MSK Flashcards
Osteoarthritis definition
Non inflammatory wear and tear of joints from loss of articular cartilage (this is a hyaline cartilage).
Osteoarthritis epidemiology
Most common type of arthritis
Age
Female
Synovial joints
Osteoarthritis risk factors
- Age -cumulative and traumatic insult
- Female - especially after menopause
- Occupation - manual labour and hands, football and knees, faming and hips
- Genetics - polyarticular disease, OA hip less common in afro Caribanan and Asian
- Obestity - links between BMI and hip and knee OA. Obestity is a low grade inflamatory state to incrase of IL-1 and TNF
- Joint trauma
- Gout
Inflamatory artheritis
Osteoarthritis pathophysiology
Age relates dynamic reaction pattern of a joint in response to injury
Articular cartilage (produced by chondrocytes) is the one which is most affected
It causes changes to underlying bones at the joint margins
* There is ore wear to the cartilage then tehere is new cartalage being made. * Threre is faulty cartilage which unergoes erosio and causes disorderd repair, fubrillations and cartilage ulceration which all increases the stress on the bnne * This leads to microfractures and cysts on the bone which cuases abnormal sclerotic subchondral bone and overgrowth at joint margins (osteophytes) * * It is a metabolically acitve and dynamic process Medicated by the cytoline - IN-1, TNF-aloha, NO
Osteoarthritis key presintations
- Elderly with joint pain
- Improves with rest and worse with activity
- Heberden’s and bouchardes nodes in fingers
- Hip - groin pain
- XR – Osteophytes, joint space narrowing, subchondral cysts and subarticular sclerosis.
Osteoarthritis signs
- Morning stiffness
- Worse at the end of the day
- Pain increases with use
- Asymmetrical joint involvement
- Joints are most commonly affected - knee, vertebrae, hip
- Joint swelling - osteophytes grow outwards- bony enlargement, effusion, synovitis, bony swelling
Tenderness and deformities
Osteoarthritis symptoms
- Joint pain on movement
- Hip and groin pain
- Pain at the end of the day
- Crepitus - crunching sensation when moving the joint
Functional impairment - walking and activities of daily living
Osteoarthritis test
X ray - LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
Bloods - normal - CRP may be slightly raised, reumatoid factor and antinuculaur antobbodies negative
MRI
aspiration of synovial fluid?
Osteoarthritis diffrential
Differential diagnosis
Rehumatoid arthritis
Gout
Psoriatic arthritis
Osteoarthritis treatmetn
Treatment
- Lifesytle - education, activity and exercise, weight loss, physiotherapy, occupational therapy, walking stick for hips, hot/cold pads
Medication -
* Topical - NSAIDs and Capsaicin
* Oral - paracetamol and sometimes NSAIDs
* Opioids - dihydrocodeinone
* Transdermal patches - buprenorphine, lignocaine
* Intra - articular steroid injections - hyaluronic acid
Surgery -
* Osteophyte removal/fusion
* Joint replacement if very severe
* Arthroscopy, Only for loose bodies, Indications ,Uncontrolled pain (particularly at night)
Significant limitation
* Arthroplasty - put in fake cartilage
* Osteotomy - cutting bone to reshape it
Rheumatoid arthritis definition
Definition
Chronic systemic inflamatory disease dur to immune complexes in the synovai joints which causes symmetrical deforming polyarthritis
Rheumatoid arthritis epidemiology
Epidemiology
Common 0.5-1% of the population
Linked to autoimmune conditions
More common in females
Rheumatoid arthritis causes
Aetiology
- Autoantibodeis presant - reumatoid factors - anti cycclic citrullinated peptide, immune complexs
- Immunoglobulins and cytokines presnet in synovial fluid
- Defective cell mediated immunity
- Association with other organ specific autoimmune conditions
Rheumatoid arthritis risk factors
Risk Factors
Increasing age
Female
Family history
Smoking
Stress
Infection
Rheumatoid arthritis pathophysilogy
Pathophysiology
- Inflammation of the lining of the synovial joints
- Synovium thickens and is infiltrated by inflammatory cells
- Generation of new blood vessels is induced which causes leucocytes into the synovium which leads to inflammation
- A tumour like pannus grows over the proliferatin leading to damae to the underlying cartilage and blockadge of th normal route of nutrition
- Cartilage becomes thin and the underlying bone becomes exposed
- This leads to a destruction of articular cartilage and subchondral bone
Rheumatoid arthritis key presintations
Key presentations
- Joint pain often worse in the morning and in the cold
- Loss of function
- Fatigue and malaise
- Extra articular involvement - pericardial effusion, pleural effusion, anaemia, uvitis
Rheumatoid arthritis signs
Signs
- Morning stiffness lasting more than 30 mins
- Pain improves with use
- Warm, red, tender joints
- Joints offten affected symetrically - Metacarpophalangeal joints, Proximal interphalangeal joint, Metatarsophalangeal joint, wrists, elbows, shoulders, knees, ankles
- Hand deformities
- Rheumatoid nodules at pressure pints - elbow
- Popliteal cysts - bulging of the synovia sack
- Carpal tunnel syndreome
Extra articular manifestations:
* Nodules on presure points
* Bursistis - inflamation of the bursa sack in the joints
* Tenosyvonitis - inflamation of tendons
* Muscle wasting
* Lymph nodes palpable
* Dleen enlarged
* Felty’s syndrome – rare
□ Triad of
® Seropositive RA
® Splenomegaly
® Neutropenia
* Anaemia - normocytic anaemia of chrons disease
* Anaemia - iron deficiency due to hepcidin inhibition from NSAIDs and prednisolone
- Nerves:
- Dry eyes
- Episleriris
- Corneal ulceration
- Sensory neuropathy
- Entrapment neuropathy - soft tissue sweeling due to inflammation at wite where rigid structues contact neres causing spinal cord compression - severe neck and occipital pain
- Myelopathy
- Atlanto-axial subluxation
Lungs
* Pleural effusion
* Diffuse fibrosinf alviolitis
* Rhuamatoid nodules
* Small airway diseas
Heart -
* Pericardial rub
* Pericarditis
* Pericardial effusion
Kidneys
* Amyloidosis
* Advanced RA
* Amyloid protein deposits
* Proteinuria
* Analgesic neuropathy
Skin:
* Vasculitis -small infarcts in the nail beds
Rheumatoid arthritis diagostic criteria
Symptoms
DIAGNOSITIC CRITERIA:
4/7
* Morning stiffness * Artherisits in 3 or more joints * Arthritis of the hands * Symmetrical * Rheumatoid nodes * Rheumatoid factor positive * Radiographic changes
Rheumatoid arthritis test
1st line test
x-ray - LESS
loss of join space
Erosions
Soft tissue swelling
Soft bones - osteopenia
* Bloods - rheumatoid factor positive in 70% of patients * Anti CCP (anticyclic citrullinated protein antibody) positive in 98% of patients highly specific!! * FBC - raised platelets, CRP, ESR, anaemia * MRI and ultrasound
Rheumatoid arthritis tretament
Treatment
- Disease-Modifying Anti-Rheumatic Drugs (DMARDs) – suppresses inflammation, Methotrexate, Must give folate supplements as methotrexate inhibits folic acid synthesis
- NSAIDs -
- Hydroxychloroquine
- Sulfasalazine
- Biologics Rituximab, Etanercept – TNF-alpha blocker, Baricitinib
- Acute exacerbations – steroids (IM methylprednisolone)
- MDT management – rheumatologist, OT, physio, GP
rehumatoid artehritis typeical presitation
Other notes
TYPICAL PRESINTAION
40 y/o female with hand stiffness and pain
Symmetrical polyarthritis – PIP, MCPs, MTPs.
