Rheumatology Flashcards
Describe the general differences between inflam and non-inflam conditions?
Inflam: pain worse after rest/in morning, morning stiffness >30 min, systemic symptoms present, actue/sub-acute symptoms
non-inflam: pain after use/at end of day, morning stiffness <30 min, no systemic sx, chronic sx
name 2 acute inflammatory monoarthritic ?
- gout
- Septic arthritis
Name a chronic inflammatory polyarthritis ? (2)
- Rheumatoid arthritis
- Psoriatic (actually oligo most the time)
name a chronic inflammatory axial arthritis ?
ankylosing spondylitis
name a non-inflammatory acute monoarthritic ?
torn cruciate ligament
name a non-inflam chronic polyarthritis ?
osteoarthritis
name a chronic non-inflammatory axial arthritis ?
scoliosis
What is osteoarthritis ? pathophysiology
degenerative joint disorder (wear and tear): result of mechanical and biological events that damage joints (degeneration + synthesis of cartilage chondrocyts)
- imbalance between cartilage worn down + chondrocyte repair => structural issues => pain
OA RF ?
- obesity (low grade inflam state)
- increasing age
- occupation
- trauma to joint
- female
- FHx of OA
OA presentation ? common joints ?
joint pain + stiffness (morning stiffness <30min), worsened by activity, crepitus
- common affected joints: knees, hips, sacroiliac, DIP (if distal the not RA!), CMC, wrist, asymmetrical
name the OA signs in hands + OE (7)
- herberden’s nodes (high => DIP)
- bouchard’s nodes (below => PIP)
- squaring at base of thumb (CMC joint)
- weak grip
- reduced range of motion
- effusions around the joint
- crepitus on movement
where might OA patients present with referred pain ?
consdier OA in the hip in patients presenting with lower bakc or knee pain
how is OA diagnosed ?
clinical diagnosis if the patient is over 45
(typical pain associated with activity and morning stiffness lasting less than 30 mins)
OA Mx ?
- lifestyle changes: weight loss, physiotherapy, arthotics
- analgesia: paracetamol + topical NSAID (diclofenac)
- add oral NSAID (Ibuprofen) + PPI (lanzoprazole)
- consider opiates: codeine, intra-articular joint infections
What is RA ?
autoimmune condition that causes chronic inflam of synovial lining of joints, tendon sheaths + bursa (synovitis)
what type of arthritis is RA ? distribution
inflammatory symmetrical polyarthritis
RA RF ?
- female
- > 50
- smoking
- fam history of RA
- genetic association (HLA DR4)
(smoking doubles risk, FHx doubles risk, both together is x20 risk)
what are the 2 antiobodies associated with RA ? present in how many ppl ?
- rheumatoid factor (RF): present in 70% of ppl with RA
anti-CCP antibodies: present in 80% of ppl with RA
what is RF ? what does it do/target?
RF is an autoantibody taht targets Fc region on IgG => activation of immune system against patients own IgG => systemic inflam + erosions
Why are RF and anti-CCP important to know in RA ?
they affect prognosis
- double positive means more likely to have persistent disease and will need lifelong meds
- double negative means could potentially come off treatment
RA presentation ? what joints affected ?
typically symmetrical distal polyarthropathy (pain, swelling, stiffness)
- wrist, ankle, MCP, PIP (almost never DIP)
- systemic symptoms: fatigue, weight loss, malaise
what are the RA signs in the hands ? (4)
- Z shape deformity of the thumb
- Ulnar deviation
- swan neck deformity
- boutonniere deformity
extra articular manifestations of RA ? (6)
- pulmonary fibrosis
- secondary Sjogren’s
- CVD
- Rheumatoid nodules
- Lymphadenopathy
- carpul tunnel
RA initial Ix ?
- RF
- Anti-CCP
- Inflam markers: CRP + ESR
- X-rays of the hands and feet for bone changes
(Dx based on clinical findings and blood results)
(also FBC, U+E, LFT for baseline Ix)
What XR changes would be seen RA ?
