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Phase 3 > Wk11 - MSK > Flashcards

Wk11 - MSK Flashcards

1
Q

Function and structure of a tendon

A

Tendon – Transmits force from muscle to achieve movement

Parallel collagen fibrils with tenocytes

Surrounded by paratenon / sheath

Largely avascular, nutrition via paratenon

As avascular - slow to heal

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2
Q

How does tendinopathy occur

A

Chronic Tendon Injury of over use – repetitive loading

  • -> Degeneration, disorganisation of collagen fibres
  • -> Increased cellularity
  • -> Little inflammation

Loss of balance between micro damage from overuse and reparative mechanisms

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3
Q

Risk factors for tendinopathy

A

Age - more middle age (elderly tend to less activity)
Chronic Disease
Diabetes, Rheumatoid Arthritis
Adverse Biomechanics

Repetitive Exercise
Recent increase in activity
Quinolone 9e.g. ciprofloxacin Antibiotics

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4
Q

Pathology of tendinopathy - what happens

A

Probably not inflamation – tendinosis not tendinitis

Deranged collagen fibres / Degeneration with a scarcity of inflammatory cells (Astrom and Rausing 1995)

Increased vascularity around the tendon

Failed healing response to micro tears

Inflammatory mediators released IL-1, NO, PG’s – cause apoptosis, pain and provoke degeneration through release of matrix metalloproteinases

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5
Q

Common sites of tendinopathies

A 
Achilles Tendinopathy
Rotator cuff tendonitis
Tennis Elbow (Lateral epicondylitis)
Golfers Elbow (Medial epicondylitis)
Patella Tendinopathy
Hamstring tendonitis
Adductor tendonitis
Plantar fasciitis
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6
Q

Clinical features of tendinopathy

A

Pain

Swelling
Thickening
Tenderness

Provocative tests - Contract that msucle group against resistance

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7
Q

Diagnosis of tendinopathy

A

X-ray? - Excludes bone pathology

Ultrasound

MRI – Tendinopathy best seen on T1.

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8
Q

Non-operative Tx of tendinopathy

A

NSAID’s
Activity modification
Physiotherapy – stretching , eccentric exercises
GTN patches
PRP injection - To bring extra growth factors into area –> promote healing

Prolotherapy – irritant injection, dextrose (The dextrose will stimulate inflammation to try get tendon to begin healing)
Extracorporeal Shockwave Therapy
Topaz – radiofrequency coblation
Steroid injection – controversial, avoid intrasubstance, ?avoid suppressing inflammatory and healing response (Steroid injection is avoided most of the time - risk of tearing the tendon)
Etc etc

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9
Q

FEatures of physiotherapy for tx of tendinopathy

A

Eccentric loading

Contraction of the musculotendinous unit whilst it elongates

Beneficial in approx 80%

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10
Q

GTN patches for Tx of tendinopathy

A

¼ patch 125 mcg

Vasodilator - Increases local perfusion

Takes up to 12 weeks to see effects (compliance is often a problem)

Side effects - headaches

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11
Q

Extra corporeal shockwave therapy for tx of tendiopathy

A

3 weekly treatments

Approx 75% improve

Breaks down calcification and stimulates healing of underlying problem

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12
Q

Operative treatment of tendinopathy

A

Debridement
Excision of diseased tissue
Possible to debride 50% of tendon without loss of function

(Tendon transfers)

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13
Q

Definition of compartment syndrome

- Common sites

A

Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise

Common sites - leg, forearm, thigh

Orthopaedic emergency - loss of function, limb or life

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14
Q

Causes of compartment syndrome

A 
Internal Pressure
Trauma – fractures, entrapment
Bleeding
Muscle oedema / myositis
Intracompartmental administation of fluids / drugs
Re-perfusion – vascular surgery
External compression
Impaired consciousness / protective reflexes
Drug / alcohol misuse
Iatrogenic
Positioning in theatre - lithotomy
Bandaging / casts
Full thickness burns

Combination

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15
Q

Pathophysiology of compartment syndrome

A

Pressure within the compartment exceeds pressure within the capillaries

Muscles become ischemic and develop oedema through increased endothelial permeability

Necrosis begins in the ischaemic muscles after 4 hours

Ischaemic nerves become neuropraxic. This may recover if relieved early, permanent damage may result after as little as 4 hours

Compromise of the arterial supply – late

Increased pressure
Increased venous pressure
Decreased perfusion
Muscle ischaemia
Muscle swelling
Increased permeability – fluid leaks into interstitial space
Increased pressure
Autoregulatory mechanisms overwhelmed
Muscle necrosis and myoglobin release
Loss of function , extremity or loss of life.
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16
Q

Effects of ischaemia of limbs at different time zones

A

1 hour
Nerve conduction normal, Muscle viable

4 hours
Neuropraxia in nerves - reversible
Reversible Muscle ischaemia

8 hours
Nerve axonotmesis and irreversible change
Irreversible muscle ischaemia and necrosis

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17
Q

End stage compartment syndrome

A

Stiff fibrotic muscle compartments

Impaired nerve function

Clawing of limbs

Loss of function

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18
Q

Diagnosis of compartment syndrome

A

Clinical Diagnosis

History

Examination

Pulses present (until late stages) unless associated vascular injury

Parasthesia and paralysis – usually later. Deep nerves affected first
1st Dorsal webspace

Impaired conscious level
Compartment pressure measurement

Normal pressure 0-4 mmHg, 10mmHg with exercise
DBP-CP <30mmHG = diagnostic
CP>30mmHG = diagnostic

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19
Q

Clinical features of compartment syndrome

A

Pain – out of proportion to that expected from the injury
Pain on passive stretching of the compartment (E.g. moving the tones or bending the fingers)
Pallor
Parathesia
Paralysis
Pulselessness (late sign)

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20
Q

Urgent treatemtn of compartment syndrome

A

Open any constricting dressings / bandages

Reassess

Surgical release

Later wound closure
Skin grafting / Plastic surgery input

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21
Q

If urgent treatment nor enough…

A

Surgical Release:
Full length decompression of all compartments

Excise any dead muscle

Leave wounds open

Repeat debridement until pressure down and all dead muscle excised

Wound closing/skin grafting

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22
Q

Compartments of the forearm

A

Flexor
Extensor
Mobile Wad of three

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23
Q

Compartment of the leg

A

Anterior
Lateral
Deep posterior
Superiffical posterior

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24
Q

Compartments of thigh

A

Anterior
Abbductor
Posterior

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25
Q

Peri-operative management of compartment syndrome

A 
Adequate hydration
Fluid loss
Monitor and regulate electrolytes (K+)
Correct acidosis
Myoglobinuria
Renal function
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26
Q