Hand deformities ulnar deviation, swan neck and boutonnieres deformity of fingers, Z deformity of thumb.
Morning stiffness >30 mins.
Complications with neck – cervical instability.
Think systemic disease with other systems frequently affected.
Ix – RF and anti-CCP, XR - LESS
Tx DMARD
rheumatoid artheritis deiiferntial
Differential diagnosis
SLE
Psoriatic arthritis
Symmetrical seronegative spondyloarthropathies
gout definiton
Definition
- Sodium urate - needle shaped and negatively birefringent under polarised light
- Neutrophils ingest the crystals and cause a proinflammatory response
gout epidemiology
Epidemiology
- Common in men over 40 - commonest tye for this catogy
- Post menopausal women
- More men than women
- Associated with hypercalcaemia
gout causes
Aetiology
- Under excretino of uric acid:
- Hyperuracaemia
- Alcohol
- Obesity
- Diabeties
- CKD
- Hypertension
- Metabolic hypothyroidism, hyperparathyroidism
Drugs:
* Low dose aspirin
* Diuretics - especially thiazide
* Cyclosporin’s
* Ethambutol/pyrazinamide
* Lead poisoning
High purine diet:
* Alcohol
* Excess meat and shellfish
* Fructose sweetened drink s
* Gravy, meat extract
* Yest extract
* Hyperlipidaemia
Other:
* Metabolic syndrome
* Hyperlipidaemia
* Proliferative
* Myeloproliferative disease
* Cytotoxic drugs
* Psoriasis
* Lesch-Nyhan Syndrome
Renal:
* Increased purine turnover
* Myeloproliferative disorder
* Lymphoproliferative disorder - leukaemia
* Carcinoma
* Psoriasis
* Cell damage - surgery
* Cell death - cancer
Most common causes:
* Aggressive introduction/ cessation to hypo uremic therapy
* Alcohol or shellfish binges
* Sepsis, MI, severe illness
* Trauma, surgery, dehydration
gout risk factors
Risk Factors
High alcohol intake
Purine rich foods
High fructose intake
Family history
High uric acid level - age, obesity, diabetes mellitus, IHD and HTN
gout pathophysilogy
Pathophysiology
- Purines from diet —> hypoxanthine —> Xanthine —> uric acid
- Monosodium urate from in joint which have das previous trauma and often cooler (more peripheral) ones
- The crystals set of the immune response causing inflammation
gout key presintations
Key presentations
- Obese man with toe pain
- Crystal induced arthropathy
- 1st metatarsal, raised serum urate levels after 4 weeks
- Joint aspiration - negatively birefringent in polarising
gout signs
Signs
- Hyperurcaemia
- Red warm joint
- Shin skin over joint
- White deposits around the joint
- Skin has peeled off
gout symptoms
Symptoms
- Asymptomatic
- Agonising pain, swelling, tenderness and redness- toe on fire
- Distal interphalangeal goints most affected in the fingers
- Base of thumb and big toe are very common
- As are wrists
gout test
1st line test
- Xray - punched out lesions, lytic lesions,
- Joint aspiration - to rule out septic arthritis this si very important!
- Polarised light microscopy shows negative bifringent monosodium crystals
- Bloods - raised serum urate
gout differential
Differential diagnosis
Septic arthritis
Tophaceous gout
Pseudogout
gout treatment
Treatment
- Lifestyle - calorie restriction, modify diet, weight loss, reduce alcohol
- Diary - cherries and vit C are good
- Allopurinol - xanthine oxidase inhibitor
- NSAIDs
- Colchicine - reduces pain and is protective, used in those where NSAIDs aren’t appropriate such as renal or heart problems
- Prednisolone
- Xanthase oxidase inhibitors - allopurinol/febuxostat is contraindicated - do not start
Colchaine daily for 6 months to avoid flareups
pesudogout definition
Calcium pyrophosphate crystals - small brick shapes, positively birefringent under polarised light
pesudogout epidemiology
Elderly - particularly women
pesudogout causes
- Trauma to joint
- Surgery
- Blood transfusion - IV fluid
- T4 replacement
Joint labage
hyperparthyroidism
pesudogout ros factors
- Old age
- Osteoarthritis
- Hyperparathyroidism
- Haemochromatosis
- Hypophosphatemia
Diabetes
pesudogout pathophys
- Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue producing chondrocalcinosis
Typical presentation of knee, wrist, shoulder, ankle, elbow
pesudogout key presinations
Asymptomatic
Sever joint pai
Acute synovitis
Hot and swollen joint
Fever
Stiffness
pesudogout tests
- Xray - chondrocalcinosis
- Joint aspiration - sepsis
- Polarised light microscopy - positive infringement
FBC - raised WBC
pesudogout differnces from OA
Differences from OA:
* Knees, wrists shoulder, elbows , ankle
* marked inflammatory component
* Superiposition of acute attacks
pesudogout treatment
Acute:
* NSAID
* Colchaine
* Nalgesia
* Aspiration
* Steroid injection
* Physiootherapy
* Res and ice packs
Chronic
* Trial of antirheumatic treatment
* Synovectomy in troublesome disease
* Surgery to wash out the crystals
pesudogout typical presintations
Typical Presentation
* Female/male with knee pain
* Crystal induced arthropathy – calcium pyrophosphate.
* Often asymptomatic, mono or oligoarticular.
* Knee (but any joint can be affected).
XR chondrocalcinosis. Weakly positive birefringent in polarizing light.
Osteoporosis definition
Definition
A systemic skeletal disease there is low bone mass, microarchitectural deteriation of the none and a consequent increase in bone fragility and susceptibility to fracture.
Osteopenia - precurosr to osteoporessi bone density 1-2.5 standard deviations below mean valure
Osteomalacia - poor bone mineralisation leading to soft bones due to lack of calcium
Osteoporosis epidemiology
Epidemiology
Risk increases with age
Post-menopausal women
Osteoporosis cuses
Aetiology
- Lack of oestrogen
- Secondary- SHATTERED
- Steroid use
- Hyperthyroidism/hypoparathyroidism
- Alcohol/smoking
- Thin
- Testosterone low
- Early menopause
- Renal/liver failure
- Erosive/inflammatory bone disease
- Dietary low calcium
Osteoporosis risk factors
Risk Factors
Think patient, diseases, medication!