- joint destruction and deformity
- periarticular osteopenia
- boney erosions
- soft tissue swelling
RA Mx ?
short course steroids initially + in flare ups, NSAIDs, PPI
- DMARDS: methotrexate
- biologics: adalimumab, infliximab, rituximab (these all cause immunosuppression)
What needs to be prescribed alongside methotrexate ?
folic acid
- methotrexate interferes with folate metabolism and suppresses the immune system. Folic acid is taken once a week (on a different day to the methotrexate)
(methotrexate uses folic acid transporter)
methotrexate SE ? what reduces the side effect risk
- nausea/diarrhoea
- mouth ulcers
- liver toxicity
- !bone marrow supression! and leukopenia
- teratogenic
- pneumonitis
(taking folic acid reduces risk of all)
What are the symptoms of low folic acid ? (5)
- fatigue
- weakness
- thinning hair
- mouth ulcers
- visual problems
What blood tests would you do for a patient on methotrexate ? (4) why ?
- LFT: as it is metabolised in the liver
- U+E: as reduced renal fun affects methotrexate metabolism and can cause levels to rise in the blood
- FBC: check white cells and platelets (assess for bone marrow failure)
- ESR/CRP: check disease progression/activity
What is Psoriatic arthritis ?
inflammatory seronegative spondyloarthropathy arthritis associated with psoriasis
(can vary in stiffness to join completely destroyed)
what % of ppl with psoriasis will develop psoriatic arthritis ?
10-20 %
(the arthritis can occur before the skin changes)
what is the complete joint destruction associated with psoriatic arthritis called ? what is it?
arthritis mutilans
-osteolysis of the bones around the joints leasing to progressive shortening of the digits (telescoping digit)
psoriatic arthritis presentation ? distribution ? signs
asymmetrical oligoarthritis
symmetrical polyarthritis
- DIP joint involvement
- Signs: plaques, nail pitting, onycholysis, dactylitis, enthesitis
(can affect any joint !)
How to check for enthesitis in a psoriatic arthritis patient ?
check for pain on foot flexion
what screening tool is used for psoriatic arthritis ?
Psoriasis Epidemiological screening tool (PEST)
what are the XR changes in psoriatic arthritis ? (4)
- periostitis (inflam of the periosteum)
- ankylosis
- Osteolysis
- Dactylysis
- Penicl-in-cup (classic finding): assocaited with arthritis mutilans
Psoriatic arthrits Mx ?
- NSAIDs:
- Steroids
- DMARDs (methotrexate)
- Anti-TNF meds (etanercept, infliximab)
what is reactive arthritis ?
sero-negative spondyloarthropathy: it involves synovitis in one of more joints in reaction to recent infective trigger (the joints are sterile therfor not septic). Immune respone => inflam that affects joints
- typically cases acute monoarthritis
most common reactive arthritis trigger ?
- gastroenteritis (salmonella, shigella)
- STI (chlamydia)
what is the classic triad of symptoms in reactive arthritis ?
- bilateral conjunctivits
- urethritis
- arthritis
(cant pee, see or climb a tree)
Reactive arthritis Ix ?
assume septic arthritis until differential excluded: aspirate joints (gram staining + culture, crystal examinations)
reactive arthritis Mx ?
- treatment of triggering infection (e.g. chlamydia)
- NSAIDs
- steroid infection into the affected joints
- systemic steroids may be required
(30-50 will develop some form of chronic ReA)
what are the seronegative arthritis ? (5) why are they called this ?
- Ankylosing spondylitis
- Psoriatic arthritis
- Reactive arthritis
- Enteropathic arthritis
- Undifferentiated spondyloarthritis
(RF and anti-CCP are typically negative)
Which RA/rheum drugs are safe during pregnancy ? (3)
- hydroxychloroquine
- sulfasalazine
- adalimumab
What is the first line bioligic in rheumatology ?
adalimumab
What is poly myalgia rheumatic (PMR) ? strong association with what ?