Late presentation/ diagnosis of compartment syndrome

A

Irreversible damage already present

Fasciotomy will predispose to infection

Consider non-operative treatment

Splint in position of function

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27
Q

FEatures of septic arthritis

A

pain, fever, swollen joint, loss of function

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28
Q

Causative organisms of septic arthritis

A

Staphylococcus aureus (Staph auereus - most common (60-75%) - MRSA emerging problem), Neisseria gonorrhoea, Haemophilus influenzae (children)

Increased risk if steroids, rheumatoid arthritis
Suspected septic arthritis is a medical emergency

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29
Q

What are the 3 main classficiation of bone tumours

A

secondary tumours in bone : very common
myeloma : common, commonest primary bone tumour
primary bone tumours : rare

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30
Q

What type of cancers commonly metasasise to bone

A

metastatic carcinoma
bronchus, breast, prostate, kidney, thyroid (follicular)
childhood
neuroblastoma, rhabdomyosarcoma

Typically goes to bones with a good blood supply - long bones (femur and humorus), vertebrae

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31
Q

Presentation of metastases to bone

A 
often asymptomatic
bone pain
bone destruction
long bones : pathological fracture
spinal metastases: vertebral collapse, spinal cord compression, nerve root compression, back pain.
hypercalcaemia
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32
Q

What type of imaging is useful for picking up metasasis on bone

A

PET CT

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33
Q

2 types of bone metastasis

A

Lytic V sclerotic bone mets

Majority are lytic

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34
Q

Sites from which sclerotic metastasis to the bone occurs

A 
prostatic carcinoma
breast carcinoma
carcinoid tumour (neuroendocrien tumour)
sclerotic on x-ray
reactive new bone formation, induced by tumour cells
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35
Q

2 tumours that produce solitary bone metastases

A

Renal and thyroid carcinomas

  • often longer survival
  • surgical removal often valuable
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36
Q

Features of myeloma

A

Commonest malignant primary bone tumour
Neoplasmic monoclonal proliferation of plasma cells
solitary (plasmacytoma) or multiple myeloma
orthopaedic consequences
“medical” consequences (as can get in bone marrow)

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37
Q

Clinical effects of myeloma

A
  • Osteolytic bone lesions (lytic ‘punched out’ lesions) - backaches, pathological fractures and vertebral collapse
  • Hypercalcaemia
  • Anaemia, neutropenia or thrombocytopenia
  • Recurrent bacterial infections
  • Renal impairment

Immunoglobulin excess

  • ESR > 100 (can be diagnostic)
  • serum electrophoresis : monoclonal band (diagnostic)
  • urine : immunoglobulin light chains (Bence Jones protein) (diagnostic)

2 types of light chains in plasma - Kappa and Lambda
If have myeloma - only have one type - either Kappa or Lambda - as monoclonal proliferation

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38
Q

Light chains present in plasma and yeloma

A

2 types of light chains in plasma - Kappa and Lambda

If have myeloma - only have one type - either Kappa nad Lambda - as monoclonal proliferation

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39
Q

Marrow replacement (due to myeloma) results in

Renal impairment with myeloma

A

pancytopenia
anaemia
leucopenia: infections
thrombocytopenia: haemorrhage

Myeloma kidney: precipitated light chains in renal tubules
Hypercalcaemia
Amyloidosis

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40
Q

The types of primary bone tumours

A

Benign

  • Osteoid osteoma
  • Chondroma
  • Giant cell tumour

Malignant

  • Oesteosarcoma
  • Chondrosarcoma
  • Ewing’s tumour
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41
Q

Features of osteoid osteoma

A

A small, benign osteoblastic proliferation
Common, any age especially adolescents, M:F 2:1
Any bone, especially long bones, spine
Pain, worse at night, relieved by aspirin, scoliosis
juxta-articular tumours : sympathetic synovitis

Tx - radio-frequency ablation

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42
Q

Features of osteosarcoma

  • definition
  • epidemiology
A

A malignant tumour whose cells form osteoid or bone

Age : peak 10 -25
Site : metaphysis of long bones, 50% around knee
Sex : male preponderance, 3:2
Incidence : 2-3 / million / year (not very common)

Classic presentation - pain, swelling (shoulder), inability to move a limb
highly malignant
early lung metastases
5 year survival : 15-20% pre-chemotherapy
modern survival : 50-60%
Tumour can often produce a new cortex of bone –> forming a codman’s triangle

Image guided biopsy - by ultrasound or CT
8 weeks of chemotherapy, surgery to remove tumour, often have another 8 weeks of chemotherapy if responded well

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43
Q

Worse prognosis of osteosarcoma - a variant

A

Paget’s
multifocal
post-irradiation

Pagets disease:
Common in elderly, Anglo-saxon origin
Disorder of excessive bone turnover
Increased osteoclasis, increased bone formation, structurally weak bone
Disorganized bone architecture (often in vertebrae, pelvis, skull, femur)
Usually lytic

  • bone pain
    OA, deafness, spinal cord compression, high cardiac output - cardiac failure, pagets sarcoma (aggressive form of osteocarcinoma)
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44
Q

Name the common cartilaginous tumours

A

Benign: Enchondroma, Osteocartilaginous exostosis

Malignant: Chrondrosarcoma

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45
Q

Features of enchondroma

A

Lobulated mass of cartilage within medulla
Common, any age.
>50% hands and feet, long bones.
Often asymptomatic in long bones.
Hands - swelling, pathological fracture.
Low cellularity, often surrounded by plates of lamellar bone

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46
Q

Features of osteocartilaginous exostosis

A

Benign outgrowth of cartilage with endo-chondral ossification,
Probably derived from growth plate
Very common, usually in adolescence
Uncommonly multiple-diaphyseal aclasis, autosomal dominant
Metaphysis of long bones, not cranio-facial

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47
Q

Features of chondrosarcoma

A

de novo (primary) or from a pre-existing enchondroma or exostosis (secondary)
Central,within the medullary canal or peripheral on bone surface
10% of malignant primary bone tumours
predominantly middle aged and elderly
Males: females; 2:1
axial skeleton, pelvis, ribs, shoulder girdle proximal femur and humerus. Hands and feet rare

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48
Q

Main difference between chondrosarcoma and osteosarcome

A

-

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49
Q

Features of Ewins

A

Malignant primary bone tumour seen in children - peak 5-15 years
long bones (diaphysis or metaphysis)
flat bones of limb girdles
early metastases to lung, bone marrow and bone
Historical 5 year survival of 5%
Modern 5 year survival 50-60%

Often tibia, fibia or pelvis

Responds well to radio and chemotherapy

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50
Q

Diagnosisng ewins

A

Stain it for C99 (/) - also do molecular geentics - has a specfic translocation (11 to 22)

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51
Q

Differentials of an acute hot joint

A

Septic arthritis
Crystal arthropathy
Trauma/haemarthrosis
Early presentation of polyarthropathy (RA, PsA)