* Patient - Old, female, low BMI, diet (lactose intolerant), athletes, alcohol and smoking * Disease - join disease (ra, sle), hypoparathyroidism and hyperthyroidism, Cushing's, low oestrogen, renal disease (vit D), previous fractures, anorexia * Medication - corticosteroids, GnHr analogues, androgen deprivation (prostate cancer)
Osteoporosis path
Pathophysiology
Primary - menopause and age
Secondary - disease or drugs
* Increased reabsorbtion by oseteoclasts and decreased formation by osteoblasts * Inadequate peak bone mass * Changes in trabaule architecture in agin, decreases in thickness and no of connections * Reduction of oestrogen - causes a net bone loss due to oestrogen restraining bone turnover. Oestrogen replacement is available, characterised by high bne turnover, cancellous bone loss, micoarchitectural disruption * Horizontal trabecuea are needed for eular buckling therory, esentially make the bone a lot stronger *
Osteoporosis key presintations
Key presentations
Asymptomatic untill fracture -
* Hip - neck of femur
* Wrist - distal radius after falling on outstretched arm
* Vertebra - sudden onset on pain in spine radiating to the front
* Fragility fractures
Osteoporosis test
1st line test
- DEXA
- X ray
- FRAX - fracture risk assesment score - age, sex, bmi previous fracture, steroids
- FBC - normal calcium phosphate and alkaline phosphate
Osteoporosis treatent
Treatment
- Lifestyle - quit smoking, drink less, vit D,
- 1st line - oral bisphosphonates (alendronate)
- 2nd line – different oral bisphosphonate e.g. risedronate (daily), ibandronate (weekly)
- 3rd line - Strontium ranelate – reduces fracture rate and Recombinant human parathyroid peptide (anabolic) e.g. teriparatide
Increases osteoblast activity and bone formation
Primary prevention:
* Adcal D3 – Vitamin D + calcium
* Calcium-rich diet e.g. dairy or sardines, white beans
* HRT – menopausal women
* Corticosteroids – consider prophylactic bisphosphonates
* Regular weight bearing exercise
* Smoking and alcohol cessation
* DEXA scans
*
septic artheritis cuaes
Aetiology
- s.aureus is most common
- N gonorrhoea
- Staph epidermis
- E coli/klebsiella
- Mycobacterium tuberculosis
septic artheritis risk factors
Risk Factors
- Elderly
- Pre-existing joint problem
- Prosthetic joints
- Immunosuppression
- Penetrating trauma
septic artheritis path
Pathophysiology
Gonococcal arthritis
* caused by gram negative neisseria gonorrhoea
* in several joints, they have a fever, pustules on distant limbs , polyarthralgia ad tenosynovtis
* Culture and bloods to diagnose
* Oral penecillin, ciprofloxicin or docycycline
Meningococcal:
* Presents as migrating polyarthirits
* Deposition of circulation immune complexes
* Penicillin
TB
* Hip, knee and intervertebral disks affected
* Fever, nigth sweats and wight loss
* 9 month therapy antibiotics
septic artheritis key presintation
Key presentations
- Knee, hip and shoulder most commonly affected
- If ti is painful, red, hot, and swollen I tcould be spetic
- Impaired range of motion
- Fever
septic artheritis test
1st line test
- Join aspiration - to look at turgid fluid
- FBC - high WBC, neutrophillia
- X rya to look for inflamatio
- Blood clutres incases its seeded bactereamia
- Polerised light microscopy - exclude gout/pseudogout
septic artheritis treatment
Treatment
- Urgent aspiration
- Antibiotics -
S. Aureus sensitive to
Flucloxacillin
Erythromycin
Doxy/tetracycline - Stop immunosurpressive drigs and anti-TNF injections for when thery on antibiotics and 2 weeks after
- Prednisolone doubled to mimic cortisol increase
- Analgesia
- Splinting if necessary
Osteomyelitis causes
taphylococcus aureus,
coagulase-negative staphylococci,
aerobic gram-negative bacilli (30%)
Streptococci (skin, oral)
Enterococci (bladder, bowel)
Anaerobes (bowel)
fungi,
Mycobacterium tuberculosis
Salmonella in sickle cell anaemia patients
Pseudomonas aeruginosa and Serratia marcescens in PWD / IVDU
S.aures is the most common overall
Staphylococcus epidermis - most common after surgery
Osteomyelitis risk factors
central line, sickle cell disease, UTI and catheterisation, IV drug users, diabetes (neuropathy)
Osteomyelitis pathophys
- Direct infection to eth bone by trauma or surgery
- Contiguous spread - form adjacent soft tissues and joints
- Hematogenous seeding - a pathogen from one part of the body is spread through the blood -this is the long bones for children and the spine for adults
- Children are more likely to have infections I eth long bones
- Adults - vertebra, (clavicle and pelvis for IV drug)
In the histology there is inframammary cells, oedema, vascular congestion and small vessel thrombosis
Osteomyelitis sugns
ystemic: fever, rigors, sweats, malaise
Local -
* Acute - tenderness, warmth, swellung, erythema
Chromic - inflamation, large deep ulcer,s on healing fractures
Osteomyelitis symptoms
- Several day onset
- Dull pain
- Fever
- Weakness
Can be aggravated by movement
Osteomyelitis tests
- Bone biopsy - sterile technique, 2 specimens s needed
- Blood culture - organism in the blood often causes organism in bone
- FBC - ESR and CRP
- X rya to see if infection if visable
- MRI
Biopsy!
Osteomyelitis treatment
- Surgcial debridement - cut it out, remove dead bone
- Hardware (artificial joint) removal
- Start SMART - guess by what their entry and risk factor was
- Then FOCUS into a specific antibiotic once the sample is back - broad spectrum at first, IV teicoplanin, IV flucloxacillin, oral fusaric acid
- Switch to oral sometimes, stopping treatment is guided by CRP
- 6 weeks of IV minimum
- Immobilisation as well to rest it
fibromyalgia definition
Non specific muscular disorder with unknown causes. No signs of inflammation. Widespread MSK pain after other diseases had been excluded. Symptoms are present for 3 months and there is au at 11/18 joints.
fibromyalgia epiemiology
Epidemiology
Females
Middle age
fibromyalgia risk factors
Risk Factors
Female is 10x more common
Middle aged
Divorce IBS, chronic headache, depression, fatigue
fibromyalgia path
Pathophysiology
Problems with pain signal:
low seratonin - inhibits pain signals
Raised p substance and nreve grotwh factor - incresd pain signals
Depression and anxiety and other psychological factrs can amplify this sensitivity
fibromyalgia key presinttions
Key presentations
- Pain worse with stress, cold weather
- Morning stiffness
- Non restorative sleep
- Headache/diffuse abdominal pain
- Exagerated pain to mildly painful stimulus
Neurocongrative features:
* Poor sleep
* Fatigue
* Mood disorders
* Poor concentration
* Memory problems
* Low mood
Patints are diagnosed by:
* Chornic pain oresant for 3 months
* Widespread pain
* Palpation of tender points
* No other reason for symptoms has been found
fibromyalgia test
1st line test
- Pain in 11/18 sites
- TFTs - rule out hypothyroidism
- ANAs and dsDNA - exclude SLE
- ESR and CRP to exclude pMR
- Vit d, calcium and electrolytes
- Examine patient and CRP - to rule out inflammatory arthritis’s
fibromyalgia differntial
Differential diagnosis
Hypothyroidism
SLE
B12 deficiency
Polymyalgia rheumatic
Inflammatory arthritis’s
fibromyalgia treatment
Treatment
- Non pharmaceutical - education, CBT, exercise
- Nalgesia
- Acupuncture
- SSRIs to raise serotonin levels
- Anti-convulsant - pregabalin and gabapentin to slow never e impulses and help with sleep
Sjogren’s syndrome defintion
Definition