It is an inflam condition causing pain and stiffness in shoulders, pelvic girdle and neck
- strong association with GCA (often occur together)
PMR epi ?
usually affects old adults (50+), women, caucasian
PMR presentaiton ? when are symptoms worse ? uni or bilateral ?
present for at least 2 weeks:
- bilateral shoulder pain (radiates to upper arm)
- bilateral pelvic girdle pain
- worse after inactivity, interferes with sleep, stiffness in morning (>45 mins)
what are addition symptoms of PMR ?
- weight loss
- fatigue
- low grade ever
- low modd
- carpal tunnel syndrome
- screen for GCA !
What are the typical GCA symptoms that you should screen for in suspected PMR patient ?
- painful and tender scalp (over the temporal arteries)
- Headaches (new temporal headache)
- jaw claudication (pain in jaw after eating/chewing)
- visual changes (blurring or loss of vision)
Describe the headache in GCA ?
severe unilateral headache around the temple
- plus scalp tenderness
what features would push you away from a GCA diagnosis ? (5)
- vomiting
- fever
- menigitis
- encephalitis
- normal inflam markers
how is PMR diagnosed ?
clinical presentation and if responds well to management
- inflam markers are usually raised but absence doesn’t exclude diagnosis
PMR mx ? (with no GCA sx)
steroids
- 15mg oral prednisolone (the wean down over yrs)
what dose of steroids for PMR if visual GCA changes present
40-60 mg oral prednisolone
(60 if visual loss has started)
What are the different categories of rheumatological drugs available ? (5)
- NSAIDs
- Steroids
- DMARDs
- Biologic agents
- JAK inhibitors
what are some side effects of steroids ? (5)
- GI: indigestion, ulcers, GI bleed
- Osteoporosis
- diabetes/glucose intolerance
- infection
- skin thinning
explain why patients should never abruptly stop their steroids ?
- exogenous steroids result in suppresion of ACTH
- Adrenal suppression with an inability to respond to appropriate to stress
=> life-threatening fluid unresponsive hypotension
biological treatment SE ?
infection: can present in a more subtle fashion, and patients may become very unwell very quickly
When would you advise a patient to stop taking their biologic treatment ? (2)
- if they have infeciton
- if they are having an operation
how long men and women need to be off methotrexate to safely conceive pregnancy ?
3 months (?)
safe for men
what are the main connective tissue disorders ?
- SLE
- scleroderma
- granulomatosis with polyangitis
- EDS
- Sjörgrens
- raynauds
what are antinuclear antibodies ?
autoantibiotides that bind to contents of nucleus (instead of foreign proteins)
- when ANAs signal body to target itself => autoimmune => scarring + damage to Orans affected
What is systemic sclerosis ?
autoimmune inflam and fibrotic connective tissue disease
- causes hardening or scarring of skin and internal organs
(cause unknown)
what are the two main patterns of disease in systemic sclerosis ?
- limited cutaneous systemic sclerosis
- diffuse cutaneous systemic sclerosis
what are the features of limited cutaneous systemic sclerosis
aka CREST syndrome
- Calcinosis
- Raynaulds
- oEsophageal dysmotility
- Scleroderma
- Telangiectasia
what are the features of diffuse cutaneous systemic sclerosis
CREST symptoms plus:
- internal organs (CVD, lung, kidney problems)
what does scleroderma mean ?
refers to the hardening of the skin => shiny tight skin without normal skin folds
what is sclerodactyly ?
describe the skin changes in the hands in systemic sclerosis
- skin tightening around the joints restrict ROM and reduces function
What is calcinosis ? associated with what condition ?
systemic sclerosis
- calcium deposits under the skin, most commonly fond on the fingertips
What are some lung complications associated with SS ? what tests should you do to monitor ?