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52
Q

Routes by which bacteria can reach the joint (–> septic arthritis)

A
  1. The hematogenous route
  2. Dissemination from osteomyelitis
  3. Spread from an adjacent soft tissue infection
  4. Diagnostic or therapeutic measures.
  5. Penetrating damage by puncture or trauma
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53
Q

Investigations for septic arthritis

A

Joint aspirate - microbiology for gram stain and culture
Blood culture
FBC - leucocytosis
X-ray - of no value

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54
Q

With septic arthritis the synovium is inflamed with…

A

fibrin exudation and numerous neutrophil polymorphs

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55
Q

Other specific types of septic arthritis

A

Lyme disease - borrelia burgdoferi
Brucellosis
Syphilitic arthritis - congenital and acquired

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56
Q

Features of crystal arthropathy

A

Gout and Pseudogout
Excess levels of uric acid
Leads to deposition of urate crystal in joints or soft tissue (tophi)
Acute gout - precipitation in joint stimulated acute inflammatory process
Chronic gout - tophi formation

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57
Q

How is gout diagnosed?

Feature of primary and secondary gout

A

Hisotry - rapid onset pain, swelling, tenderness, max intensity within 6-12 hours
Diagnsoed by aspirate - negatively birefringent needel shaped cyrstals in polarized microscopy
Serum urate levels and U&Es
Definitive diagnosis = MSU crystals

Primary - hyperuricaemia due to genetic predisposition e.g. Lesch-Nyhan syndrome
Secondary - high uric acid due to myeloproliferative disorder (PCRV), leukaemia treated by chemo, thiazides, chronic renal disease

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58
Q

Where is the most common site affected by gout?

A 
1st metatarsal (big toe)
Podagra - inflammation of 1st metatarsal joint - classical presentation of gout
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59
Q

Management of gout (both acute and chronic)

A

Acute:
NSAIDs - high doses rapipdly reduce pain and swelling
Cochicine - works best when initiated within 24 hours of attack; works in several ways e.g. IL-1 interference, microtubule interference; Need to stop statins with cochicine treatmen
Corticosteroids

Long term:
Aim SUA <300 using ULT (urate lowering therapy)
Emphasise lifestyle alterations
Allopurinol - excrteed renally; ; Xanthine oxidase inhibitor; Risks include DRESS syndrome - occurs wihtin first few months usually, particulalry HLA mutations at risk
FEbuxostat - XO inhibitor, hepatic metabolism, very expensive (20x allopurinol)
Uricosuric agent (probenecid) - increases secretion of uric acid into urine
Rasburicase - given via IV - progressive risk of anaphylaxis, recombinate urate oxidase

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60
Q

Management of pseudogout

A

Aspiration helps reduce the pain and swelling
NSAIDs
Colchicine

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61
Q

Features of reactive arthritis

A

Sterile synovitis which occurs following an infection
Trigger organisms - salmonella, shigella, yersinia, chlamydia thrachomatis
Preceding illness usually a urethritis or diarrhoral
Association with HLA B27 (75%)

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62
Q

Clinical features of reactive arthritis

A

Acute, asymmetrical lower limb arthritis
More common in men
Days - weeks post infection

Asymetry oligoarthritis, larger jiont of lower limbs, daylitis, enthesitis (e.g. plantar fasciitis), bursitis, onjuctivits/uveitis, circinate balanitis, mouth ulcers, conjuctivities, keratoderma blenorrhagica (dark rash on base of foot)

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63
Q

Management of reactive arthritis

A

Little evidence that treating the triggering infection alters the course of the disease
Pain control - NSAIDs, intra-articular steroids

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64
Q

Prognosis of reactive arthritis

A

Usually self limited, lasts up to 6 months
May be chronic
Very occassionally there may be cardiac complications e.g. aortic regurgitation, aortitis, and amyloidosis

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65
Q

Features of enteropathic arthritis

A

Form of reactive synovitis seen in association with UC and Crohn’s disease
An asymmetrical lower limb arthritis
Treatment of the bowel disease and NSAIDs

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66
Q

Define OA

Features of osteoarthritis

A

Definition: Degenerative joint disease involving loss of articular cartilage, influenced by mechanical and biological factors.

Degenerative joint disease
Commonest form of arthritis
Middle aged/elderly
Weightbearing joints - hip, knee
Pathology - disorder of articular cartilage

Primary generalized - multiple joints, hands
Secondary - fracture, previous sepsis, RA, osteonecrosis, CDH, steroids, chronic overuse, gout, haemochromotosis, ochronosis, peripheral neuropathy

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67
Q

Signs and symptoms of osteoarthritis

Differential diagnosis of OA

Ix/Tx of OA

A

Pain and stiffness - worse at end of day
Cerpitations
Reduced ROM
Loss of articular cartilage, exposure of underlying bone, subchondral cysts and slcerosis, osteophytes
Synovium becomes hyperplastic, mild inflammation, bony detritus

Differential diagnosis:
bursitis, gout/pseudogout, RA, PA, AVN, meniscal tear

X-ray - LOSS
Bloods
Exercise
Physio/OT
NSAIDs + paracetamol
Steroid injection
Arthroplasty
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68
Q

Function of bone

A

Structural - support, protection, movement

Mineral storage - calcium and phsophate

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69
Q

Structure of bone

A 
Cortical bone:
Compact or tubular bone
80% of the skeleton
Slow turnover rate/ metabolic activity
Higher Young's modulus and resistance to torsion and bending

Cancellous bone:
Spongy or trabecular bone
Higher turnover rate and undergoes greater remodelling
Lower YOung’s modulus, and is correspondingly more elastic

Composition - Matrix & Cells

Matrix:
Organic - collagen, non-cllagenous proteins, mucopolysaccharides
Inorganic - calcium, phosphorus

Cells: Osteoprogenitor, osteocyte,, osteoblast, osteoclast

Diaphysis (shaft)
Epiphysis (end)
Metaphysis (transitional flared area between diaphysis and epiphysis)

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70
Q

Features of physis of bone

A

Unique feature of children’s bone
Responsible for skeletal growth
Allows remodelling of angular deformity after fracture
If physeal blood supply damaged, will lead to growth arrest (either partial or complete)

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71
Q

Stages of indirect fracture healing

A
  1. Fracture haematoma and inflammation:
    Blood from broken vessels forms a clot.
    6-8 hours after injury
    Swelling and inflammation to dead bone cells at fracture site.
  2. Fibrocartialge (SOFT) callus:
    (lasts about 3 weeks)
    New capillaries organise fracture haematoma into granulation tissue - ‘procallua’
    Fibroblasts and osteogenic cells invade procallus.
    Make collagen fibres which connect ends together
    Chondrocytes begin to produce fibrocartilage
  3. Bony (HARD) callus
    (after 3 weeks and lasts about 3-4 months)
    Osteoblasts make woven bone
  4. Bone remodelling
    Osteoclasts remodel woven bone into compact bone and trabecular bone
    - Often no trace of fracture line on X-rays
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72
Q

Stages of direct fracture healing

A

Unique ‘artifical’ surgical situation
Direct formation of bone (via osteoclastic absorption and osteoblastic formation), without the process of callus formation, to restore skeletal continuity.
Relies upon compression of the bone ends

No callus
Cutting cones cross fracture site
Lay down new osteones

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73
Q

Blood supply to bones

A

Endosteal - inner 2/3rds
Periosteal - outer 1/3rd
Injured by a fracture
Further damaged by surgery

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74
Q

Certain fractures are prone to problems with union or necrosis because of potential problems with blood supply… e.g.

