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Phase 3 > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

Define compartment syndrome

Where are the common sites compartment syndrome occurs?

A

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

Common sites: leg, forearm, thigh

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2
Q

Describe briefly the structure of limbs and the impact of increased volume

A
  • Central skeleton structure with muscles over the top, all covered with fascia
  • Fascia covered the subcutaneous and the skin
  • If there is bleeding/extra fluid under the skin, the body can cope to a degree as skin is elastic
  • Any increased volume under the fascia leads to an increase in pressure because fascia isn’t elastic to allow for extra volume
  • This could cause vessels and lymphatics to collapse and impede the circulation
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3
Q

What are the causes of compartment syndrome?

A
  • Increased internal pressure e.g. bleeding, swelling, iatrogenic infiltrate
  • Increased external compression e.g. cast/bandage (causing constriction), full thickness burns (skin becomes tight and loses elasticity and constricts the limb)
  • Combination
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4
Q

Describe the pathophysiology of compartment syndrome

A
  • Pressure within the compartment exceeds capillary pressure
  • Capillaries collapse and can’t maintain patent lumens, reducing blood flow
  • Muscles become ischaemic and develop oedema through increased endothelial permeability
  • Vicious cycle as muscles that aren’t getting enough oxygen leak fluid and become swollen, further increasing pressure*
  • Autoregulatory mechanisms overwhelmed: to begin, these can cause smooth muscle relaxation of the compartment and constrict inflow
  • Necrosis begins in ischaemic muscles after 4 hours
  • Damaged muscles release myoglobin (toxic to kidneys)
  • Ischaemic nerves become neuropraxic (permanent damage may result after just 4hrs)
  • Irreversible damage: loss of function, limb or life
  • Arterial compromise is later as arteries have strong walls, so will still bring blood to muscle until very late therefore will still feel a pulse in an established process
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5
Q

What happens in an expansible compartment when there is increased compartment content?

A
  • Temporary rise in pressure which may impede venous outflow but the body can recover
  • Compartment expands and pressure stabilises
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6
Q

Compare effects of increased internal and external pressure in a rigid compartment

A

External Compression or Internal pressure e.g. bleeding

  • Pressure increases
  • Venous flow reduced, but arteries inflow continues
  • Pressure continues to rise

If these aren’t resolved

  • Pressure increases, ischaemia and permanent damage result
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7
Q

Describe how ischaemia develops throughout compartment syndrome

A

1 hour

  • Normal nerve conduction, muscle viable, reversible

4 hours

  • Reversible neuropraxia, reversible muscle ischaemia

8 hours

  • Nerve axonotmesis and irreversible change
  • Irreverisble muscle ischaemia and necrosis
  • Permanent changes
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8
Q

What are the end-stage limb changes in compartment syndrome?

A
  • Stiff fibrotic muscle compartments: muscles have no flexibility and no possibility of the muscles working
  • Impaired nerve function: loss of sensation and loss of motor function in the limb
  • Clawing of limbs: flexor compartment is stronger than extensor compartment (wrists and fingers will be flexed)
  • Loss of function
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9
Q

Give 3 examples of causes of internal pressure causing compartment syndrome

A

Trauma e.g. fractures or entrapment

  • Sig. trauma to a limb, even without fracture will cause bleeding within the muscle tissue
  • Fractures bleed from end bones

Muscle oedema/myositis

Intercompartmental administration of fluid/drug

  • hospital setting e.g. dislodgement of a cannula
  • substance abuse

Re-perfusion: vascular surgery

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10
Q

Give 3 examples of causes of external compression causing compartment syndrome

A

Impaired consciousness/protective reflexes

  • If unconscious for 48hrs, can get very localised damage and pressure build-up

Positioning in theatre e.g. lithotomy

  • Iatrogenic as during surgery, the doctors have to control pressures and need to ensure adequate padding

Bandaging/Casts

  • If put in cast early in when swelling is still evolving, therefore cast needs continually reasssessed

Full thickness burns

  • Skin loses elasticity and becomes tight, causing constriction
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11
Q

What are the clinical features of compartment syndrome?

A

Pain: out of proportion to that expected from the injury eg. if analgesia hasn’t worked. Pain on passive stretching of the compartment

Later signs (don’t wait for these to develop before treating)

  • Pallor: poor peripheral blood flow
  • Paraesthesia: sensation lost due to damage to deeper nerves
  • Paralysis: muscles can’t function (neuropraxis)
  • Pulselessness: circulation fully compromise (arterial collapse is a very late sign)
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12
Q

How is compartment syndrome diagnosed?

A

Clinical diagnosis

  • Site (commonly forearm, leg, thigh)
  • Swelling
  • Shiny skin
  • Autonomic responses: tachycardia and sweating
  • Pulses present (until late stage) unless associated vascular injury
  • Paraesthesia and paralysis (usually later): deep nerves affected first

DBP-CP measurement: difference between diastolic BP and compartment pressure

  • Normal: >30
  • Compartment syndrome: <30 ie. compartment pressure is too high
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13
Q

What is the treatment for compartment syndrome?

A

Open any dressings/bandages

  • Ensure skin can be seen and reassess
  • If symptoms settle: observe and reassess
  • If no improvement or deterioration: urgent surgical release, then pt taken to theatre after >48hrs to reassess and delayed wound closure +/- skin grafting/plastics

Surgical release:

  • Full length decompression of all compartments, excision of dead muscle (debridement), leave wounds open (to ensure no further pressure build up)
  • Repeat debridement until pressure is down and all dead muscle is excised
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14
Q

What happens if a patient has presented with compartment syndrome and symptoms have been present for >48hrs?

A
  • No urgent surgical release as the muscle has already lost capacity to recover
  • Irreversible damage already present
  • Non-operative treatment (NB renal failure)
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15
Q

Define rheumatoid arthritis (RA)

A

An autoimmune disease characterised by chronic progressive inflammation of the joints, especially in the hands, wrists, feet and ankles

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16
Q

What are the complications of rheumatoid arthritis if left untreated?

A
  • Joint destruction
  • Deformity
  • Loss of function
  • Extra-articular complications
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17
Q

What is the pathophysiology of RA?