- pulmonary fibrosis
- ILD
- Lung Function test (TLCO, FVC), Echo
What autoantibodies iare associated with systemic sclerosis ?
- antinuclear antibodies (ANA)
- anti-centromere
systemic sclerosis Mx ?
steroids + immunospressents
- non-medical: avoid smoking, gentle skin stretching, regular emoliatns, avoid cold triggers
What is raynauds phenomenon ? what are the two types?
episodes of vasospasm in the extremities (usually in fingers and toes) in response to cold or stress
- can be either primary or secondary
explain primary raynauds phenomenon ? typical patient and presentaiton ?
raynaud’s disease (occurs without any associated underlying disease)
- young women
- symptoms less severe, typically ffects both hands and feet
- final risk of complications
explain secondary Raynaud’s phenomenon ?
associated with other underlying medical condition (usually systemic sclerosis, lupus, RA, sjögren’s)
- older
- symptoms are more severe and prolonged and can present with digital ulcers
describe the colour changes in raynauds phenomenon ? why ?
- first white (due to vasoconstriction)
- then blue (due to cyanosis)
- then red (due to repercussion and hyperaemia)
how can you investigate if raynauds is primary or secondary cause ? what would suggest secondary cause ? (3)
nail fold capillaroscopy (to examine the peripheral capillaries)
- SS: abnormal capillaries, avascular areas, micro-haemorrhages)
(if ulcers present on fingertip then is secondary cause)
raynauld’s mx ? (2)
- keep the hands warm
- CCB (nifedipine)
What is systemic Lupus Erythematosus ?
SLE: it is an inflam autoimmune connective tissue disease (with autoantibodies)
- systemic (affects multiple organs + systems)
- erythematosis (red molar rash)
what is the leading cause of death in SLE ?
CVD (and infection)
- chronic inflam => shortened life expectancy
SLE epi ?
- women
- asian, African, Caribbean and hispanic ethnicity
- young to middle-aged adults
SLE pathophysiology ?
anti-nuclear antibodies => immune system target these proteins => inflam response
SLE presentation
relapsing-remitting + flares
- fatigue
- weight loss
- arthralgia (joint pain)
- non-erosive arthritis
- myalgia
- fever
- photosensitive molar rash
- sob
- pleuritic chest apin
- mouth ulcers
- hair loss
- raynauds phenomenon
SLE investigations ?
- ANA (85% patient +ve)
- anti-dsDNA (highly specific) (anti-double stranded DNA)
- FBC
- ESR/CRP
- urinalysis (sign of lupus nephritis)
what condition can occur secondary to SLE in 40% of patients ?
antiphospholipid syndrome
=> increased risk of VTE
SLE complications ?
- CVD (chronic inflam in blood vessels => hypertension => fatty deposits => CAD)
- Infection
- anaemia
- pericarditis
- ILD
- Lupus nephritis
SLE Mx ?
First line: hydroxychloroquine, NSAIDs, Steroids, suncream (and sun avoidance)
Second: DMARDs, Biologics
What is discoid lupus erythematosus ?
chronic scarring skin condition (different to lupus)
- sub-type of chronic cutaneous lupus erythematosus
Discoid lupus evythmatosus presentation ?
initial dry red patches that form plaques with scale
- can progress to atrophic scarring and alopecia
What is antiphospholipid syndrome ? with what other things is it associated ? (2)
it is a disorder associated with persistently elevated antiphosphlipid antibodies => blood become prone to clotting (hyper coagulable state) => throbus + miscarriages
- SLE (secondary to it), recurrent miscarriages
what are the key antiphospholipid syndrome complications ? (3) (go into each one a bit)
- VTE (DVT/PE)
- Arterial thrombosis (stroke, MI, renal thrombosis)
- Pregnancy-related complications (recurrent miscarriage, stillbirth, pre-eclampsia)
what skin condition is associated with antiphospholipid syndrome ?
lived reticularis
- purple lace-like rash that gives a mottle appearance to the skin
antiphospholipid syndrome Dx + Mx ? in pregnancy Mx ?