A

Proximal pole of scaphoid fractures
Talar neck fractures
Intracapsular hip fractures
Surgical neck of humerus fractures

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75
Q

What patient factors can inhibit fracture healing?

A 
Increasing age
Diabets
Anaemia
Malnutrition
PVD
Hypothyroidism
Smoking
Alcohol
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76
Q

What medications can inhibit fracture healing

A

NSAIDs (COX 2 NSAIDs inhibit fracture healing more than non-specific NSAIDs)
Steroids
Bisphosphonates (Inhibit osteoclastic activity; Delay fracture healing as a result; Long half-life

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77
Q

Epidemiology of RA

A

FEmales:males 3:1
Clusters in families
If 1st degree relative affected, 2-10 times greater risk

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78
Q

Aetiology of RA

A

HLA-DR4 and other genetic factors
Smoking - definite, multiple studies, ACPA
Infection (EBV< TB, prophyromonas gingivalis)
Hormonal (pregnancy, female prepond)
(Rheumatoid can go into remission with pregnancy and then flares again after pregnancy)

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79
Q

Risk factors for RA

A

Genetic risk factors (60% of risk0

  • Susceptibility genes (e.g. HLA-DRB1)
  • Epigenetic modifications

Non-genetic risk factors (40% of risk)

  • Smoking
  • Microbiota
  • Female sex
  • Western diet
  • Ethnic factors
80
Q

Pathophysiology of RA

A 
Synovitis = immune cells invading a normally relatively cellular synovium in the form of a pannus
Pannus = hyperplastic, invasive tissue leading to cartilage breakdown, erosions and consequent reduced function
81
Q

What is the first area where erosions occur in rheumatoid?

A

The synovial lining = the bare area

And moves in from the margins

82
Q

Clinical features of RA

A

Synovitis - any synovial joint
Symmetrical
Small jts hands and feet early on; shoulder/hip at onset rare
MCPs/PIPs/wrists
Inflammatory - pain, erythema, swelling, EMS
Tenosynovitis, bursitis, CTS
Constitutional sx: fatigue, weakness, low grade fever, weight loss, anorexia

83
Q

Joint features - late signs of RA

A 
Boutonniere
Swan neck
Z-thumn (Boutonniere of thumb)
Volar subluxation of wrist
Ulnar deviation of digits
Radial deviation wrist
Paino key ulnar head
84
Q

Extra-articular features of RA

A

Respiratory - e.g. pulmonary fibrosis
Cardiac - e.g. pericarditis
Dermatological - Rheumatoid nodules, thinning, ulceration
Ophthalmic - scleritis, keratoconjunctivitis
Neurological - carpal tunnel syndrome, peripheral neuropathy
Haematological - anaemia, thrombocytosis

85
Q

RA investigations

A

Bloods: FBC, U&Es, LFTs, ESR/CRP, RF, ACPA

Rheumatoid factor

Imaging - Xray, MRI

86
Q

Rheumatoid factor

A

Autoantibody against Fc portion of IgG
Usually IgM against IgG, though can be any isotype
60% sens, 80% spec
other conditions that also show +ve RF = SLE, SBE, TB, EBV etc.
Part of assesment but is not diagnostic

87
Q

Anti-CCP/ACPA

A

Newer antibody than RF
Sens 60%, spec 80-90%
Picks up those who may be RF -ve.
Predictor of worse prognosis, more erosions, resistant disease
Linked with smoking (increases citrullination)

88
Q

Imaging for RA

A

X-rays: Soft tissue swellign, joint spcae narrowing, erosions, periarticular OP
USS: more sensitive for synovitis and erosions
MRI: bone marrow oedema

89
Q

Differentials of RA

A

OA, SLE, PMR, psoriatic arthropathy, reactive arthritis, sarcoid, Lyme’s

90
Q

Treatment of RA

A

Non-pharmacological:
OT/PTc(mobility help, walking aids etc.), Podiatrists (specialty foot assessment, footwear adjustments). Dieticians

Pharmacological:
Symptomatic
- NSAIDs, Analgesia etc.
DMARDs:
- Glucocorticoids (oral, IA, IM)
- Biologics (anti-TNF, anti-CD20, anti-IL6 etc)
91
Q

How does Methotrexate (a DMARD) work in the Tx of RA

- Side effects

A 
MTX is a systemic immunosuppressant (1 mark). MTX stops the actionof the enzyme dihydrofolate (1 mark) needed for production of DNA 
Is a Dihydrofolate reductase inhibitor
7.5mg-25mg per week orally
Common side effects - GI, hair, skin, rashes
Serious side effects: lungs, liver, BM
Concomitant folic acid
Pregnancy - total contraindication
Withhold during infection and if on abx
(Can't give with trimethoprim)
92
Q

How does Sulfasalazine (a DMARD) work in Tx of RA?

A 
MOA
Salazyopyrin and mesalazine (5-ASA)
RA, IBD etc.
500mg-4g OD orally
Common side effects: GI, rashes
Serious side effects: BM
Safe in pregnancy
Fine in infection unless cytopenic (cf guidelines)
93
Q

Name the biologics used to treat RA

A

Anti-TNF:
Etanercept, infliximab, adalimumab, golimumab, certolizumab
TB, infection risk, MS, CHF

Anti-CD20 (depletes T cell, reduces immunoglobulin levels)
Rituximab
Infection, PML, Hypogammaglobulinaemia

Anti-IL6:
Tocilizumab
Minimal CRP, infections, high lipids

CTLA4-Ig:
Abatcept
Infections

JAK inhibitors:
Tofacitinib and others e.g. Baricitinib
High lipids, infections esp VZV, reduced CRP

94
Q

SLE epidemiology

A

Commoner in Afro-Caribbean, South Asian, Mexican populations
Female preponderance
Symptom onset commonly during reproductive years
Diagnosed 40-50 years
Premature death - average 25 years earlier - infection, cardiovascular disease, ESRF