A

Genetic predisposition alongside environmental precipitators

  • Genetics: HLA-DR4
  • Environmental: insult, bacteria, smoking

Cells involved:

  • B and T cells
  • Dendritic cells in the circulation
  • Lots of cytokine response amplifying the process until there’s tissue damage
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18
Q

What is the epidemiology of RA?

A
  • Female (3:1 ratio with men)
  • Age: 30-60yrs
  • More aggressive disease in African Americans and Hispanic populations
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19
Q

What are the symptoms of RA?

A

Symptoms:

  • Pain: Location and pattern important for differential diagnosis
  • Stiffness: Early morning stiffness lasting 1hr before significant improvement

: Joint gelling aka inactivity stiffness

  • Swelling
  • Mainly affected small joints (hands, feet etc)
  • Symmetrical
  • Persistant ie. symptoms last at least 6 weeks
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20
Q

What are the signs of rheumatoid arthritis?

A
  • Synovitis: Swelling at the knuckles
  • Deformity: swan neck, Boutonniere, Z-thumb, ulnar deviation
  • Rheumatoid nodules on extensor surfaces
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21
Q

Describe the differentials for a new arthritis presentation

A

Polyarticular gout:

  • Gout usually affects a single joint but can have polyarticular presentation
  • Hands often involves (MCP joints and whole fingers swollen)
  • More acute presentation (24hr) with lots of pain, erythema and heat

Psoriatic arthritis:

  • 90% patients will have psoriasis
  • Major difference: DIP involved (RA doesn’t reach that far)

Osteoarthritis:

  • Particularly in menopause, there’s a flare up of osteoarthritis
  • Increase in pain and stiffness but no synovitis

SLE (Systemic Lupus Erythematous):

  • Presents with arthralgia rather than arthritis
  • Pain and stiff but not inflamed

Rheumatoid Arthritis:

  • Synovitis, pain, swelling, small joints
  • MCP joints (knuckles)
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22
Q

What laboratory investigations are important in a patient presenting with joint pain and swelling?

A
  • CRP/ESR: acute phase proteins
  • Bone/urate
  • FBC: patients with profound inflammatory response are usually anaemic as they can’t utilise iron with acute inflammation
  • Rheumatoid factor (RF): IgM antibody, directed against IgG. Present in RA, SLE, PBC, Hep B and C, therefore not very specific or sensitive for RA
  • ACPA (anti-citrullinated cyclic peptide antibodies): marker for RA. Very specific but less sensitive, so if present it’s likely to be RA
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23
Q

What is ACPA?

A
  • Marker for rheumatoid arthritis
  • Inflammation leads to cellular damage
  • Enzymatic process leads to the conversion of arginine residues to citrulline
  • Alteration of shape creates a foreign antigen from self: ACPA
  • 90% specific, 60% sensitive
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24
Q

What is RF and what condition(s) is/are they found in?

A
  • Rheumatoid Factor: IgM antibody directed against IgG
  • Seen in RA, SLE, primary biliary cholangitis (PBC), Hepatitis B and C
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25
Q

What criteria are involved in classification criteria for RA?

What is classification useful for?

A

Joint Involvement: large/small joints and number of joints

Serology: presence of RF or ACPA and levels of them

Acute phase reactions: normal or abnormal (elevated) CRP/ESR

Duration of symptoms: under or more than 6 weeks

No diagnostic, useful for evidence-based medicine

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26
Q

What imaging is used for a patient with joint pain and stiffness?

A
  • Plain radiograph
  • Doppler ultrasound: measures synovitis (thickness of synovium) and erosin of the joint space
  • MRI: if ultrasound isn’t easiliy available or an area that isn’t compatible with ultrasound
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27
Q

What is the progression of RA on X-ray?

A

Early RA: normal X-Ray

First changes

  • Peri-articular osteopenia (bones are thinner or less dense around the joint) and soft tissue swelling

Late changes

  • Erosin, joint destruction, subluxation (partial dislocation)
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28
Q

What are the aims when treating RA?

A
  • Reduce inflammation
  • Maintain joint function
  • Prevent progression
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29
Q

What are potential treatment options for rheumatoid arthritis?

A

Reduce inflammation

  • NSAIDs: ibuprofen, naproxen
  • COX-2 inhibitors: celecoxib
  • Steroids: prednisolone, methylprednisolone

cDMARDs - offered first line and within 3 months of symptom onset: Methotrexate

bDMARDs: Infliximab (monoclonal Ab)

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30
Q

What is the class, indication and action of ibuprofen?

A

Class: non-selective NSAIDs (non-steroidal anti-inflammatory)

Indications:

  • Mild-moderate pain relief
  • Rheumatic disorders eg. RA and osteoarthritis
  • Fever (anti-pyuretic effect)

Action:

  • Non-selective inhibition of cyclo-oxygenase (COX 1 and 2) enzymes, descreasing prostaglandin (key inflammatory mediator) production
  • Therefore reduces inflammation, pain and swelling
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31
Q

List 3 side effects of ibuprofen

A
  • Gastric and duodenal ulceration
  • Nausea
  • Diarrhoea
  • Renal impairment
  • Hyperkalaemia
  • Avoid in pregnancy, esp 3rd trimester
  • Avoid in elderly (risk of GI bleed)
  • Avoid in pts with renal impairment (lowest dose)
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32
Q

What is the class, indication and action of celecoxib?

A

Class: selective NSAID

Indication: pain and inflammation in OA, RA and ankylosing spondylitis

Action:

  • Selective inhibition of COX-2, decreasing prostaglandin (key inflammatory mediator) synthesis
  • Thereby reducing pain, inflammation and swelling
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33
Q

List 3 side effects of celecoxib

A
  • Gastric and duodenal ulcers (less so than non-selective NSAIDs)
  • Nausa
  • Diarrhoea
  • Renal impairment (caution)
  • Hyperkalaemia
  • Avoid in pregnancy, esp 3rd trimester
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34
Q

What is the class, indication, administration and action of Infliximab?

A

Class: Anti-TNF agent

  • bDMARD

Indication:

  • RA, ankylosing spondylitis, psoriatic arthritis, juvenile arthritis

Action:

  • Monoclonal antibody
  • Anti-TNF alpha and beta
  • Blocks it’s interaction with TNF receptors
  • TNF a&b are produced ny T cells and macrophages to stimulate cytokines (IL-1,-6,-8)
  • Inhibiting this reduces inflammation

Administration:

  • IV or subcutaneous
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35
Q

What are the side effects and contraindications for infliximab?