Autoimmune destruction fo exocrine glands especially lacrimal (tear ) and salivary
Sjogren’s syndrome epidemiology
Epidemiology
- Stong assocatioo with gluten sensitivity
- Other autoimmune conditions
- More common in women
- HLA-D8/DR3
- Onset in 40-50s
Sjogren’s syndrome causes
Aetiology
Primary sicca syndrome
Secondary -
* SLA
* RA
* Scleroderma
* Primary biliary cirrhosis
* Other autoimmune diseases
Sjogren’s syndrome path
Pathophysiology
Lymphatic infiltration (anti-SS-A and anti-SS-B) - fibrosis of exocrine glands especially lacrimal and salivary
Sjogren’s syndrome signs nd symptoms
Signs
- Salivery nd parotic gland swelling
- Vasculitis leading to a skin rash
- Loss of teeth due to slivery disruptions
Symptoms
- Lacrimal gland involvement - kerat
- conjunctivitis (inflammation and ulceration of the cornea and conjunctiva) blurring of vission, itching, redness, burning
- Salivary gland involvement - difficulty tasting and swallowing, cracks and fissures
- Nose and respiratory passages- ulceration and perforation of nasal septum
- Larynx - difficulty speaking
- Dryness of skin and vagina
- Fatigue
- Joint pain
Sjogren’s syndrome test
1st line test
- Schirmer’s test - measures tear production - a filter paper is put in the lower conjunctival sack, is it positive if less than
- 5mm of the paper is we after 5 mins
- Anti -60kD (antiSS-A) - antibodies fou din 90% of Sjogren’s syndrome
- Anti-la (SS-B) are found in lots of autoimmune diseases
- Anti Ro Ss-a Anti60kd Found in 90% of patients with Sjogren’s
Anti la Ss-b ——– Common in autoimmune disease - Positive RF
- Raised immunoglobulins
- Lip biopsy to look for identities
- Schirmer’s tear Test – measures conjunctival dryness
- Rose Bengal staining – staining of eyes shows punctate or filamentary keratitis
- Ultrasound – abnormal salivary glands
*
Sjogren’s syndrome treatment
Treatment
- Artificial tears - eye drops to help lubricate
- Ophthalmic ciclosporin drops - increases tear production
- Cholinergic drugs to stimulate exocrine glands - pilocarpine (avoid in patients with respiratory disease and those taking hypertensive medications)
- Salivary substitutes
- Paracetamol and Nsaids to joint pain
- Corticosteroids to treat vasculitis
- Intravenous immunoglobulin
Sjogren’s syndrome complications
Complications
- Risk of B-cell lymphoma with Sjogren’s syndrome as the lymph nodes are often hyperplastic- emergence of dominant b-cell clone responsible for marginal zone lymphoma
- Congenital heart block in the foetus
vasculitis definition
Definition
Inflammatory disorder of the blood vessels wall which can affect any organ by causing destruction or stenosis of the vessel
vasculitis causes
Epidemiology and causes
- Infective - subacute infective endocarditis
- Non-infective - vasculitis with RA, SLE, scleroderma, polymyositis/dermamyosotis, good pastures
vasculitis path
Pathophysiology
- Large vessle - aorta and majto tribuaties (gaint cell arteritis/polymyalgia rheumatic
- Medium vessle - polyarteritis nodosa
- Small vessles -
ANCA-associated – granulomatosis with polyangiitis
ANCA-negative – Wegener’s - Inflamation and necorsis of blood vessle walls wit gimpared blood flow
- This leadst o vessel wall destruction causing haemorrhage into tissues and endothelial injury causing infarction of dependant tissues
- Histology - neutrophils, mononuclear cells or giant cells with fibrinoid necrosis and leukocytoclastic
vasculitis ley presintations
Key presentations
- Systemically unwell, fever, arthralgia, weight loss, headache, foort drop, stroke, bowel events
vasculitis differntials
Differential diagnosis
Sepsis
Malignancy
Cholesterol emboli
Giant cell arteritis definition
nflammatory granulomas arteritis of the large cerebral vessels and other large vessels such as the aorta.
Giant cell arteritis epidemiology
- Women
- Over 50
Associated with polymyalgia rheumatica
Giant cell arteritis key presintation s
- Severe headache
- Scalp tenderness
- Temporal arteries are tender, palpable, reduced pulsation
- Jaw claudication when eating
- Visula changes
- Risk fo CVA
- Malaise, legarthy, fever
To diagnose there must to be 3 or more of;
* Ver fo
* New headache
* Tempoal artery tenderness or decreased pulsation
* Raised ESR
Abnormal artery biopsies showing necrosing and mononuclear infiltrate
Giant cell arteritis test
- Raised ESR, ANCA negative
Temporal artery biopsy is ogold standard
Giant cell arteritis differntial
- Migrane
- Trigeminal neuralgia
Polyartheritis nodosa
Giant cell arteritis treatment
rednisolone
* Prophylaxis of osteoporosis - DEXA scan, calcium/vit D, bisphosphonate, iV methylprednisolone for visual changes,
steroid sparing agents e.g. azathioprine/methotrexate/biologics
Takayusu arteritis ? what is thiso??? tell me??
Very similar to giant clle, but it affects asian women under 40, and it affects the arteries that branch off of the aortic arches
Asian women aged 40
- It can cuases weka and no pulse, and visula nd neurological symptoms
steroids
Wegner’s granulomatosis (Granulomatosis with Polyangiitis) definition
Necrotisin gransulmatois vasculitis of arteroiles, capillers ad venuels.
Wegner’s granulomatosis (Granulomatosis with Polyangiitis) epidemiology
- 25-60
- Associated with antineutrophil cytoplasmic bodies (c-ANCA)
Wegner’s granulomatosis (Granulomatosis with Polyangiitis) key presintations
- Affectes vasculature of all organ systems
- Most commonly lungm nasal passage kidnyes
- Upper respiratry tract - sinusitis nasal crusting and bleeding
- Lungs - nodules and hemorages
- kidnye - glomerulonephritis
- Skin - pupura/ ulcers
- Nervous system - monoeuritis multiplex
- Eye - proptosis scleritis, sepiscleritis, uvitis
- Chemosis
- Sadle nose deformity
- Collapsed trachesa
*
Wegner’s granulomatosis (Granulomatosis with Polyangiitis) test
- Raised ESR
- c-ANCA posiitve
- Biposy pf kidnye, lungs resp tract and you will see granulomas
CXR - nodules
Wegner’s granulomatosis (Granulomatosis with Polyangiitis) treatment
High cortiticosteroids
Cycolophosphamide
Biologics
Rule of 5 Cs-
Cs in the body (nose, kidnye, resp tract,
c-ANCA
Cross secion biopsy
Corticosteroids
Polyarteritis nodosa - medium epidemiology
- Middle aged men
- Hep B
RA, SLE< scleroderma
Polyarteritis nodosa - medium path
Necrosing vasculitis that causes anyerisms and thrombosis in medium size vessles leading to infarction.
Polyarteritis nodosa - medium key presintations
- Fever, malaise, weight loss, myalgia
- Neurologucal - numbness tinigiling, lack of sensatoin, inability ot move part of the body
- Abdominal - pain due t arterial involvement of abdominal viscera
- Renal - presentation with haematureia and protnuria
- Cardiaic - coronary arteries - MI anf HF
Sin - subcutanoues hemmoage and gangrene
Polyarteritis nodosa - medium tests
- Bloods- anaemia, WBC raised, raied ESR, ANCA negative
- Biopsy of kidney
Angiography will show miroanyerisms and strig of beads resintation
Polyarteritis nodosa - medium differentials
- Fever form infection
- Chrons
SLE/RA
Polyarteritis nodosa - medium tx
- BP controll - ramapril
- Corticosteroids and azathioprine or cyclophosphamide
Hep B treated with antiviral after steroid treatment
Paget’s disease of bone (osteoitis definition
Definition
Chronic bone disorder characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone.
Paget’s disease of bone (osteoitis epideimiology
Epidemiology
- Older population
- Commoniner in temperate climates
- UK has highest preveleance in world !