95
Q

Diagnosing SLE

A

ACR classification criteria

  • Malar rash
  • Discoid rash
  • Photosensitivity
  • Oral ulcers
  • Non-erosive arthritis
  • Pleurisy or pericarditis
  • Renal
  • Neurological
  • Haematological
  • Immunological
  • Positive ANA

At least 4 criteria needed for the classification of SLE (don’t need to have them at the same time)

SLICC classification:
Need at least 1 clinical and 1 serological manifestation (need 4 in total)
Diagnosis possible with just biopsy proven LN and positive immunology
Less specific

96
Q

Problems with ACR criteria (used for diagnosing SLE)

A

Classification rather than diagnositc criteria
Subset of the clinical manifestations - seizure and psychosis only induced for NPSLE; Proteinuria and casts only renal criteria (renal biopsy not included)

97
Q

Clinical presentation of SLE

A 
Variable
Mild to severe disease
Common features:
- Constitutional symptoms (fatigue)
- Cutaneous manifestations
- Arthralgia and arthritis
98
Q

Musculoskeletal manifestations with SLE

A

Inflammatory arthritis
Jaccoud’s arthropathy (ligaments are loose but no erosive properties)

AVN - seen out with steroid use
Fibromyalgia
Osteoporosis

99
Q

Renal involvement with SLE

A

20% will develop ESRF in 10 years
Typically presents within first year or two
Urinalysis, U&E, BP monitored at clinic
ds-DNA - if have level more likely to have renal involvement

Renal biopsy helpful for diagnosis, prognosis and determining treatment

100
Q

Pulmonary effects from SLE

A 
Pleurisy
Pleural effusions
Acute pneumonitis
Diffuse alveolar haemorrhage
Pulmonary hypertension
Shrinking lung syndrome
101
Q

Cardiovascular effects from SLE

A 
Pericarditis +/- effusion
Myocarditis
Vavular abnormalities
Cornoary heart disease - high risk of morbidity and mortality long-term
Risk of MI 50x
102
Q

Neuropsychiatric effects from SLE

A 
Headache (constant)
Anxiety and mood disorder
Seizure
Demyelination
GBS
Mononeuritis
Requires tailored investigation
EEG
MRI
LP
Psychiatric evaluation

Anti-ribosomal P
Associated with mood disorders

103
Q

Gastrointestinal involvement with SLE

A 
Rare
Dysphagia
Reduced peristalsis
Peritonitis
Pancreatitis
Lupus hepatitis
104
Q

Haematological involvement with SLE

A

Anaemia of chronic disease
Autoimmune haemolytic anaemia
Thrombotic thrombocytopenic purpura (TTP) – MAHA, low plts, fever, neuro/renal involvement - check aPLS antibodies
Leukopenia

Can have associated lymphadenopathy and splenomegaly
Thrombocytopenia
- Mild or ITP

105
Q

ANA

A

Present in 95-98% of patients
SLE results due to activation of innate and adaptive immunity
Interaction of self antigens on or released by apoptotic cells
Sensitive but not specific
5% healthy population have positive ANA – need clinical context

106
Q

ENA

A

If ANA positive, helpful to know which antigens affected

Ro/La – SLE, Sjogrens
Ds-DNA – SLE
Sm - SLE
RNP – mixed CTD
Centromere – limited SScl
Scl-70 – diffuse SScl
Histone - drug induced lupus
107
Q

Compliment involvement with SLE

A 
Complement consumption in active disease
C3 more specific
C4 can be chronically low
Trends more important than absolute numbers
> 90% negative predictive value
108
Q

Investigation for suspected SLE

3 medications for SLE

A
  • FBC - leukopenia
  • U&Es - looking for renal manifestations
  • Urinalysis - for renal manifestations
  • ESR/CRP
  • Activated PTT
  • ANA
    ○ Best diagnostic test and is positive in virtually all patients with SLE
    ○ Clinically relevant ANAs are IgG antibodies
    ○ Can also be positive in other connective tissue disease e.g. RA, systemic sclerosis, Sjogren’s syndrome, thyroid disease
  • CXR - if has cardiopulmonary symptoms - looking for pleural effusion etc.
  • ECG - if has cardiopulmonary symptoms

In the UK 3 medications are licensed:

  • Steroids
  • Hydroxychloroquine
  • Belimumab
109
Q

Treatment of mild disease of SLE

A

Cutaneous disease – topical therapies, UVA/UVB sunblock
MSK – NSAIDS, IA/IM steroid, low dose oral prednisolone, HCQ +/- MTX
Serositis – NSAIDS, MTX

110
Q

Treatment of moderate disease of SLE

A

Treatment as per mild disease plus:

Oral prednisolone (0.5mg/kg)
MTX, Aza, MMF, Ciclosporin, Tacrolimus
Belimumab

Refractory disease – Rituximab

111
Q

Treatment of severe disease of SLE

A

Treatment as per mild and moderate disease activity plus:

High dose steroid
DMARDs
B cell therapy
Cyclophosphamide
IVIG – Refractory cytopenias, TTP, Catastrophic APLS
Plasmapheresis – TTP, Catastrophic APLS, Diffuse alveolar haemorrhage, Refractory NPSLE or LN

112
Q

Adjunctive therapy for SLE

A

Topical lubricants for sicca symptoms

Fatigue management groups

Calcium channel blockers for Raynauds

Treatment of co-existent Fibromyalgia

CVS risk

Osteoporosis risk

Co-existent APLS: Anticoagulation in confirmed thromboembolic disease. Use of antiplatelets debatable

113
Q

What is vasculitis?

A

Inflammation of blood vessels
Skin, kidneys, lungs, joints, nerves, ENT

It is an autoimmune reaction

114
Q

What are the different types of vasculitis?

A

Large vessel vasculitis
Medium vessel vasculitis
ANCA-Associated Small Vessel Vasculitis
Immune complex Small Vessel Vadculitis

115
Q

Subtypes of Large Vessel Vasculitis

A

Takayasu Arteritis

Giant Cell Arteritis

116
Q

Features of giant cell arteritis

A

Systemic vasculitis that affects the aorta and its major branches
Prevalence increases with advancing age - Peak incidence between 70-79 years

Female:Male ratio 2-3:1

117
Q

Clinical presentation of giant cell arteritis

A 
Headache - temporal headache with tenderness, subacute onset, constant, little relief with analgesics
Visual symptoms
Jaw claudication
Polymyalgia rheumatica symptoms
Constitutional upset
118
Q

Complications of GCA

A

1) Visual loss
- Acute ischaemic optic neuropathy
- Sudden painless loss of vision, occassionally preceded by amaurosis fugax

2) Large vessel vasculitis
- Vascular stenoses nad aneurysms

3) CVA
- Obstruction or occlusion of internal carotid artery or vertebral arteries

119
Q

Diagnosing GCA

A

Clinical presentation - typical headache, appropriate age, associated clinical features - jaw claudication , constitutional symptoms, PMR

Clinical examination findings - temporal artery asymmetry, thickening, loss of pulsatility

Acute phase response - ESR/CRP

Further investigations

120
Q

Investigations for GCA

A

Temporal artery biopsy - Gold standard: Interruption of internal elastic laminae with mononuclear inflammatory cell infiltrate within vessel wall. Multinucleated giant cells are typical (40-60%) but their absence does not exclude a diagnosis.