A

Side effects
- Flu-like symptoms (fever, headache, runny nose)

  • Immune deficiency (can reactivate TB)

Contraindications:

  • Active infection
  • Active/Latent TB
  • Pregnancy
  • Malignancy
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36
Q

What other measures need taken before and during Infliximab usage?

A

Screening before:

  • Viral hepatitis and HIV
  • Varicella
  • TB (anti-TNF can destabilise protection against TB)
  • Vaccinations: influenza, pneumococcal

Monitoring during:

  • Infections, malignancy, bloods, updated vaccinations
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37
Q

What is the class, indication and action of prednisolone?

A

Class: Corticosteroid (Glucocorticoid)

  • Prednisolone: oral prep
  • Methylprednisolone: parenteral prep

Indication:

  • replacement therapy in adrenal insufficiency
  • post-transplantation immunosuppression
  • exacerbation of a no. of inflammatory conditions inc. eczema, RA, IBD
  • acute asthma

Action:

  • Binds to glucocorticoid receptors
  • Upregulates anti-inflammatory mediators and down-regulates pro-inflammatory mediators
  • This provides immunosuppression
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38
Q

List 3 side effects of prednisolone

A
  • Sleep disturbance
  • Psychosis
  • Hyperglycaemia
  • Moon face and increased abdo fat
  • Immunodeficiency
  • Easy bruising
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39
Q

What is the class, indication and action of methotrexate?

A

Class: Immunosuppressant

  • cDMARD

Indications:

  • Post-transplantation immunosuppression, IBD, Renal vasculitis, Paediatric leukaemia, RA

Action:

  • Folate antagonist
  • Disrupts DNA synthesis
  • Stops the action of the enzyme dihydrofolate needed for DNA production
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40
Q

List 3 side effects of methotrexate

What is the contraindication for methotrexate?

A
  • GI upset
  • Mucosal ulceration
  • Bone marrow suppression
  • Risk of infection

Contraindication: Pregnancy

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41
Q

Compare and contrast the different types of bone

A

Cortical and Cancellous bone

Cortical: Compact

Cancellous: Spongy/trabecular

Cortical: found in long bones (80% of the skeleton)

Cancellous: found at ends of long bones and small bones of hands and feet

Cortical: Slow turnover rate / metabolic activity (impacts fracture healing)

Cancellous: higher turnover rate and undergoes greater remodelling

Cortical: Higher Young’s Modulus i.e. stiff and fractures easily when too much force is applied, and resisitance to torsion

Cancellous: lower Young’s Modulus, therefore more elastic

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42
Q

Name the parts of the bone and the part present in childrens’ bones (and it’s function)

A
  • Diaphysis (shaft)
  • Epiphysis (end)
  • Metaphysis (transitional flares area between diaphysis and epiphysis)

In children: physis (growth plates)

  • Responsible for skeletal growth
  • Allows remodelling of angular deformity after fracture
  • Fractures heal deformities more easily and heal better than adult bones
  • Damage to physeal blood supply will lead to growth arrest (either partial or complete)
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43
Q

What is the composition of bone?

A

Cellular Component and Matrix

Cellular component:

  • Osteoblasts: produce new bone under influence of PTH
  • Osteocytes: 90% of cells in mature bone and mantain extracellular calcium levels. Involves in daily function of looking after the bone
  • Osteoclasts: resorb bone
  • Osteoprogenitor cells: cell differentiate into other cells

Matrix:

  • Organic (40%): Collagen Type I, proteoglycans, growth factors, cytokines. Provides elasticity to bone
  • Inorganic (60%): Calcium hydroxyapatite and calcium phosphate. Provides strength
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44
Q

What is the function of bone?

A
  • Support
  • Protection of organs
  • Movement
  • Mineral storage (stores 90% bodily calcium and 85% of phosphate)
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45
Q

Define indirect fracture healing (secondary)

A

Formation of bone via a process of differential tissue formation until the skeletal continuity is restored via callus formation

  • Inflammation, repair and remodelling
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46
Q

Describe the processes involved in indirect fracture healing

A

Fracture haematoma and inflammation

Blood from broken vessels forms a clot (haematoma) that forms 6-8 hours after injury. Swelling and inflammation to dead bone cells at the fracture site

Fibrocartilage (soft) callus formation

  • New capillaries organise fracture haematoma into granulation tissue, called pro-callus. This lasts 3 weeks
  • Fibroblasts (start lying down collagen) and osteogenic cells invade pro-callus
  • Chondrocyte begin to produce fibrocartilage

Bony (Hard) callus

  • After 3 weeks and lasts 3-4 months
  • Osteoblasts arrive and make woven bone of the fibrocartilage callus

Bone remodelling

  • Osteoclasts remodel woven bone into compact and cancellous bone. Continuity of the bone is restored and over time, the bone is broken down by osteoclasts and compact and trabecular bone is laid down.
  • No trace of fracture line on X-ray
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47
Q

Define direct fracture healing (primary)

A

Direct formation of bone, without the process of callus formation, to restore skeletal continuity

  • Surgical situation with the aim of anatomically reducing the fracture and stabilising it so there is little movement around the fracture site
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48
Q

Describe the processes occuring in direct fracture healing

A
  1. Inflammatory process with haematoma formation
  2. No callus formation
  3. Direct bone formation via osteoclastic absorption and osteoblatsic formation (cutting cones across the fracture site)
    - Compression of end bones via surgery (reducing fracture site)
    - No fracture site (reduced by surgery) so there’s quick invasion of osteoclasts, which form cutting cones
    - Initially clearing out the fracture area then forming new bone
  4. Lay down new osteons (new bone) directly
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49
Q

What advice is given on movement in indirect and direct fracture healing?

A

Indirect fracture healing:

  • A degree of movement is desirable to promote tissue differentiation (even if bone is stabilised in a plaster, there is a little movement)
  • Excessive movement disrupts the healing tissue and affects cellular differentiations

Direct fracture healing:

  • Undesirable
  • Even small amounts of movement are likley to disrupt primary healing and promote callus formation (secondary healing)
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50
Q

What are the different types of bone healing?