Paget’s disease of bone (osteoitis causes
Aetiology
- Trigger by infection - measales
- Linked to genetic mutations - SQSTM1
Paget’s disease of bone (osteoitis risk factors
Risk Factors
Family history
Over 50
Infections
Paget’s disease of bone (osteoitis path
Pathophysiology
3 phases of the disease
* Lytic - osteoclasts have up to 200 nuclei and aggressively demineralise the bone
* Mixed - rapid disorganised proliferation for new bone tissue b a large number of osteoblasts, collagen deposited haphazardly
* sclerotic - new bone formatio exceeds bone eabsorbtio, the bone is disorganised and weak. The osteoblasts activity slows down leading ot a burned out state
Paget’s disease of bone (osteoitis ey presintaions
Key presentations
- Can affcect singla bone or whole skeleton
- Skull, lumbar vertabrea, pelvis, femur
- Pain
- Skull growth - leontiasis - lion like face, hearing loss, vision loss
- Kyphosis (curved spine)
- Pelvic asymetry
- Bone enlargement
- Bowlegs
Paget’s disease of bone (osteoitis test
1st line test
- Alp elevated, calcium and phosphate normal
- x-ray - bone enlargement and deformity, osteoporosis cicumscripta, lystic lesions duig lytic phase., cotton wool appearnae of the skull,
- Bone biopsy too exclude malignancy
Paget’s disease of bone (osteoitis tx
Treatment
- Pain relief
- Anti resorptive medication- bisphosphonates - alderonic acid
- Vit D and calcium supplementation
- Surgery- correct deformities, decompress nevers, decease fracture risk
- Effective treatment should normalise ALP
Paget’s disease of bone (osteoitis complications
Complications
- Pageants sarcoma - osteosarcoma - bony overgrowth leading ot genetic mutations and sarcoma
- Arthritis
- Spinal cord compression
- Vision loss
- Fractures
- Hearing loss
Spondyloarthropathies definition
Definition
A group of autoimmune diseases which share certain features of:
* axial inflammation of spine and sacroiliac joints
* Asymmetrical peripheral arthritis’s
* Prescence of RF - so seronegative
* Strong association with HLA-b27
Spondyloarthropathies causes
Aetiology
- HLA-B27 - human leukocyte antigen B27
- A class 1 surface antigen which is on all cells except RBSs
- There is infection which leads to immune response which causes confusion leading to auto-immune response against HLA-B27
Spondyloarthropathiesnpath
Pathophysiology
- HLA-B27
- A class 1 surface antigen which is on all cells except RBSs
- There is infection which leads to immune response which causes confusion leading to auto-immune response against HLA-B27
Spondyloarthropathies key presintations
Key presentations
SPINE ACHE
* Sausage digit - inflammation of tendons * Psoriasis * Inflamatory back pain * NSAIDs good response * Enthestsis (heel) * Arthiritis * Chrons/colitis * HLA B27 * Eyes - uvitis * Inflammatory back pain, bowels, eyes, skin psoriasis, asymmetrical arthritis!!!!
Ankylosing spondylitis definition
nflamtory artheritis of the inervertebral joint sin the spine and rib cage leading to sutio of joiints
Ankylosing spondylitis epidemiology
- Young adult male in twenties
- Symptoms come over 3 months
- 88% HLA-B27 positive
- Male 3:1
Ankylosing spondylitis risk
eronegative arteritis
Family history
Smoking
Ankylosing spondylitis path
- Inflamatio cuases destruction of intravetebral joints, facet joints and sacroilliac joints
- Fibroblasts replace the destroyed units with fibrin
- Ossificatio occurs eading to the spine being immmobile
Syndesmophytes – new bone formation and vertical growth from anterior vertebral corners
Ankylosing spondylitis key presintations
- Pain is worse at night and better with movement after 30 mins
There are flares and worse
Ankylosing spondylitis signs
- Bamboo spine on xray
- SPINEACHE
- Moening stiffness
- Can causes severe kyphsosi of the thoracic and cervical spine - het become hunches over
PRISM
* Pain
* Rash’s and skin change
* Immune
* Swellings
* Malignancy
Ankylosing spondylitis symptoms
- Fever
- Weight loss
- Fatigue
- Bum pain (sacroilitis)
Neck pain and stiffness
Ankylosing spondylitis test
- X ray showing sacroillitis , dagger sign, bamboo sine due to fusion
- MRI
- Bloods - HLA-B27 positive
- Normocytic anaemia
- Decrease Hb
- Raised ALP
To diagnose they need sacroilitis and more than one of the SPINE ACHE mnumonic
Ankylosing spondylitis treatment
- Physio and hydrotherapy
- Long term NSAIDS - naproxen
- DMARDs - methotrexate to treat peripheral arthritis’s
Anti TNF - etanercept, adalimumab these stop sydemophyts from forming, one formed nothing can reverse the progress
ankylosing spondylitis complications
Vertebral fractures
psoracic arteritis difinition
Autoimmune arthritis characterised by red scaly patches
psoracic arteritis risk factors and path
Family history
- T cell medicated attack of joint in people with psoriasis
*
psoracic arteritis signs and symptoms
- Inflamatory arthititis and psoriasis
- Can involve connective tissue
Ther are 5 different patterns of diseases :
* Oligoartheritis - mild asymetircal few joints
* Polyarticular/rheumatoid pattern - resembels RA, symetrical and >5 joints affected
* Spondyloarthritis - asymetrical and involves spine and sacroilliac fusion
* Distal interphalangeal predominant - affects DIP joints leading to dactyltis - sausage digits and nail abnormalaties
* Arthiritis mutilans - oerarticualr osteolysis and bone shorteneing, pencil in cap x ray changes
* There is akso psoratic plaques on scalp trunk and extensor surfaces, scaly and itch
- Polyartheritis or asymetric oligoarticular
- Joint swelling and stiffness
- Red and warm joints
psoracic arteritis test
- Bloods - HLA-B27 positive, raised ESR, FR and anti-CCP absent
Xray - erosive changs, penicl in cap on xray
psoracic arteritis treatment
imilar to RA:
* NSAIDS
* DMARDS
* Anti TNF - Etanercept, adalimumab, infliximab
* IL 12/23 blockers - ustekinumab
Exercise
Reactive arthritis definition
Sterile inflammation f synovia membranes, tendine, fascia following infection, typically by STIs or GI infections
Reactive arthritis epidemiology
- Occus following distal infection (GI or STI)
Men more than women afected
Reactive arthritis cases
GI infection - salmonell, shigella, e.coli, camplylobacter
STI - chlaymidia, gonnohoreoa
Reactive arthritis pathophysiology
An infection triggers joint inflamation elsewhere in the body
Usually a single joint e.g a knee
Reactive arthritis key presintations
Reiter triad - cant see, cant pee, cant climb a tree. Convjunctivits, urethritis, oligoarthritic
* Pain and sweling of a single joint Psoriatic like skin lesions 0 rahs on fee and on penis
Reactive arthritis tests
- Bloods - HLA-B27, ESR, CRP
- Stool culture if diarrhoea
- Urethral swab
- STI screen
- Joint aspration - should be sterile
Xray
Reactive arthritis differntials
Septic arthritis
GOUT
Reactive arthritis tx
- Treat infection with antibiotics
NSAIDs - steroid jpin injections`
what drig is associated with gout
thiazide diuretics
Systemic lupus erythematosus ddfinition
Definition
Type 3 hypersensitivity reaction
Systemic lupus erythematosus causes
Aetiology
Autoimmune, associated with raynards and anti-phospholipid syndrome
Systemic lupus erythematosus epidemioloy
Epidemiology
More common in females
Peak age - 20-40
Systemic lupus erythematosus risk facors
Risk Factors
- Premenopausal women
- Family history
- Afro Caribbean
- Genetics - HLA genes
- Drugs - hydralzine, isonazid procaamide, penicillamine
- Uv light
- Smoking
- EBV
Systemic lupus erythematosus pathophys
Pathophysiology
- Multisystemic autoimmune inflammatory disease in which autoantibodies target autoantigens which leads to the formation of immune complexes
- This activated the complement system and causes and influx of neutrophills into the tissues
Systemic lupus erythematosus key presintation
Key presentations
Diagnosis- must have 4/11
MD SOAP BRAIN
* Malar rash – butterfly rash on face
* Discoid rash
* Serositis – pleuritis, pericarditis
* Oral ulcers in mouth
* Arthritis – similar to RA
* Photosensitivity – rashes on sun exposed area
* Blood (haematological) disorder – all low (anaemia, leukopenia, thrombocytopenia)
* Renal disease – proteinuria (glomerulonephritis)
* Anti-nuclear antibody positive
* Immunological disorder – anti-dsDNA
* Neurological disorder – seizures, cerebrovascular disease, myasthenia gravis
Systemic lupus erythematosus signs
Signs
Haematological
Anaemia
Thrombocytopenia
Neutropenia
Lymphopenia
Reynard’s phenomenon
Systemic lupus erythematosus symptoms
Symptoms
- Remitting and relapsing
- Very non specific
- Fever, fatigue, rash, myalgia and arthralgia
- Skin problems
- Lymphadenopathy
- Weight loss
Systemic lupus erythematosus test
1st line test
- Autoantibodies - antinuclear antibody (sensitive but nit specific)
- Anti-double stranded DNA (anti-dsDNA) is specific to SLE, meaning patients without the condition are very unlikely to have these antibodies. Around 70% of patients with SLE will have anti-dsDNA antibodies.