- clinical Dx + persistent antiphospholipid antibodies
- long-term warfarin (INR 2-3)
- LMWH and aspirin used in pregnancy (warfarin contraindicated in pregnancy)
What are spondyloarthropathies ?
range of rheumatic autoimmune inflammatory arthritis which can predominantly affect the spine (axial spondyloarthritis) or peripheral joints (peripheral spondyloarthritis)
What are zero negative spondyloarthopathies ? name them (4) ?
group of conditions associated with HLA-B27 antigen
- psoriatic arthritis
- enteropathic arthritis
- reactive arthritis
- ankylosing arhtirits
What similarities do serotonin-negative spondyloarthopathies share ?
similar clinical, radiographic and lab features (spinal inflam, HLA-B27 antigen)
- joint pain + inflam in absence of RF
which cells express the HLA-B27 antigen ?
all cells except RBC
zero negative spondyloarthopaties pathophysiology ?
molecular mimicry: get infection => immune response => infection agent has antigens similar to HLA-B27 => body presents antibody defence => autoimmune
What is ankylosing spondylitis (AS) ?
- zero negative spondyloarthropathy (related to HLA B27 gene)
chronic progressive inflammatory condition affecting the axial skeleton causing fusion of the joints
what are the key joints affected in AS ?
- sacroiliac joints
- joints of vertebral column
AS pathophysiology ?
inflam => erosive damage repair => lay down of fate => fusion of joints (bamboo spine)
AS presentation ?
young adult male in their 20s, slow onset >3 months
- pain and stiffness (in the lower back)
- sacroiliac pain (in the buttock region)
- can affect other systems: systemic sx, chest pain (costoverterbal joints, dacyltit, anaemia, aortitis, IBD, enthesitis)
when AS symptoms worse ?
- pain and stiffness worse with rest and improve with movement
- pain worse at night and in the morning (may wake from sleep)
mornings tiffness last >30 min - symptoms improve with activity and worsen with rest
what test can be used in AS to assess spinal mobility ? explain it
schobers test
- measure 10cm above and 5cm below L5 vertebrae
- ask patient to bend over
-> 20cm = normal. less than this indicates a restriction in lumbar movement and helps support AS dx
AS Ix ? (4)
- Inflam markers (CRP/ESR)
- HLA B27 genetic testing (present in 90% of patients)
- XR of the spine and sacrum
- MRI of the spine can show bone marrow oedema
AS XR changes ?
- bamboo spin (typical finding)
- squaring of vertebral bodies
- subchondral sclerosis and erosions
- fusion of the sacroiliac and costovertebral joints
AS Mx ? (4)
rheum MDT
-NSAIDs are first line
- anti-TNF meds (adalimumab): stops pain and boy formations
- intra-articular steroid injections for specific joints
- additional: physiotherapy, avoid smoking, bisphosphonates (osteoporosis)
What is sjögren’s syndrome ?
autoimmune condition that affects the exocrine glands => symptoms of dry mucus membranes (often lacrimal and salivary glands)
what are the two distributions of Sjögren’s syndrome ?
- primary: where condition occurs in isolation
- secondary: where is occurs due to other disease such as SLE and RA
what are the antibodies associated with sjögren’s ?
- anti-Ro
- anti-La
sjögren’s epi ?
usually starts in ppl aged 40-60 and more common in women
- F:M 9:1
- 60% of the disease secondary to RA, SLE
sjögren’s presentaiton ?