A
  • Primary: direct bone healing (surgical intervention)
  • Secondary: indirect bone healing (callus formation)
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51
Q

What can compromise the blood supply to bone?

A

Surgical factors ie. iatrogenous

Anatomical factors eg. avascular necrosis

  • Certain fractures are prone to problems with avascular necrosis due to problems with blood supply:
  • Proximal pole of scaphoid bone fractures
  • Talar neck fractures
  • Intracapsular hip fractures
  • Surgical neck of the humerus
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52
Q

What factors can inhibit proper fracture healing?

A

Patient factors:

  • Increasing age, diabetes, anaemia, malnutrition, hypothyroidism, smoking, alcohol
  • Peripheral vascular diseaseL microcirculation is affected which will affect all vessels

Medicine:

  • NSAIDs, steroids, bisphosphonates
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53
Q

How does ibuprofen affect bone healing?

A

Ibuprofen = NSAID

  • Reduces local vascularity at fractrure site
  • Additional reduction in healing effect independent of blood flow
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54
Q

What is the class, indication, action and side-effects of Alendronate?

A

Class: Bisphosphonate

Indication:

  • Post-menopausal OA
  • Reduces risk of vertebral and hip fractures
  • Paget’s disease

Action:

  • Inhibits osteoclastic bone resorption
  • No effect on bone formation

Side Effects:

  • Abdo pain, dysphagia, dyspepsia, headache
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55
Q

How do bisphosphonates affect bone healing?

A
  • Inhibits osteoclast activity
  • Delayed fracture healing as a result
  • Problem: used for OA
  • Atypical femoral fractures related to those on bisphosphonates without trauma
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56
Q

Define osteonecrosis

A

Aka avascular necrosis

  • Refers to bone infarction and tissue death caused by an interruption of the blood supply near a joint
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57
Q

What is complication of osteonecrosis?

A
  • Death of subchondral bone (ie. bone right under joint surface) can lead to collpase of the joint surface and end-stage arthritis
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58
Q

What are the symptoms of avascular necrosis?

A
  • Most common sites: hip and shoulder
  • Often asymptomatic and found incidentally on imaging: bone death occurs initially and disrupted blood supply, but these only cause problems later down the line. Infarction can cause pain (usually not) but as the joint surface is affected there is pain as secondary arthritis develops

Pain

  • Either from infarction itself or secondary arthritis
  • Osteonecrosis of femoral head: groin pain that worsens with weight-bearing and motion, with limitation in internal rotation and abduction (similar to arthritis)
  • Osteonecrosis in the back: buttock pain
  • Rest pain and night pain
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59
Q

What would be the findings in a physical exam in a patient with osteonecrosis?

A
  • Initially: non-specific, but after osteonecrosis progresses and joint function deteriorates the patient presents with arthrosis
  • Limp
  • Tenderness around the affected bone
  • Restricted motion
  • In femoral head: limation in internal rotation and abduction
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60
Q

What is the epidemiology for osteonecrosis?

A
  • Accounts for >10% total hip replacements
  • 40-50yrs
  • Bilateral in 55% cases
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61
Q

What is the general pathophysiology of osteonecrosis?

A
  • Necrosis always involves subchondral bone first
  • Loss of blood supply, inflammatory processes and involvement of subchondral bone, leading to collapse of cartilage of the femoral head which then cannot repair itself well. As a result, there is a predisposition to post-osteonecrotic arthritis
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62
Q

How does osteonecrosis lead to arthritis?

A
  • Bone is deprived of oxygen (ischaemic), so the tissue dies and cannot undergo remodelling
  • If bone can’t remodel, there is no repair of micro-damage and the mechaical properties of the bone are impaired. If enough damage accumulates, the subchondral bone can be weakened to the point of collapse.
  • Collapse will lead to irregularity of the joint surface which is no longer smooth and can damage the other surface
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63
Q

How is osteonecrosis diagnosed?

A

Plain radiograph or MRI: affected subchondral bone

  • MRI: 91% sensitive and can show changes earlier on that on plain X-ray
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64
Q

What changes are seen on plain xray with osteonecrosis?

A
  • May be normal for months after onset of symptoms

Early findings:

  • Mild density changes, then sclerosis and cysts as it progresses
  • Pathognomonic crescent sign: precedes subchondral collapse. Once this has occured, it’s hard to recover

Late stages:

  • Loss of sphericity, collapse of femoral head, joint space narrowing, degenerative changes in the acetabulum
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65
Q

Give 3 RFs for osteonecrosis

A
  • History of trauma, esp. joint dislocation
  • Corticosteroid use (high dose for prolonged time) or Cushing’s disease
  • Alcohol abuse
  • Sickle cell disease/haemoglobinopathies
  • Often no definite cause, especially if no obvious arthritis on X-Ray
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66
Q

What treatment options are available for osteonecrosis?

A
  • Depends on presence of collapse
  • Aim: reperfusion of the hip (difficult)

Most options: surgical

  • Early stages: core decompression with or without bone graft (removing area of nectrotic subchondral bone and allowing bone to repair to restore blood supply)
  • Late stages: totaly hip arthroplasty (used if evidence of collapse or crescent sign is present
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67
Q

What is the commonest primary bone tumour?

A

myeloma (clonal proliferation of plasma cells)

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68
Q

List 3 common primary sites that can cause metastatic carcinoma in bones?

Which bones do these secondary tumours usually arise?