- Other antibodies - RF, anti-cardiolipin antibodies, anti-RO/lupus antibody, SM, RNP
- Complement - decreased C3 and c4
- Inflammatory markers - raised ESR
- MRI/CT of the brain
- FBC - normocytic anaemia
Systemic lupus erythematosus differentail
Differential diagnosis
- Acute pericarditis
- Anti-phospholipid syndrome
- B cell lymphoma
- Fibromyalgia
- Scleroderma
- Sjorgens syndrome
Systemic lupus erythematosus treatent
Treatment
- Avoid triggers (UV)
- Weight loss and smoking cessation
- Topical - suncream and steroids
- Steroids - prednisolone
- NSAIDs
- Anticoagulants
- Hydroxychloroquine
- Other immunosuppressants - Methotrexate, Mycophenolate mofetil, Azathioprine, Tacrolimus, Leflunomide, Ciclosporin
- Biological therapies for severe disease - rituximab - a monoclonal antibody that targets CD20 proteins on the surface of B cells. Belimumab is a monoclonal antibody that targets B-cell activating factor
sle complications
Complications
- Cardiovascular disease
- Infection secondary t immune suppression
- Anaemia of chronic disease - affects the bone marrow
- Pericarditis and pleuritis
- Nephritis
- Venous thromboembolism
Antiphospholipid syndrome definition
PATINET IS IN A HYPERCOAGULABILITY STATE!
Syndrome characterized by thrombosis (arterial or venous) and/or recurrent miscarriages with positive blood tests for anti-phospholipid antibodies (aPL)
Antiphospholipid syndrome`epidemiology
Epidemiology
- Associated with SLE
- More common in women
Antiphospholipid syndromeauses
Aetiology
HLA-DR7 mutation and environmental trigger
Infection - HIV< Malaria,
Drugs - CV drugs (propranolol, dyralazine) and antipsychotics
Antiphospholipid syndrome path
Pathophysiology
- Anti phospholipid antibodies attack phospholipases on the cell membrane or protein bond to phospholipids
- aPL play a role I thrombosis by binding to phospholipid on te surface of the cell such as endothelial cells, platelets and monocytes, this then alters the function of the cells leading to thrombosis or miscarriage
- Primary occurs by itself and secondary occurs with other autoimmune diseases - SLE
Antiphospholipid syndrome key presintaiton
Key presentations
CLOT
* Coagulation defect * Livedo reticularis - lace like purple discoloration on skin * Obstetric issues - miscarriage * Thrombocytopenia
Major clinical featires are results of thrombosis:
* Arteries - stoke, TIA, MI
* Vetins - DVT, PE, Budd charri syndreom
* MISSCARIGE - PLACENTLAL INFARCTION
* Kidneys - renal falire
* Valvular heart disease
* Epilepsy
* Migrane
* Throbocytopenia
Antiphospholipid syndrome test
1st line test
Anti-cadiolipin antibody test
Anti BETA2 glycoproien test
Lupus anticoagulent test
Antiphospholipid syndrome tx
Treatment
Manage thrombosis TRs - smoking , weight loss, diet, HTN, exercise
Warfrin or LMWH as warfrin is contraindicated in pregnancy
Prophylaxis - aspirin or clopidogrel
Dermatomyositis/polymyositis definition
Definition
Rare muscle disorder where ther is inflammation and necrosis of skeletal muscle fibres causing a rash and muscle weakness.
Dermatomyositis/polymyositis
Dermatomyositis/polymyositis cuases
Aetiology
- Viruses - coxsackie, rubella, influenza
- Genetic predisposition - HLA-D8/DR3 appear to be at hight risk
Dermatomyositis/polymyositis path
Pathophysiology
- Polymyositis - immune system attack the muscles due to molecular minimicary
- Dermatomyositis - immune system attacks muscle and skin
Dermatomyositis/polymyositis key presintation
Key presentations
Polymyositis
* Symmetrical progressive musec weakness affecting large proximal muscles - shoulders and hips
* Dermatomyotosis - heliotrope -purple eyelids
*
* Gottoreon sign - scaly plaques over knuckles
Dermatomyositis/polymyositis tests
1st line test
- Electromyography - muscle changes
- Antibodies - Jo-1, PM-Scl, Mi-2
- Muscle/skin biopsy - diagnostic
- Serum creatine kinase - sensitive muscle enzyme test
- Aldolase is also raised
- Antinuclear antibody
- MRI
- CXR
Dermatomyositis/polymyositis tx anc complications
Oral steroids - prednisolone
Exercise therapy
Hydroxychloroquine for skin rashes
Tacrolimus
Interstitial lung disease
Scleroderma definition
Definition
Multisystem diseases with involvement of skin and Raynaud’s phenomenon.
Scleroderma risk factors
Risk Factors
Exposure to viny
l chloride, silica dust, rapeseed oil
Drugs
Genetic
Scleroderma path
Pathophysiology
- Genetic predisposition, immune activation, infection and an environmental toxin initiates endothelial lesion and widespread vascular damage
- The immune system and endothelium cells are activated and cuases - cell adhesions between t, b , neutrophils and monocytes causing inflammation
- There is collagen laid down which c=narrows the vessle and thickens the wall
- This leads to ischaemia
- T-helper cell activation——> damage to skin and blood vessels ———>fibrosis (FGF sensitivity)
- limited cutaneous SSc - less severe internal organ involvement better prognosis
- diffuse cutaneous SSc - crest syndome + affection the internal organs - hypertension and coronary problems, pulmonary hypertension, fibrosis of the lungs, glomeruloneohritis and scleroderma renal crisis
Scleroderma presintation s
Key presentations
* Calcinosis - calcium deposits in the skin * Reynard's phenomenon - digital ischemia due to vasospasm * (O)oesophageal dysfunction - acid reflux and decreased motility * Sclerodactyly- thickening and tightening of skin of fingers and hands * Telangiectasis - dilation of capillaries causing red marks and spider veins * Skin involvement - hands, face, feet, forearms
Scleroderma signs
Signs
- GI involvement with dilation and atony (loss of strength) - heartburn, dysphagia, colon pseudo obstruction
- Renal involvement -acute and chronic kidney disease, hypertensive crisis
- Lung disease - fibrosis and pulmonary vascular disease
- Myocardial fibrosis
Scleroderma test
1st line test
- Bloods - normocytic anaemia
- Raised ESR and CRP occasionally
- Serum autoantibodies -
- anticentromere antibodies- associated with limited cutaneous SSC
- Anti - SCL 70 - positive in diffuse cutaneous SS
- Antinuclear antibodies positive - positive for most patients with SSc
- anti-topoisomerase-1 antibodies
- anti RNA polymerase 3
- RF positive
- Antinuclear antibodies positive - positive for most patients
- Urinalysis - look for creatine, protein for AKI
- CXR to exclude other pathology
- Hand xray to see calcium deositis in fingers
*
Scleroderma treatment
Treatment
Overall:
* Steroids and immunosuppressants - prednisolone
* Nifedipine vasodilator for rayunards
* Gastroesophageal reflux - proton pump inhibitors
* Ace inhibitors to prevent renal cursus
* Topical skin emollient
* Annual echocardiogram to look for pulmonary arterial hypertension
Polymyalgia rheumaticadefinition
Definition
Autoinflammatory diseases affecting joints and muscles there is a stong association with giant cell arthritis!