Temporal Artery USS
MRI
PET CT

121
Q

Treatment of GCA

A

1mg/kg/day prednisolone (max 60mg) for 1 month
Taper to 15mg by 12 weeks
IV methylprednisolone if visual symptoms
Aim to discontinue corticosteroids by 12-18 months

Aspirin 75mg daily - reduces ischaemic complications

122
Q

Differential diagnosis for cutaneous (small vessel) vasculitits

A

Idiopathic
Drugs
Infection: HCV, HBV, gonococcus, meningococcus, staph.
Secondary RA/CTD/PBC/UC
Malignancy
Manifestation of small/medium vessel ANCA associated vasculitis

123
Q

FEatures of Henoch-Schonlein Purpura (HSP)

A 
Small vessel vasculitis
More common in children, 2-11y
Observed in adults, mean age 43y
Male > Females
FRequently self limiting illness, 4-16 weeks
Good overall prognosis
Mortality 1-2%
124
Q

Clinical features of Henoch Schonlein Purpura (HSP)

A

Classic purpuric rash: buttocks, thighs>lower legs
Urticarial rash, confluent petechiae, ecchymoses, ulcers
Arthralgia/arthritis (lower limb) in 75%

125
Q

Complications of HSP

A

Gastrointestinal: pain, bleeding, diarrhoea, rarely intussuseption. More common in children
Renal: IgA nepphropathy, more common in adults
urological: orchitis
CNS: very rare

126
Q

HSP management and prognosis

A

Often no treatment required
Corticosteroids for certain complciations; testicular torsion, GI disease, occasionally arthritis
Steroids in renal disease: evidence limited. Steroids do not prevent development or progression of renal disease.

127
Q

Clinical presentation of ANCA associated small vessel vasculitis

A

2 month history of: weight loss, fatigue, joint pain, headaches/facial pain

128
Q

Investigations for ANCA associated vasculitis

A

FBC
CRP
U&Es

Urine dipstick: +++ protein, + blood
Urine portin: Creatinine ratio (PCR): 30

129
Q

Initial treatment for ANCA associated vasculitis

A

Intravenous antibiotics

Intravenous fluids for presumed respiratory tract infection with dehydration

130
Q

Immunology of ANCA associated vasculitis

A

cANCA stongly positive

PR3 130 IU

131
Q

Diagnosing ANCA associated vasculitis

A

GRanulomatosis with polyangitis (GPA):
Characterised by granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and often a pauci-immune glomerulonephritis

132
Q

GPA: the classic triad of disease

A

Upper airway/ENT: - rhinitis, chronic sinusitis, chronic ottits media, nasal septal perforation, saddle nose deformity

Lower respiratory: Parenchymal nodules + cavitation, Alveolar haemorrhage

Renal: (rapidly progressive) pauci-immune glomerulonephritis

Constitutional symptoms: Fatigue, weight loss, fever/sweats, myalgia/arthralgia, failure to thrive in elderly

133
Q

Immunological diagnosis of ANCA

A

Autoantibodies directed against cytoplasmic constituents of neutrophils and monocytes

2 means of testing:

  • Indirect immunofluorescence
  • ELISA for PR3/MPO

Looking for cANCA and pANCA

134
Q

cANCA with PR3 suggesstive of…

A

GPA

135
Q

pANCA with strong MPO suggestive of…

A

MPA (or EGPA)

136
Q

2 broad reasons for using immunosuppressant drugs

A

Abnormal inflammation:

  • Inflammatory arthropathies
  • Ulcerative colitis/Crohns
  • Psoriasis

Unwanted normal inflammation

  • Solid organ transplants
  • Bone marrow grafts
137
Q

Steroids (e.g. prednisolone) being used for immunnospuressants
& adverse effects

A

Steroids are excellent immunosuppressants:
Rapid onset (within hours)
Easy to administer
Able to treat wide variety of inflammatory conditions
Limited by intolerable adverse effects, especially at high dose

Weight gain and fluid retention
Glaucoma
Osteoporosis
Infection
Hypertension and hypokalaemia
Peptic ulceration and GI bleed
Psychological/psychiatric symptoms
138
Q

MOA of corticosteroids

A

Modulators of transcription factors

Cortciosteroids enter the cell and bind to a glycocorticoid receptor (either in cytoplasm or nucleus) –> will upregulate transcription factors which will promote anti-inflammatory products

139
Q

Examples of non-steroid immunosuppressive drugs

A

Inhibitors of DNA synthesis:
Methotrexate
Azathioprine
Mycophenolate

Lymphocyte signalling inhibitors:
Cyclosporin
Tacrolimus
Sirolimus
Leflunomide
140
Q

What are the 2 roles that methotrexate has?

A

When given as a high does - is a cytotoxic chemotherapeutic agent

Low dose - immunosuppressant

141
Q

MOA of methotrexate

A

Methotrexate inhibits the folate cycle (has very similar structure to folic acid) and pentose-phosphate pathway –> prevents the development of nucleotides that go into DNA synthesis; therefore preventing DNA synthesis

From 50 drugs database:
Stops the action of the enzyme dihydrofolate needed for production of DNA

142
Q

Methotrexate: effect on cells

A

Causes cell cycle arrest due to inhibition of DNA synthesis

143
Q

Different cellular functions of methotrexate

A 
Folate Antagonism
Inhibiton of adenosine signalling
Inhibits Methyl donors
Eicosanoids and MMPs
Cytokines
Adhesion molecules
144
Q

Adverse effects of methotrexate

A

GI: nausea, vomitting, diarrhoea, hepatitis, stomatitis, hepatotoxicity
Haematological: leukopenia (predisposition to infection, nausea and vomiting)
Kidney failure
Abdominal pain
Birth defects
Others: frequent infections, pulmonary fibrosis

145
Q

What medication is often given alongside methotrexate

A

Folic acid 5mg usually given 4 days after MTX

“Methotrexate on Mondays; Folic acid on Fridays”

146
Q

Indications for methotrexate in practice

A

Most commonly used for rheumatological disease: RA, psoriasis and psoriatic arthropathy
Steroid sparing agent in giant cell arteritis

147
Q

Describe common indications for immunosuppressant drugs and biologic therapies

A

Autoimmune conditions - IBD, Grave’s disease, RA etc.
Post-transplant immunosuppression
Renal vasculitis
Paediatric leukaemia (methotrexate)

148
Q

Mechanism of action of Azathioprine

A

Blocks purine synthesis, mainly in lymphocytes, disrupting DNA synthesis and therefore blocking continued immune response

149
Q

Side effects of Azathioprine

A 
Birth defects
Nausea and vomiting
Hepatitis 
Cholestasis
Dizziness/fatigue
Diarrhoea
Leukopenia
Thrombocytopenia
Skin rashes
Anaemia - bone marrow suppression
150
Q

Azathioprine metabolsim

A

TPMT enzyme vital in reducing active drug in cells
A small percentage of people lack this enzyme
Without TPMT there is an accumulation of the most active metabolites of azathioprine within cells and development of severe toxicity
Checking TPMT activity prior to treatment with azathioprine prevents this problem.