A
  • Bronchus
  • Breast
  • Prostate
  • Kidney
  • Follicular thyroid

Bone Mets: those with good blood supply ie. long bones (femur, tibia, humerus) and vertebrae

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69
Q

List 3 effects of metastases to bone

A
  • often asymptomatic
  • bone pain (due to destruction)
  • long bones: pathological fractures (minimal trauma and fracture at the neck of the femur or crush vertebral fractures)
  • spinal mets: vertebral collapse, spinal cord compression, nerve root compression, back pain
  • hypercalcaemia
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70
Q

Describe the two types of metastasis in long bone

A

Lytic bone metastasis

  • More common
  • Bone tumour cells produce cytokines
  • these activate osteoclasts (bone resorption): not the tumour cells themselves that resorb bone
  • bone is darker on PET-CT

Sclerotic bone metastasis

  • Eg. prostatic carcinoma, breast carcinoma, carcinoid tumour
  • Tumour cells produce cytokines that stimulate osteoblasts (inc. bone formation)
  • Bone is very white on PET-CT
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71
Q

Define a myeloma

A

Monoclonal proliferation and tumour of plasma cells (which produce antibodies) which reside in the bone marrow, forming a tumour

  • Commonest malignant primary bone tumour
  • Can be solitary ie. single proliferation or multiple myeloma ie. multiple tumours, multiple bones
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72
Q

Explain 3 clinical effects of myeloma

A

Bone lesions

  • punched out lytic foci: pepperpot skull
  • generalised osteopenia: tumour cells replace part of bone, reducing it’s density

Marrow replacement with tumour cells

  • Pancytopenia: anaemia (RBCs pushed out), leukopenia (inc. risk of infection), thrombocytopenia (inc. risk of haemorrhage)

Immunoglobulin (Ab) excess

  • Plasma cells produce immunoglobulin: ESR >100 and immunoglobulin light chains identified in urine

Renal impairment

  • myeloma kidney: precipitated light chains in renal tubules
  • hypercalcaemia
  • amyloidosis
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73
Q

List 3 benign and 3 malignant primary bone tumours

A

Benign

  • osteoid osteoma
  • chrondroma
  • giant cell tumour

Malignant

  • osteosarcoma
  • chrondosarcoma
  • Ewing’s tumour
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74
Q

What is an osteoid osteoma?

What’s the epidemiology?

How does it present?

A

= A smll, benign osteoblastic proliferation

Epidemiology: common, any age esp. adolescents, 2x common in males

Presentation:

  • Esp long bones and spine
  • Pain, worse at night, relieved by aspirin
  • Scoliosis if present in spine
  • juxta-articular tumours: sympathetic synovitis
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75
Q

What is Ewing’s sarcoma?

What is the epidemiology?

How does it present?

A

= A malignant tumour that arises in a primative nerve cell within bone or soft tissue and affects children and adolescents

Epidemiology: peak age is 5-15

Presentation:

  • long bones and flat bones of limb girgles (pelvis, spine and ribs)
  • swelling/pain at site
  • fever
  • fracture
  • Aggressive tumour: early mets via bloodstream to lung, bone marrow and bone
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76
Q

Define osteosarcoma

What is it’s epidemiology

Outline the natural history

A

= A malignant tumour whose cells form osteoid/bone

Epidemiology:

  • Peak age: 10-25, second peak >70yrs (only occurs if patient has pre-exisiting bone abnormality eg. Paget’s, necrosis, radiotherapy)
  • More common in males

Natural history:

  • Highly malignant and early lung metastases (haematogenous spread)
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77
Q

Where is the usual site for osteosarcoma to develop?

List 3 clinical features

How is osteosarcoma managed?

A

Site: metaphysis of lone bones

  • 50% around the knee

CLinical Features:

  • late presentation
  • pain, swelling, loss of function

Management:

  • neo-adjuvant chemotherapy for 8 weeks
  • followed by surgery - remove tumour and replace with customised prosthesis
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78
Q

What is Paget’s disease?

Describe the pathology and which bone’s it mostly affects

What is risk of Paget’s disease?

A

= Chronic bone disorder of excessive bone turnover

  • Enhanced resorption by giant multinucleated osteoclasts followed by formation of disorganised woven bone by osteoblasts
  • formation of structurally weak bone

Site: vertebrae, pelvis, skull, femur

Risk: at increased risk of osteoid sarcoma

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79
Q

List 4 manifestations of Paget’s disease

A
  • bone pain
  • deformity: bowing of long bones
  • pathological fractures
  • osteoarthritis
  • deafness
  • spinal cord compression
  • cardiac failure: high CO
  • Paget’s sarcoma: second osteosarcoma peak in elderly, usually lytic, poor prognosis, early meta to lung and bone
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80
Q

List 2 cartilagenous tumours

A
  • enchondroma
  • chrondrosarcoma
  • osseocartilagenous exostosis
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81
Q

What is an enchrondroma?

Epidemiology

Clinical features

A

= benign cartilage tumour

  • lobulated mass of cartilage within the medulla

Epidemiology: common at any age

Site: 50% hands and feet, long bones

Clinical presentation:

  • Long bones: asymptomatic
  • Hands: swelling, pathological fracture
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82
Q

What is osseocartilaginous exostosis?

What is the risk with osseocartilaginous exostosis?

Epidemiology

Where is it’s origin

A

= benign outgrowth of cartilage with endochondral ossification

Risk: can become malignant (chondrosarcoma)

Epidemiology: common, usually in adolescents

Derived from the growth plate

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83
Q

What is the epidemiology of chondrosarcoma?

List 3 sites they usually arise from

What is the mainstay of treatment

A

Epidemiology:

  • can be de novo (primary) or from a pre-existing enchondroma or osseocartilagenous exostosis (secondary)
  • Central, within the medually canal or peripheral on bone surface
  • 10% of primary malignant primary bone tumours ie. uncommon
  • More common in males

Sites:

  • flat bones ie. pelvis, ribs, axial skeleton, shoulder girgle
  • proximal femur and humerus

Treatment:

  • Surgical removal (tend not to metastasise so removal of tumour with clear margin may come back at later date but won’t metastasise)
84
Q

What is the clinical presentation of acute monoarthritis

A
  • Cardinal features of inflammation: rubor (redness), color (heat), tumor (swelling), dolor (pain) and loss of function

+/- fever

+/- leukocytosis, raised CRP

85
Q

A patient presents with acute monarthritis and fever

What is the main differential diagnosis?

What is the key investigation for diagnosis?

A

this is septic arthritis until proven otherwise

-if any doubt of diagnosis: aspirate (key investigation)

86
Q

Define septic arthritis

What joints are usually involved?