Scleroderma risk factors and oath
Risk Factors
- SLE
- Polymyositis/dermatomyositis
Pathophysiology
- Inflammatory disorder causing pain in shoulder and hips
- Pain come from bursae and tendons
- Muscels are spared
Polymyalgia rheumatica key presintations
Key presentations
- Bilateral shoulder pain that may radiate to elbow
- Bilateria pelvic girdle pain
- Worse with movement
- Interferes with sleep
- Stiffness for 45 mins in the morning
- Systemic symptos - wight loss, fatigue low grade fever kow moof
- Pitting odema,
- Carpal tunnel syndrome
Polymyalgia rheumatica test
1st line test
- Clinical history and tests to rule out other conditions
- bloods - raised CRP and ESR
- ANCA negative
- Raised alkaline phosphate
- Calcium serum
- RF, CK for myositis
- Serum protein electrophoreiss for prtien disorders
- LFTs
- Temporal artery biopsy will show giant cell arteritis in 10-30% of cases
- diagnosis is based of clinical presintation and response to steroioids
Polymyalgia rheumatica differentials
Differential diagnosis
- RA
- SLE
- OA
- Malignancy
- Chronic pain
- Osteomalacia
Polymyalgia rheumatica treatmetn
Treatment
- Prednisolone - you should see an impprovemt of symptom s and then after a while for inflammatory markers to return to normal to diagnose PMR
- Long term bone and I protections - lansoprazole, alendronate
- Ca2+ and vitamin D
things to wrn people who are on steroids
Complications
Don’t STOP
Don’t - they might become steroid dependant afterr 3 week sna dif they stop will go into an adrenal crisis
Sick day rules - increases steroid if unwell
Trearment card - to alert other that thye are steroid dependant
Osteoporesis prevention - bisphosphoates, calcium and vit D
P - proton pummpinhibitor - omeprazole
Mechanical lower back pain causes
Aetiology
Lumbar disk prolapse, osteoarthritis, fractures, spondylolisthesis, heavy manual lifting, stooping and twisting, exposure to whole body vibration
Mechanical lower back pain risk factors
Risk Factors
Manual labour
Smoking
Poor working conditions
Low socioeconomic stats
Age
Pre-existing chronic pain
Mechanical lower back pain signs and symptoms
Signs
- Sudden onset
- Worse in the evening
- Exercise aggravates pain
- Scoliosis
- Red FLAGS - TUNAFISH
- Trauma
- Unexplained weight loss
- Neurological defects - bowel and bladder incontinence
- Age - younger than 20 and older than 55
- Fever
- IV drug user
- Steroid use
- History of cancer/morning stiffness
Symptoms
- Back pain - duh
- Muscular spasms - causes local pain and tenderness
Mechanical lower back pain tests
1st line test
- If young - CRP/esr to rle out myeloma, infecition, tumour
- Xrya if red flags present
- MRI better than CT
- Bone scans
Mechanical lower back pain differential
Differential diagnosis
Raised ESR and CRP will help distinguish from polymyalgia rheumatica
Mechanical lower back pain definition
Definition
Pain after heavy manual liftin stooping and twisting, exposure to while body vibration, psychosocial stress
Mechanical lower back pain epidemiology
Epidemiology
- Common in general population - 20-55
mechanical lower back pain tx
Treatment
- Most resolve after 6 weeks
- Don’t rest - continue normal activities
- Avoid slouching, proper lifting techniques, heat pads, swimming
- Analgesics ladder - paracetamol, NSAIDs
- Physio, acupuncture, CBT
- Workplace adaptations and changed duties
mechanical lower back pain benefits of wor, high risk work activities, returning to work, legal sides
Benefirts of work:
* Lower mortality
* Pat
* Better self asteem and mental health
* Socia relationshiops
* Structure t life
High risk activitys:
* Heav manual lfiting
* Lifting from beliw knee, or to above the shoulder
* Repetative work
* Foreceful movements
Returning to work:
* Talk abot barriers
* Fitnote
* Rehabbilitation - phased return, restirctions and modifications
* Confidence may be lost
Staturatory and legal:
* Equality act and resonalye adjustent for the disabled or Ill
* Presnaly injury lirifation for work related injury/illness
* A patient can be lawfully dissmissed for incapatibility due to ill health - this si different from reducndancy
* Reporting of Injuries, Diseases and Dangerous Occurrences Regulations (RIDDOR) to the HSE – CTS, HAVS or tenosynovitis
what is carpal tunnel syndroe
Carpal tunnel syndreom
- Compression of the median never by flexor tendons, gives pain, numbness, tingiling, wekaness and muscle wasting
- Extreames of wrist externtion may causes it, - painers, meat preocessors
- Associated with: hyppthyroidism, diabeitses, prognancy
- Can lead to paralysis, sometime steh fascia neesd to be cut
vertebral disk degeneration
definition
Osteoarthritis’s of the spine which includes degeneration of the disc or facet joints.
vertebral disk degeneration
Degeneration of the annulus fibrosus - tough outer coating og the intervertebral disk - leading to narrowing f the spinal canal. Dysfunction Stage, the Dehydration Stage, the Stabilization Stage, and the Collapsing Stage.
Small tears happen in the annulus and this creates scar tissue, the wall is weakens, the nuclus popuses become dehydrates and collapses, this cuases the faces joint to fring and it can cuases bone spurs and may cause nerve pinching.
vertebral disk degeneration key presintations
- Mechanical pain
- Sciatic radiation may occur with pain in the bum and thigh
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
vertebral disk degeneration tx
- NSAIDs
- Physiotherapy
- Weight loss
- Surgery for when there is pain at a single level - decompression of the nerve root
vertebral disk degeneration - what is sciatica
- Sciaticica - L3 and L4 form the scaitic never which exitis the pelvis at the sciatic foramen
Sciatica causes pain form bum radiating down twh back of the tigh to the knee or deet
herniated disk definition
- Progressive breakdown of the vertebral disk leading to prolapse resulting in acute back pain
herniated disk risk factors
- Genetics
- Advanced age
- Menopause
Spina trauma
herniated disk pathophysiology
ntervertebral disc’s nucleus pulposus (mostly water) dehydration → decreased proteoglycan and collagen → decreased padding between vertebrae → unable to absorb shock → disc collapse → annular tears, herniation of disc contents into spinal canal → nerve impingement → pain
herniated disk key presintations
- Sudden onset back pain
- Decreased range of motion
- Muscle spasms
- Muscle weakness and atrophy
- Radiation of pain
Headache, dizziness, vertigo
herniated disk tests
- Xrya
- MRI - evaluate spinal canal
- Evaluate annular tears
Increased dignal may indicate disk dehydration
herniated disk tx
- NSAIDs
- Bed rest on firm matress
- Corticosteroid injection locally
- Surgery to remove and replace
- [physio to help resotre movement
Osteomalacia definition
Metabolic bone disease characterised by incomplete mineralisation of underlying mature organic bone matric. This causes bone softening.