- dry eyes + mouth
- arthritis
- rash
- neurological features
- vasculitis
what test is useful in assessing sjögren’s presentation ? describe
schemer test
-insert folded filter paper under the lower eyelid with the end handing out
- wait 5 min for moisture to travel along
- should be >15mm (<10mm is significant)
sjögren’s Mx ?
clinical dx
- symptomatic: artificial tears, artificial saliva, vaginal lubricants
- hydroxychloroquine (may be considered in patients with associated joint pain)
What is vasculitis ? and what are the different categories ?
it is inflammation of the blood vessels
- categories: small, medium-sized or large vessels
how does vasculitis cause damage ? (generally)
- vessel wall destruction => perforation + haemorrhage into tissues
- endothelial damage => thrombosis + ischaemia/infarction of dependant tissues
name some small vessel vasculitis ? (4)
- Honoch-schonlein Purpura
- granulomatosis with polyangitis
- microscopic polyangitis
- eosinophilic granulomatosis with polyangitis
name some medium vessel vasculitis ? (2)
- Kawasaki disease
- polyarteritis nodosa
name some large vessel vasculitis ? (2)
- giant cell arteritis
- takayasu’s arteritis
general vasculitis presentation ? (6)
- joint and muscle pain
- peripheral neuropathy
- renal impairment
- purpura
- GI symptoms
- systemic symptoms
what are the ANCA associated vasculitis ? (3)
- GPA
- EGPA
- Microscopic polyangitis
what is granulomatosis with polyangitis (GPA) ?
small vessel (ANCA associated) vasculitis mainly affecting the resp tract and kidney (glomerulonephritis)
what 3 areas does GPA generally affect ?
1) URT/LRT
2) systemic vasculitis
3) Kidney involvement
GPA pathophys ?
granuloma formation => partial/total occlusion of blood vessels
GPA typical presentaiton ?
think GPA when:
- nose bleeds, crusty nasal secretions, kidney failure
- cough with wheeze + haemoptysis
GPA Ix ? what specific blood test ?
- CXR may show consolidation
- C-ANCA (+ve)
- CT chest (lung nodules if lung involvement)
GPA Mx ?
- high dose red + methotrexate
(wean off steroids)
what are polymyositis and dermatomyositis ?
they are autoimmune disorders where there in inflam in the muscles (myositis)
- polymyositis is condition of chronic inflam of muscles
- dermatomyositis is connective tissue disorder where there is chronic inflam of skin + muscle
polymyositis and dermatomyositis presentation ?
gradual onset, symmetrical, proximal muscle weakness (difficult standing form chair)
- +/- myalgia
- potential skin changes: heliotrope rash, cotton lesions, periorbital oedema, photosensitive erythematous rash
what is important blood test for polymyositis and dermatomyositis ? (2) describe
creatine kinase
- it is an enzyme found inside muscle cells that is released from muscles when there is inflam
antibodies: anti-Jo-1 antibodies
causes of raised creatine kinase ? (5)
- rhabdomyolysis
- AKI
- MI
- statins
- strenuous exercise
polymyositis and dermatomyositis Mx ?
corticosteroids
- if inadequate then methotrexate
important dermatomyositis hand sign ?
gottron papules
What is Ehlers-Danlos Syndrome ? (EDS)
group of genetic conditions involving defects in collagen => hyper mobility in the joints and abnormalities in the connective tissues (of skin, bones, blood vessels + organs)
what are the different types of EDS ? which most common ? which most severe ? explain each a bit
- hypermobile EDS (most common): hyper mobility + soft/stretchy skin
- Classical EDS: smooth/velvetty skin, joint pain/hypermobility, abnormal wound healing
- Vascular EDS (most severe): blood vessels prone to rupture (FHx of sudden death)
EDS presentation ?
joint pain, hyper mobility, joint dislocations
- association with POTS
what score is useful in EDS Dx ?
Leighton score (assesses hyper mobility)
EDS Mx ?
no cure
- physio
- hyper mobility => additional wear + tear => premature OA
What is Behcets disease ? main feature ?
complex inflam condition affecting blood vessels + tissues
- Main feature: recurrent oral and genital ulcers (can affect eyes, skin, GIT, lungs, blood vessels, MSK, CNS)
Behcets disease features ?
ulcers > 3 times per year
- painful, sharply circumscribed erosion with a red halo in oral mucosa
What is crystal arthropathy ? what causes it ? 2 types ?
crystal deposition in joints results in local inflammation and tissue damage
- gout
- pseudogout
What is gout ? associated with high levels of what in blood ? what crystals ?
gout is a crystal arthropathy associated with chronically high uric acid
- urate crystals
what are gouty tophi ? where are they located ?
gouty tophi are SC deposits of uric acid under the skin (rather than in joint)
What is uric acid produced from ? where is it excreted ?