A

Infection within the joint space with micro-organisms

  • It’s a medical emergency

Joint

  • Knee (55%)
  • Elbow, hip, shoulder, ankle, wrist
  • polyarthritis
  • can affect any joint
87
Q

List 3 risk factors for septic arthritis

A
  • previous arthritis
  • rheumatoid arthritis (and management with steroids)
  • trauma
  • diabetes mellitus
  • immunosuppression
  • bacteraemia
  • sickle cell anaemia
  • prosthetic joint
88
Q

Describe the causative organisms of septic arthritis and how they can be differentiated clinically

A

S. aureus

  • Healthy adult, skin breakdown, previously damaged joint
    e. g. RA, prosthetic joint

Strep species

  • healthy adult with splenic dysfunction

Neisseria gonorrhoea

  • young (sexually active) healthy adult, associated tenosynovitis, vesicular pustules, -ve synovial fluid culture and gram stain

Gram -ve infection (aerobic and anaerobic)

  • immunocompromised host with GI infection

Mycobacterial species

  • immunocompromised, recent travel

Fungal species

  • immunocompromised host
89
Q

Outline the pathogenesis of septic arthritis

A

Bacteria enter the joint and deposit in the synovial fluid either by

  • haematogenous spread
  • local invasion/inoculation eg. infeciton from adjacent soft tissue, penetrating damage by puncture/trauma

Rapid entry into synovial fluid

  • no basement membrane and close relationship to blood vessels

Prolonged and severe septic arthritis: risk of damage to underlying cartilage

  • Loss of articular cartilage: may get secondary osteoarthritis
90
Q

What is polyarticular septic arthritis?

Epidemiology

What joints are most commonly involved

How would it present

A
  • Septic arthritis affecting multiple joints

Ave joints affected: 4 (knee, elbow, shoulder and hip)

Epidemiology: >60years, RA prevalent

Presentation: without fever and leucocytosis

  • Usually Staph and Strep species
  • Poor prognosis: 32% mortality
91
Q

What are the key investigations to diagnose septic arthritis?

A

Joint aspirate (synovial fluid)

  • Use a wide bore needle as pus can be viscous and difficult to aspirate
  • use this for Gram stain and culture
  • cell count: >50,000 WBC/mm3
  • insensitive for gram stain but positive culture

Synovium (only received with hip replacement)

  • inflamed synovium with fibrin exudate and numerous neutrophil polymorphs

Blood culture: if systemically unwell

FBC: leucocytosis (high WBC count)

92
Q

What is the management for septic arthritis?

A

Joint aspiration: daily or more frequently as needed

Abx therapy:

  • immediately treated with IV abx
  • based on gram stain/culture and clinical factors

Surgical intervention:

  • only necessary if patient is not responding after 48hrs of appropriate therapy
93
Q

Define crystal arthritis

A

Aka gout

  • form of inflammatory arthritis that develops in those with excess levels of uric acid in the blood and deposition of urate crystals in the joint
94
Q

List 3 modifiable and 3 non-modifiable risk factors of crystal arthritis (gout)

A

Non-Modifiable:

  • age, male, race
  • genetics
  • impared renal function, myeloproliferative disorders

Modifiable:

  • obesity
  • alcohol consumption
  • high-purine diet
  • Medications: aspirin (low doses reduce serum uric acid renal excretion), diuretics
95
Q

What are the clinical presentations of acute and chronic gout?

A
  • recurrent, acute attack of joint inflammation (swelling, heat, redness, pain, loss of function)

Acute gout: stimulates acute inflammatory process

Chronic gout: tophi formation (crystals deposit in surrounding tissues forming hard calcified nodules under the tissue, commonly aorund the elbow

96
Q

How do you investigate a patient with suspected gout?

A

Aspiration of synovial fluid

  • negatively birefringent needle shaped crystals on polarised microscopy

Presumptive diagnosis may be made in absense of synovial fluid aspirate if:

  • typical presentation of podagra (gout affecting the metatarsophalangeal joint between big toe and foot)
  • history of gout flares or hyperurinaemia

Raised sUA (serum uric acid) between attacks: >6.8mg/dL

97
Q

A patient presents with acute, severe monoarthritis

What are the differential diagnoses?

A

Septic arthris: always needs considered with acute monoarthritis

Gout

CPPD (Calcium pyrophosphate deposition disease)/Pseudogout: less commonly affects the metatarcopharyngeal joint, more commonly affects the knee, wrist and sholder

98
Q

What are the goals for treating gout?

A

Acute attacks:

  • relieve pain and reduce inflammation
  • non-pharmacological: cold packs
  • pharmacological: high dose NSAIDs/aspirin/corticosteroids

Long-term:

  • prevent further acute attacks
  • prevent joint damage and elimiate tophi
99
Q

List 3 lifestyle modifications recommonded for a patient with gout?

A

Diet

  • Reduce purine intake (eg. seafood and alcohol)
  • reduce fructose-containing drinks
  • include skimmed milk, low-fat yogurt

Weight loss

  • 1kg/month (avoid crash diets)
  • avoid high protein diets

Moderate exercise

Reduce alcohol

100
Q

What is the pharmacological treatment for gout?

List 3 situations in which treatment for gout would be considered?

A

Treatment: allopurinol

  • recurring attacks (>2 in 12 months)
  • tophi (typical of gout)
  • chornic gouty arthritis
  • renal impairment (<60ml/min)
  • Urolithiasis history (stones in urinary tract)
  • diuretic therapy use
  • primary gout starting at young age <40yrs
  • very high serum urate >500mmol/l
101
Q

What is the treatment for gout?

A

Acute attacks

  • cold packs
  • high dose NSAIDS/aspirin/corticosteroids

Lifestyle modifications

  • diet: low purine diet (seafood, alcohol), low fructose, avoid alcohol, avoid high protein diet
  • weight-loss: 1kg per month, avoid crash diets
  • moderate exercise
  • avoid alcohol

Pharmacological treatment: allopurinol

  • for those with recurring attacks, tophi, chronic arthritis, renal impairment, diuretic therapy use etc.
102
Q

What is the class, indication and action of allopurinol?

In what situation should allopurinol not be used (in relation to gout)?

A

Class: Xanthine oxidase inhibitor

Indication:

  • prophylaxis of gout
  • prophylaxis of calcium oxalate renal stones
  • hyperuricaemia associated with cancer chemotherapy

Action:

  • reduces uric acid synthesis by competitively inhibiting xanthine oxidase
  • reduces serum uric acid level

Avoid:

  • Avoid during acute attacks of gout because it can exacerbate the inflammation
103
Q

What is calcium pyrophosphate deposition disease?

How does this differ from gout?