Osteomalacia causes
- Vitamin d deficiency
Calcium and phosphate deficiency
Osteomalacia risk factors
- Dark skin
- dietary vit d deficiency
- Liver/kidney dysfunction
Malabsorption
Osteomalacia pathophysiology
Vitamin D requires activation by the liver (25-hydroxylation) and then by the kidney (1-alpha-hydroxylation/ calcitriol). Active vitamin D raises serum calcium and phosphate by increasing intestinal absorption, as well as resorption from the bone and kidney
If there is less vitamin d or less calcium there calcium phosphate for the bones can’t be properly calcified.
Osteomalacia signs
- Skeletal deformities
- Waddling gat
Hypocalcaemia - Chvostek’s sign
Osteomalacia symptoms
- Bone pain
- Proximal muscle weakness
- Difficulty walking up stairs
- Muscle spasms
- Fractures
Osteomalacia test
- Serum calcium and phosphate low
- Serum 25-hydoxyvitamin D low
- PTH levels
- Serum ALP - raised in 80% of patients #
- Renal and liver function assessment for primary causes
Osteomalacia gold standard test
Iliac bone biopsy with double tetracycline labelling allows the bone formation to be seen
osteomalacia differential
Differential diagnosis
Osteoporosis
Paget’s disease
osteomalacia tx
Treatment
Treat underlying causes:
* Calcium and D3
* D2 id liver disorder
* Give calcitriol if kidney problems
osteomalacia complications
Complications
Insufficiency fracture
Complication of treatment - hypercalcaemia, secondary hyperparathyroidism
what is rickets
Other notes
Rickets is when there is deficiency in children leading to growth retardation and skeletal deformities.
whihc tumours metastasis to bone
Secondary is much more common than primary.
BLT KP
Breast
Lung
Thyroid
Kidney
Prostate
bone tumours epidemiology
Rare and more commenly seen in children
bone tumours risk factors
Radiation
Paget’s disease
bone tumours path
Oncogene causes overstimulated cell growth and mutated tumour suppressor genes which can causes uncontrolled proliferation.
Benign:
* Osteochondroma- males < 25, develop in metaphysis (growth plate) of the long bones
* Giant cell tumour - bone fracture and radiation exposure increases risk, develop in epiphysis (end)of the long bones
* Osteoblastoma and osteoid osteomas - arise form osteoblasts,. Osteoblastoma affect the axial skeleton.
*
Malignant:
* Osteosarcoma - under 20. most common primary bone malignancy in children. Arises from osteoblasts in metaphysis (growth plate), associated with pagets diseases in adult life, knee and proximal humorous, rapidly metastasises to lung.
* Ewing’s sarcoma - hips and long bones, very rare, presents with mass/swellings on the arms, pelvis and chest, occasionally skull and chest flat bones too. Tumours, malaise, anorexia, WL, incontinence if affecting spine
* Chondrosarcoma - pelvis. Come from chondrocytes, most common adult bone sarcoma, dull, deep pain, pelvis, femur, area is swollen and tender. Pelvis, femur, humorous, scapula, ribs.
bone tumours signs
- Fatigue
- Weight loss
- Anaemia
- Unexplained bone fractuers
- Pain swelig
- Limp or loss of limb
- Faliure to thrive
Pyrexia
bone tumours symtoms
- Redness
- Swelling
- Fractures
- Osteoid osteoma - pain worse at night
- Osteochondroma and blastoma - press on spinal cord to create, numbness, weakness, avascular necrosis,
- Fever, weight loss, night sweats
SOB and coughing
bone tumours tests
- X-ray
- Osteochondroma - exostosis
- Gina cell tumour - soap bubble
- Osteosarcoma - sunburst
- Ewing’s - onion skin appearance
- Bone isotope scan - hotspots of bone metastasis
- MRI
- Biopsy
Labs - PSA< serum electrophoresis for Bence jones protein, ESR, CRP
bone tumour treatmetn
Benign - surgery
Malignant:
* Chemo
* Radiotherapy
* Surgery
* Bisphosphonates to reduce pain and fracture risk
Marfans definition
Genetic disorder which leads to defective connective tissue - this effects the skeleton, heart, blood vessels, eyes and lungs.
Marfans path
A mutation on gene FBN1 on chromosome 15 which is autosomal dominant. This causes the fibrillin 1 to be dysfunctional or less abundent which means less tissue integrity and elasticity. TGF-beta doesn’t get toned down which causes excessive growth.
Marfans symptoms
all stature, long arms, long legs
* Pectus excavatum/carinatum (chest sinks in or out)
* Scoliosi s
* Hypermobility
* Downward slant of eyes
* Narrow high arch palate
* Stretch marks
Marfans diagnosis criteria
Clinical diagnosis if there are more than 2 features of:
* Lens dislocation #
* Aortic dissection/dilation
* Dural extasia - widening of Dural sack
* Skeletal features
* Pectus deformity
* Scoliosis
Flat feet
Marfans differential
ellos danhlos
Marfans treatment
- Physiotherapy for joint strengthening
- Genetic counselling for parents
- Replacement of dislocated lens with artificial
- Avoid intense exercise
- Avoid caffeine
- Beta blocerks to stop aortic dilation
- Angiotensin receptos to decease aortic dialation
- Surgical repair of wide aorta
Marfans complications
- Retinal distachment
- Joint dislocations
- Bulla formaiton on lungs
- Aoric dilation
- Cystic medial necotis s
- Incrased risk of dissectino and anyerysm
- Mitral vale prolaps e
Aortic valve prolapse
Ehlers Danlos definition
A group pf connective tissue disorders cause by mutation of connective tissue proteins with collagen being the most commonly affected.
Ehlers Danlos type epidemioloy and ris factors
Hypermobile eds in the most common
Family history
Ehlers Danlos path
Mutations which h leads to weakedn connective tissue I the skin, bones, blood vessles, oragans,
Ehlers Danlos key presintations
- Joiny hypermobility and pain
- Recurrant dislocation
- Scoliosis and spine pain
- Hyperelasic skin
- Easy brusing
Atrphic skin
Ehlers Danlos test
- Clinical diagnosis als based on familt history
- Joint examinations
- Genetic testing to identify faulty genes
Spine x-ray for scoliosis
Ehlers Danlos tx
- Physioltherapy
- Orthopedis insturments - bracing, wheelchair and casting
- Lifestyle advie
- Analgesia
Psychologial input
prosthetic infection bacteria
S. Aureus
Coagulase negative staphylococci e.g. S. Epidermidis – most frequent infecting organism after hip replacement
Gram positives mainly
prosthetic infection risk factros
Poor infection controll
Old age
Obestiy
Diabeties
prosthetic infection tests
- History
- Examination
- Aspiration
- X rays
- FBC - eSR and CRP raised
- Alpha defensin raised
- Microbiology culture
prosthetic infection treatment
- Eradicat sepsis- antibiotics
- Analgeia for pain
- Debridment of infectios
- Excisio arthroplaty - take it oubt
Amputatio
what are rhemuatoid nodules made up of
Mobile subcutatnous nodules at point of pressure are in rheumatoid nodules - tere is an area of fibrinoid necorisis in the middle and then pallaside layer of histocytes and then a ring of macrophages
what are teh xr signs of RA and osteoartheritis
- Periarticualr erosions are the classic feature of RA on Xray
- Subchonral cysts, periarticular scelrosis, osteophytes are osteoartherits x ray signs
what shoudl people with gout eat more off
dairy1 it promotes uric acid excretinos
what are the 4 side effects of biphosphenates
Reflux and oesophageal erosions. Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this.
Atypical fractures (e.g. atypical femoral fractures)
Osteonecrosis of the jaw
Osteonecrosis of the external auditory canal
