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