- produced from nucleic acids (xanthine oxidase (inhibited in treatments))
- excreted by intestine + kidneys (underexcretion can be caused by alcohol)
Gout RF ? (6)
- Male
- Obesity
- High purine diet (meat + seafood)
- Alcohol
- Diuretics
- CKD
Gout presentation ? and natural disease course ?
- single acute, hot, swollen + painful joint (excruciating)
- typical joints: base of big toe, writs, base of thumb (carpometacarpal joint)
- will naturally resolve in around 3 weeks but is excruciating (so analgesia)
gout Ix ? and results ?
- aspirate fluid from joint (no bacterial growth, needle shaped crystals, negatively birefringent of polarised light, monosodium nitrate)
- x-ray: lytic lesions, punched out erosions
Gout Mx ? (3) which groups would you avoid what in ?
NSAIDs, or colchicine or steroids
- but high dose colchicine => diarrhoea (so start with lower dose in elderly)
- NSAIDs not good for kidney (which could be causing gout)
- steroids not good in elderly (osteoporotic)
Gout prevention ?
- allopurinol, febuxistat (xanthine oxidase inhibitor)
- lifestyle changes: lose weight, good hydration, reduce alcohol + red meat
- losartan (anti-HTN but also increases renal uric acid clearance)
What is pseudogout ? What crystals ? triggered by ?
it is a crystal arthropathy caused by calcium pyrophosphate crystals
- triggered by direct trauma, surgery, blood transfusion of spontaneous (most common)
pseudogout presentation ?
older adult with hot, swollen, stiff, painful knee (monoarthiritis) or asymtpomatic
psuedogout Ix ? and results
calcium pyrophosphate crystals
- rhomboid crystals that are positively birefringent in polarised light
- x-ray: chondrocalcinosis (diagnostic)
pseudogout Mx ?
symptoms usually resolve spontaneously over weeks
- NSAODs, colchicine, aspirate fluid
What is fibromyalgia ?
chronic condition characterised by widespread pain + pressure hypersensitivity
- unknown aetiology but thought stress and sleep play important role
fibromyalgia RF ?
- female 35-45
- poor sleep
- smoking
- obesity
- sedentary lifestyle
fibromyalgia signs and symptoms ?
- chronic widespread pain
- increase pain to pressure (allodynia)
- fatigue
- sleep disturbance
- anxiety
- parasthesia
- dysmennorhoea
(linke with IBS, chronic fatigue)
fibromyalgia investigations ?
diagnosis of exclusion so other test unremarkable, often come back normal, clinical dx
- widespread pain index (0-19 points) + symptom severity score (0-12)
- symptoms present for >3 months + no other differential
fibromyalgia treatment ?
no cure, symptom management
- non-pharma: exercise, reduce stress, avoid caffeine, sleep hygiene
- SNRI (duloxetine), amitriptyline
What is osteoporosis ?
skeletal disease characterised by reduced bone density, microarchetectual defects => increased bone fragility => increased bone fracture susceptibility
- osteopenia isa less severe reduction intone density
osteoporosis RF ?