151
Q

Indications for Azathioprine in practice

A

Most commonly used for IBD

Used in other autoimmune disorders: Myaesthenia Gravis & Eczema

152
Q

Clinical use of Azathioprine in practice

A

Given orally on a daily basis
Effects take several weeks to become evident
Need to monitor bloods on a monthly basis

153
Q

MOA of cyclosporine

A

This lowers the activity of T cells by binding to cyclosporin, a protein which facilitates protein binding and regulates activity of other proteins. Inhibition of this inhibits phosphatase activity which is required for activation of transcription factors which up-regulate expression of inflammatory cytokines

154
Q

Side effects of cyclosporin

A 
Nephrotoxicity
Hypertension
Hepatotoxicity
Anorexia and lethargy
Hisituism
Gum enlargement
Peptic ulcers
Fever
Vomiting and diarrhoea
Confusion
HYpercholesterolaemia

When used in post-renal transplantation, is associated with development of gout

155
Q

What is the drug Tacrolimus?

A

Different class of drug to cyclosporin but similar MOA.
More potent activity.
Very similar use to cyclosporin but may be a little tolerated

156
Q

Indications for Tacrolimus use in practice

A

Usually given for organ transplantation - liver, kidney, heart/lung

157
Q

Disadvantages of immunosupressants

A

Immunosuppressants often insufficient to control inflammatory disease with subsequent progression.
Usually have a slow rate of onset limiting usefulness in acute severe disease
Even at low doses they have significant toxicities
Class effects include: Bone marrow suppression, infections.

158
Q

What route are biologic therapies usually delivered by?

A

Parenteral

159
Q

Know the features of mechanical back pain

A

This is non-specific low back pain, accounting for 97% of back pain
Onset at any age and generally worsens with movement or prolonged standing - early morning stiffness for less than 30 minutes

160
Q

Causes of mechanical back pain (non-specific lower back pain)

A

Lumbar strain/sprain is most common cause
Degenerative discs/facet joints - Degenerative disc disease is spondylosis (asymptomatic/pain increases with flexion, sitting and sneezing); Degenerative facet disease (more localised pain, increased with extension)
Disc prolapse/spinal stenosis
Compression fractures - common in elderly patients

161
Q

What are the 3 broad differentials of back pain

A
  1. Mechanical (97%)
  2. Systemic - infection, malignancy, inflammatory
  3. Referred (i.e. no pathology in the back)
162
Q

Non-specific LBP management

A

Education, promote self-management –> advise to stay active
Exercise programme and physiotherapy
Analgesics as appropriate (avoid opiates)
Also acupuncture

163
Q

Mechanical back pain - radiculopathy

A

Disc prolapse: Herniated nucleus pulposus:
May be acute, increase cough
Typicaly leg> back pain; sciatica is the most common nerve affected
Leg pain = dermatomal distribution
Straight leg raising test +ve
Reduced reflexes
Most resolve spontaneously within 12 weeks
Wait 12 weeks before doing MRI scan

164
Q

Mechanical back pain - spinal stenosis

A

Anatomical narrowing of spinal canal:
Congenital and/or degenerative
Often presents with ‘claudication’ in legs/calves - worse walking, rest in flexed position
Natural history variable
Investigations = xray, MRI
Only operate on those whose symptoms are getting worse and worse
Neuropathic agents used e.g. gabapentin

165
Q

Features of cauda equina syndrome

A

Spinal cord ends at L1/2 (need to do lumbar puncture below this)
Neuropathic symptoms - bilateral sciatics, saddle anaesthesia
Bladder or bowel dysfunction - reduced anal tone (need to test perianal sensation and anal tone)

usually a large prolapsed disc
Urgent neurosurgical review

166
Q

Mechanical back pain - spondylolisthesis

A 
'Slip' of one vertebra on the one below:
Pain may radiate to posterior thigh
Increased pain with extension
Born with defect (?)
Often found incidentally on imaging
Often asymptomatic
Rarely needs surgery (only if severe)
167
Q

Mechanical back pain - compression fracture

A

Elderly patient
Often sudden onset, severe
Radiates in ‘belt’ around chest/abdomen
most pain settles in 3/12; chronic mechanical and kyphosis
Associated osteoporosis - risk of recurrence high
Investigations - x-ray, DEXA scan
Treatment:
Conservative (analgesia)
Vertebroplasty (cement) or kyphoplasty (balloon)

168
Q

Referred pain in back

A

Retroperitoneal structures:
Aortic aneurysm - CVS features (BP, inc. HR), collapse
Acute pancreatitis - epigastric pain, relief lean forwards, unwell
Peptic ulcer disease (duodenal) - epigastric pain (meals), history PUD, vomit, blood/malaena
Acute pyelonephritis/Renal colic - history UTI/stones, unwell, radiation, haematuria, frequency
Endometriosis/gynae

169
Q

Systemic causes of back pain

A

Infection - discitis, osetomyelitis, epidural abscess

Malignany

Inflammatory

170
Q

Features of infective discitis

A

High index of suspicion
Fever (may be PUO), weight loss
Constant back pain - rest, night pain
Immunnosppuressed, diabetes, IV drug use

Bloods: FBC, ESR, CRP, blood cultures
Imaging xray, MRI
Radiology-guided aspiration
Most common Staph aureus
IV antibiotics +/- surgical ddebridement
Look for source
171
Q

Malignancy causing back pain

A

History of malignancy: “LP Thomas Knows Best” - Lung, prostate, thyroid, kidney, breast
Onset age >50 years
Constant pain, often worse at night
Systemic symptoms, primary tumour signs and symptoms

X-ray (lytic/destructive), MRI, bone scan
Look for primary site

172
Q

Inflammatory back pain (IBP)

A

Onset <45 years (often teens)
Early morning stiffness >30 mins
Back stif after rest and improves with movement
May wake 2nd half of night, buttock pain

173
Q

Approach to investigating back pain

A

History (red flags)
Examination - back, neurology, abdomen
Most = non-specific LBP = No further investigation

Keep diagnosis under review - investigate if unusual/new features
Imaging - x-ray, MRI
Bloods - if suspect infective/inflammatory, myeloma screen