A

aka pseudogout

  • A painful form of arthritis that occurs suddenly, producing symptoms of gout but caused by different types of crystals

Crystals: calcium pyrophosphate crystals

Differences:

  • Generally older age group
  • Can also be acute or chronic
  • Positive befringent rhomboid shapes crystals on polarised microscopy (smaller more sparse crystals)
  • Blue crystals ppoint right and yellow crystals point left: diagnostic of pseudo gout
104
Q

What two conditions can predispose to pseudogout?

A

Haemochromatosis

Hyperparathyoidism

105
Q

How do the crystals in gout and pseudogout differ?

A

Gout: urate crystals

Pseduogout: calcium pyrophosphate

Gout: negative befringent needle shapes crystals

Pseudogout: positive befringent small rhomboid shaped crystals

Gout: blue crystals point left, yellow crystals point right

Pseudogout: blue crystals point right, yellow crystals point left

106
Q

Define reactive arthritis

A

A sterile synovitis which develops following an infection elsewhere in the body

A chronic form of arthritis featuring the three following conditions:

  • inflamed joints
  • inflammation of the eyes (conjunctivitis)
  • inflammation of the genital, urinary or GI system
107
Q

What are the genetics associated with reactive arthritis

What serology is associated with it?

A

Genetics

  • Strong association with HLA-B27

Serology

  • a serogenative spondyloarthropathies (a group of inflammatory rheumatic diseases)
  • seronegative for rheumatoid factor
108
Q

List 3 caustive organisms from enteric infections and 3 from GU infections causing reactive arthritis

A

Enteric infections:

  • salmonella
  • shigella
  • campylobacter
  • clostridium

GU infections:

  • chlamydia trachomatis
  • neisseria gonorrhoea
  • mycoplasma genitalium
109
Q

What is the clinical picture seen with reactive arthritis?

A
  • acute onset: 2-6 weeks post infection
  • asymmetrical lower limb arthritis (warm, swollen etc.)
  • more common in men
  • systemically unwell - elevated inflam markers and malaise
  • triad of arthritis, conjunctivitis and urethritis may occur
  • inflammation elsewhere can occur: enthesitis, sacroiliitis, anterior uveitis, conjunctivitis
110
Q

List 3 joint changes seen with reactive arthritis?

A
  • lower limb asymmetrical oligoarthritis (arthritis affecting 2 to 4 joints in the first 6 months)
  • dactylitis (sausage digits)
  • enthesopathy (Achilles tendonitis, plantar fasciitis): disorder involving the attachment of a tendon or ligament to a bone
  • inflammatory back pain
111
Q

List 3 extra-articular changes are seen with reactive arthritis?

A
  • conjunctivitis, iritis
  • keratoderma and naily dystrophy
  • urethritis, porstatitis, cystitis, cervicitis
  • stomatitis, diarrhoea
112
Q

Describe the pathogenesis of reactive arthritis

A
  • unclear
  • may involve cross reactivity between bacterial antigen and joint tissue leading to a perpetuating T-helper cell mediated response
  • persistence of antigenic material due to failed clearance possibly due to polymorphisms of toll-like receptos
113
Q

What investigations are suggested for a patient with suspected reactive arthritis?

A
  • joint aspiration to exclude sepsis
  • swabs (cervical/urethral)
  • screen for related infections
  • Bloods: inflammatory markers ie. CRP and ESR
  • chlamydia serology
  • HLA-B27 (prognostic)
114
Q

What is the management of reactive arthritis?

A

Mild: NSAIDs and simple analgesia

Moderate: NSAID, joint aspiration and corticosteroid injection

Severe/Prolonged: Consider DMARD

Antibiotics:

  • initial treatment should be directed to underlying infection
  • some abx have anti-inflammatory properties
115
Q

Define primary vasculitides

What is their general pathology?

A
  • A group of autoimmune conditions characterised by inflammation of the blood vessels
  • Multisystem nature: affects skin, nerves, kidneys, airways, lungs, ENT, joints

General pathology: genetic predisposition interacts with environmental factors, eliciting an autoimmune reaction and causes inflammation of the blood vessels

116
Q

Classify the following vasculitides by vessel size and immune pathology:

Eosinophilic Granulomatosis with polyangiitis (eosinophilic GPA)

Giant Cell Arteritis (GCA)

Granulomatosis with polyangiitis (GPA)

IgA vasculitis (Henoch-Schonlein)

Microscopic Polyangiitis

A

Large vessel vasculitis:

  • Giant cell arteritis (GCA)

Small vessel vasculitis:

  • ANCA-associated vasculitidies: eosinophilic GPA, GPA and microscopic polyangiitis
  • Immune Complex small vessel vasculitis: IgA vasculitis
117
Q

Define Giant Cell Arteritis

What is it’s epidemiology?

A

= Systemic vasculitis causing inflammation of the lining of the aorta and it’s major braches, especially those in the head

Epidemiology:

  • Rare <50years
  • Peak age: 70-80years
  • Female predominant (3x more likely)
  • Prevalence highest in caucasians
118
Q

List 3 clinical presentations of giant cell arteritis (GCA)

A

Headache

  • Bilateral temporal headache with tenderness
  • Subacute onset, constant, little relief with analgesics

Visual symptoms

  • temporary blurring, vision loss or double vision

Jaw claudication (50%)

  • Pain on chewing, relieved on stopping mastication
  • Can be a cause of weight loss and often as problematic as the headache

Polymyalgia rheumatica (PMR)

  • can overlap with GCA on 50% GCA cases
  • subacute onset of shoulder and pelvic girgle stiffness, pain and inflammation with no alternate diagnosis

Constitutional upset

119
Q

List 3 complications of giant cell arteritis

A
  • vision loss
  • cerebrovascular accident ie. stroke
  • vascular stenoses and aneurysm
120
Q

What is the major complication of giant cell arteritis

  • What causes it
  • How does it progress
A

Visual loss

  • caused by acute ischaemic optic neuropathy due to vasculitis and interruption of blood flow in the posterior ciliary arteries
  • sudden painless loss of vision
  • evolves within 24-48 hours
  • if strong clinical suspicion of GCA - treat rapidly due to risk of vision loss
121
Q

Describe the diagnostic pathway to diagnosing giant cell arteritis

A
  1. Clinical presentation
    - typical headache, appropriate age, no alternate diagnosis and presence of associated clinical features eg. jaw claudication
  2. Clinical examination
    - temporal artery asymmetry, thickening, loss of pulsatility and tenderness
  3. Acute phase response
    - elevated ESR/CRP

Diagnosis relies on typical history (tender headache with ass. symptoms) coupled with elevated acute phase response

  1. Further investigations
    - temporal lobe biopsy (TAB): gold standard
    - temporal artery high resolution USS
    - PET-CT

TAB and/or temporal artery USS important for confirmation of diagnosis

122
Q

What is seen on a positive temporal artery biopsy for GCA?