- increase age
- female (PM)
- reduced mobility
- low BMI
- RA
- alcohol
- Smoking
- Long term steroids
- SSRI
- PPI
explain osteoporosis and Post menopausal women ? pathophys
oestrogen is protective against osteoporosis
- osteoblasts severed OPG which inhibit RANKL (RANKL => osteoclast action)
- PM women with ostergoen deficiency have over expression of RANKL with overrides OPG)
What is FRAX tool for ? takes what into account ?
predication of the risk of a fragility fracture over the next 10 yrs
- Age, BMI, comorbidities, smoking + alcohol, FHx
what is a DEXA scan ? what are the different relevant ranges ?
checks bone mineral density
- more than -1 => normal
- -1 to -2.5 => osteopenia
- less than -2.5 => osteoporosis
osteoporosis mangement ?
- activity + exercise, maintain healthy weight, ensure enough calcium + vit D, avoid falling, stop smoking, reduce alcohol
- calcium + vit D suppléments
- bisphsphonates (interfere with osteoclasts)
how should a patient take a bisphosphonate ?
need to take on empty stomach and sitting up (prevent reflux)
What is pages disease of bone ? pathophys ? increased risk of what ?
it is a disease of bone turnover, excessive bone turnover (formation + reabsorption)
- due to excessive osteoblast + class activity
- not coordinated => patchy areas of high density (sclerosis) + low density (lysis) => enlarge + misshapen bones with structural problems => increase risk of fracture
pagets disease of bone presentations
- bone pain
- bone deformity
- fractures
- hearing loss
pagets disease of bone Ix ?
- XR (enlarged + deformed, osteoporosis, cotton wool appearance of skull, va shaped defects)
- raised Alkaline phsphatase, normal Ca + phosphate
pagets disease of bone Mx ?
- bisphsphonates, NSAIDs, calcium + vit D supplementation
What is osteomyelitis ? most common aetiology ?
It is inflam in a bone + bone marrow, usually caused by bacterial infection
- mainly staphylococcus aureus
osteomyelitis presentation ?
- fever, pain + tenderness, erythema, swelling (usually single bone)
osteomyelitis Ix and Mx ?
- XR (often doesn’t show changes in early disease)
- MRI (best imaging)
- blood tests (raised WBC, ESR, CRP), blood cultures (before Abx)
Mx: surgical debridement of infected bone + tissue, Abx (6 weeks flucloxacillin)
What is septic arthritis ?
its occurs where there is infection within a joint (emergency - 10% mortality)
- common complication of joint replacement
septic arthritis presentation ?
mono arthritis (90%), often knee, rapid onset of red, hot, swollen, painful joint + stiffness and reduced ROM
- systemic symptoms (fever, lethargy, signs of sepsis)
septic arthritis aetiology ?
- s-aureus
- neisseria gonorrhoea (sexual transmission
- strep pyogneis
septic arthritis mx ?
(always suspect septic arhtirits in red hot swollen joint)
- aspirate the (prior to abx), send sample for gram string + crystal microscopy + culture + abx sensitivity
- antibiotics (2 weeks IV, 4 weeks oral), analgesia, aspirate joint to dryness
What is osteomalacia ?
it is where defective bone mineralisation causes soft bones, as a result of low vit D (aka rickets in children)
explain vit D synthesis - what is the precursor ? where is it activated ?
Vit D is created from cholesterol by the skin in response to UV radiation, also obtained from food as fat soluble vitamin
- activated in the kidney
what medical conditions would be a risk factor for low vit D ? other RF ?
- IBD (due to malabsorption)
- CKD (kidneys convert vit D to active form)
- Darker skin (require more UV to synthesis vit D)
- spending time indoors
what metabolism is vit D important in ? how does low vit D affect this
- calcium and phosphate absorption in intestines
- calcium and phosphate reabsorption in kidneys
- low vit D => low serum Ca + Phos => reduce bone mineralisation (osteomalacia)
osteomalacia presentation ?
- fatigue
- bone pain
- muscle weakness and aches
- pathological fracture
osteomalacia Ix ?
- serum 25-hydroxy vitmin-D
- XR osteopenia
- DEXA: reused bone mineral density
- low serum Ca + Phos, high PTH (secondary hyperparathyroidism)
osteomalacia Mx ?
cholecalciferol (vit D3)