174
Q

Red flags for back pain

A 
Symptoms:
New onset <16 or >50
Following significant trauma
Previous malignancy
Systemic = fevers/rigors, general malaise, weight loss
Previous steroid use
IV drug abuse, HIV or immunosuppressed
Recent significant infection
Urinary retention
Non-mechanical pain (worse at rest "night pain")
Thoracic spine pain
Signs:
Saddle anaesthesia
Reduced anal tone
Hip or knee weakness
Generalised neurological deficit
Progressive spinal deformity
175
Q

Yellow flags for back pain

A 
Bio-psycho-social model = patients likely to develop chronicity:
ABCDEFW
Attitudes
Beliefs
Compensation
Diagnosis
Emotions
Family
Work relationship
176
Q

Mechanical vs Inflammatory back pain

A

Age of onset - Any age (M); Usually <40 yrs (I)
Onset - Variable, may be acute (M); Insidious (I)
Morning stiffness - <30 mins (M); >30 mins (I)
Exercise: May worsen pain (M); Improves pain (stiffness) (I)
Rest - Often improves (M); No improvement (I)
Night - May imporve (M); May wake during second half of night (I)

177
Q

Features of ankylosing Spondylitis

A

A type of inflammatory back pain.
Low back pain and stiffness for more than 3 months which improves with exercise, but is not relieved by rest.
Limitation of movement of the lumbar spine in both the sagital and frontal planes.
Limitation of chest expansion relative to normal values correlated for age and sex.
Radiological criterion: Sacrolitis grade>=2 bilaterally or grade 3-4 unilaterally

178
Q

Features of Axial Spondyloarthritis (axSpA)

A 
Type of inflammatory back pain.
Enthesitis and dactylitis
Axial involvement
New bone formation/Ankylosis
Extra-articular manifestations *Heterogeneity*
179
Q

ASAS classification criteria for axial SpA

A

In patients with >= 3 months back pain and age at onset <45 years

Sacroilitis on imaging (active (acute inflam on MRI) plus >=1 SpA feature - e.g. inflam back pain, arthritis, enthesis, uveitis, datylitis, psoarsis, IBD, family histoy, elevated CRP

OR

HLA-B27 plus >=2 other SpA features

180
Q

Who gets axSpA and AS?

A

Onset <45 years
Many in late teens-early childhood 15-35 years
AS = mainly male
axSpA = approaching 1:1 gender split

181
Q

Sympotms in axSpA

A 
Inflammatory back pain
Fatigue
Arthritis in other joints e.g. hip, knee
Enthesitis: Achilles tendon, plantar fasciitis
Inflam outside joints = extra-articular:
- Eye: Uveitis
- Skin: Psoiasis
- Bowel - Crohns/UC
- Other: heart, lungs, osteoporosis
Family history of above
182
Q

Recommended imaging for axSpA

A

x-rays = pelvis AP films
Lumbar spin films
MRI allows earlier identification of sacro-ilitits

183
Q

Diagnosis of AS and axSpA

A

Remains a clinical diagnosis

  • suggestive symptoms (inc IBP)
  • Imaging
  • Associated features e.g. family history, psoriasis, colitis, uveitis

Other investigations:
HLA-B27 status
CRP/ESR (usually normal)

184
Q

Treatment options for axSpA

A

-

185
Q

Clinical presentation of OA

A

Joint pain and stiffness
Joint swelling and decreased range of movement
Bouchards nodes - middle finger joint
Heberdens nodes - DCP joints

186
Q

Causes of OA

A

Previous injury
Abnormal anatomy
Obesity
Jobs with high stress on joint/sports

187
Q

Pathophysiology of OA

A

Proteolytic breakdown of the cartilage matrix from an increased production of enzymes, e.g. metalloproteinases.
The proteoglycan and collagen fragments released into the synovial fluid as the disease progresses, Erosion to the cartilage roughens the surface and fibrillation which narrows the joint space.
There is increased production of synovial metalloproteinases, cytokines and TNF that can diffuse back into the cartilage to destroy the soft tissue around the knee.

188
Q

Diagnosis of OA

  • General examination
  • Imaging
A 
General examination - include gait
Systemic examination
Specific joint examination
Look/feel/move/special tests
Neurovascular status distally
Leg length measurement

Imaging - x-ray will show loss of joint space
Blood
Urine
Aspirate

189
Q

Kellgren Lawrence Stages of OA on radiographs

A

Stage 0 - no radiographic evidence of OA is present
Stage 1 - doubtful JSN and possible osteophytic lipping
Stage 2 - definite osteophytes and possible JSN on anteroposterior weight-bearing radiograph
Stage 3 - multiple osteophytes, definite JSN, sclerosis, possible bone deformity
Stage 4 - large osteophytes, marked JSN, severe sclerosis and definite joint deformity

190
Q

Management of OA at different stages

A

Stage 1: Lifestyle - e.g. regular exercise, weight loss
Stage 2: Physiotherapy, strict regimen of exercise and strength training for inc joint stability and weight loss, analgesia as required
Stage 3: NSAIDs, paracetamol or stronger pain-reliefs e.g. codeine, oxycodone; acupuncture, head/cold therapy, massage, local anti-inflam gels; Intra-articular injections of steroid/hyaluronic acid into the joint.
Stage 4: If do not respond to analgesia, physical therapy, weight loss, use of NSAIDs, brace, acupuncture, heat/cold therapy the surgery may be required:
Realignment
Replacement - most common
Excision
Fusion

191
Q

Joint replacement

A

-

192
Q

Features of juvenile idiopathic arthritis

A

This is a disease of childhood onset, characterised primarily by arthritis persisting for at least weeks and currently having no known cause
Chronic inflammatory arthropathy, commonest rheumatic disease in childhood

193
Q

Diagnosis of JIA

A 
Clinical diagnosis but following tests should be considered:
Acute phase response
Anaemia
ANA
RF
X-rays
194
Q

Differential diagnosis of swollen joint in a child

A

Trauma
Inflammation - infection or autoimmune
Malignancy - leukaemia, bone tumours

195
Q

Know similarities and difference between types of chronic inflammatory arthritis in children compared to adults

A

-

196
Q

Recognise the key clinical presentations of arthritis in children and how these differ from adults

A

Clinical signs which occur in children over adults include:
Oligoarthritis
Uveitis
Systemic dises occurs in systemic JIA - fever, rash
Micrognathia occurs in polyarthritis

197
Q

Understand the differences between seropositive and seronegative arthritis

A

Seropositive:
Symmetrical
Affects small and large joints, often widespread
Commonly affects wrists and MCPS

Seronegative:
Asymmetrical
AS/ERA/Reactive/IBD after lower limb weight-bearing joints
Psoriatic affects large and small joints

Phase 3 (15 decks)

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