyelitis?
Imaging:
• Plain X-ray may show osteopenia
• MRI may show marrow oedema from 3-5 days (sign of osteomyelitis) -
done after X-ray
Blood: • Blood culture to determine aetiology • ESR & CRP raised • Acute - raised WCC • Chronic osteomyelitis - can have normal WCC
- Bone biopsy & culture to determine aetiology
treatment of osteomyelitis?
Immobilisation
- Antimicrobial therapy:
• Tailored to culture and sensitivity findings
• IV TEICOPLANIN - side effects; rash, pruritus, GI upset
• IV FLUCLOXACILLIN
• ORAL FUSIDIC ACID
prosthetic joint infections; causes?
Staphylococcus Aureus
• Coagulase negative staphylococci (these are the MOST FREQUENT
INFECTING ORGANISM AFTER HIP REPLACEMENT) e.g.
Staphylococcus Epidermis
clinical presentation of prosthetic joint infection?
Majority are not acutely infected
- Systemically well
- Tender, hot, swollen joint (the one thats been replaced)
investigation of prosthetic joint infections
JOINT ASPIRATION:
• GOLD STANDARD DIAGNOSTIC
Tissue sample from surgery
- X-ray
- Both ESR & CRP raised - sign of infection:
treatment of prosthetic joint infections?
- antibiotics
- excision arthroplasty
- amputation
juvenile idiopathic arthritis?
Defined as joint swelling/stiffness/limitation in those older than 6 weeks but
under 16 with no other causes
clinical presentation of juvenile idiopathic arthritis?
- synovitis
- arthritis (might be RF neg)
- enthesis
- thrombocytosis
- daily fever
- rash
- splenomegaly
treatment of juvenile idiopathic arthritis?
- physio
- steroid injections, NSAIDs and methotextrate
TYPES OF FRACTURES?
Oblique - is common is ankle due to axial load injury
- Spiral - generated from twisting injury
Comminuted - generated from high energy impact
- Greenstick fracture:
• SPECIFIC to CHILDREN
• Unicortical fracture in which the bone BENDS & BREAKS due to thick
periosteum
• Very easy to treat
• Bone not completely broken
compartment syndrome - fractures?
Painful condition in which the pressure within the fascia builds to
dangerous levels usually caused by bleeding within the fascia
• Common in tibia
• Caused by cast (too tight) or post-op bleeding of the fascia
• Treated with fasciotomy whereby the fascia is removed