What must be taken into consideration with a TAB?

A

Positive:

  • interruption of internal elastic laminae with mononuclear inflammatory cell infiltrate within the vessel wall
  • multinucleated giant cells are typical but absence doesn’t exclude diagnosis

Consider:

  • GCA affects vessels focally and segmentally (skip lesions) therefore length of biopsy is important
  • Time taken: due to risk of visual loss, patients are started on corticosteroid treatment prior to undergoing definitive investigations
123
Q

What is the classical sign for GCA seen with a temporal artery USS?

What are the benefits?

How specific/sensitive is it?

A

Classic sign: halo sign (hypoechogenic mural thickening in inflamed temporal arteries)

  • Quick and non-invasive

High specificity: +ve USS in symptomatic patients removes need for TAB

Low sensitivity: -ve USS but high pre-test probability for GCA would be sent for TAB

Low pre-test probability and negative USS: excludes GCA

124
Q

How is giant cell arteritis treated?

A

60mg prednisolone for 1 month

  • Aim to discontinue corticosteroids by 12-18 months

If patients relapse on corticosteroids:

  • Relapse: clinical presentation with acute phase response markers
  • Methotrexate: conventional DMARD
125
Q

Define Henoch-Schonlein Purpura (HSP)

Describe the epidemiology

A

IgA, cutaneous small vessel vasculitis

Epidemiology:

  • More common in children (can affect adults)
  • Males > females
  • frequently self-limiting (4-16 weeks)
  • good prognosis
126
Q

List 3 clinical features of henoch-schonlein purpura (HSP)

A
  • classic purpuric rash on buttocks, thighs, lower legs
  • urticarial rash (raised itchy rash appearing on skin)
  • confluent petechiae (pinpoint areas of haemorrhage)
  • Ecchymoses (discolouration of skin due to underlying bleeding)
  • Ulcers
  • arthralgia/arthritis (lower limb)
  • self-limiting (4-16 weeks)
127
Q

List 3 complications of henoch-schonlein purpura (HSP)

A

GI (children): pain, bleeding, diarrhoea

Renal (more adult): IgA nephroapthy

Urological: orchitis (testicular inflammation)

128
Q

How is henoch-schonlein pupura managed?

A
  • often no treatment required as self-limitating
  • corticosteroids for certain complications eg. testicular torsion, arthritis, GI disease
129
Q

What is an occassional trigger for HSP?

A

Strep throat infection (sore throat)

130
Q

Outline the epidemiology for ANCA-associated vasculitis

A
  • associated with the most morbidity and mortality
  • associateed with significant end-organ damage and mortality if untreated or treated late
  • most frequently seen
131
Q

What conditions are grouped together under ANCA-associated vasculitides?

A
  • Eosinophilic Granulomatosis with polyangiitis
  • granulomatosis with polyangiitis (GPA)
  • microscopic polyangiitis (MPA)
132
Q

Define granulomatosis with polyangiitis and it’s pathology

A

= Small vessel vasculitis causing inflammation of the blood vessels in the respiratory and renal systems

Pathology:

  • characterised by granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and often a pauci-immune glomerulonephritis
133
Q

Describe the classic triad of disease seen with glomerulomatosis with polyangiitis

A

Renal:

  • rapidly progressive pauci-immune glomerulonephritis

Upper Airway/ENT:

  • rhinitis, chronic otitis media, chronic sinusitis, saddle nose deformity

Lower Respiratory:

  • parenchymal nodules +/- cavitation
  • alveolar haemorrhage
134
Q

What is the clinical presentation of glomerulomatosis with polyangiitis (GPA)?

A

Classical triad:

  • renal: pauci-immune glomerulonephritis (nephritic syndrome)
  • ENT: rhinitis, chronic sinusitis, otitis media
  • lower resp: alveolar haemorrhage (haemoptysis and dyspnoea) and parenchymal nodules +/- cavitation

Constitutional symptoms:

  • fatigue, weight loss, fever/sweats, malaise/myalgia, failure to thrive in the elderly
135
Q

When undergoing the diagnosis pathway for vasculitis, give 3 situations should vasculitis be a differential?

A
  • Classical presentation
  • Constitutional symptoms
  • Multi-system disease
  • Disease not behaving as expected
136
Q

What does a diagnosis of vasculitis depend on and what specific tests are important?

A
  • comprehensive history and review of symptoms (past and present) NB specifically ask about constitutional symptoms eg. weight loss, malaise, night sweats etc.
  • exlcusion of secondary causes: infection, malignancy, drug-induced

Specific tests:

  • Immunology: ANCA, MPO (in MPA), PR3 (in GPA)
  • Pathology: exlcuding secondary causes (infectious, malignant or drug-induced drivers)
137
Q

Explain the two aims of treatment in vasculitis

A
  1. Remission reduction
    - ie. turning of vasculitis activity
    - higher dose: higher toxicity
    - time pressure: the longer it takes to induce remission, the higher the likelihood of vasculitis induced organ damage and death
    - Prednisolone
    - If severe disease: Rituximab (anti B-cell biologic agent)
    - if moderate severity: methotrexate
  2. Remission maintenance
    - prevent relapse and lower drug toxicities
    - involves prolonged therapies
138
Q

Outline the mechanism of action of glucocorticoids and identify 3 side effects

A

Mechanism of action:

  • bind to glucocorticoid receptors
  • causes up-regulation of anti-inflammatory mediators and down regulates pro-inflammatory mediators
  • this provides immunosuppression
  • rapid onset (within hrs), easy to administer

Side effects:

  • weight gain
  • osteoporosis
  • glaucoma
  • infection
  • HTN and hypokalaemia
  • peptic ulceration and GI bleed
  • psychological/psychiatric symptoms
139
Q

What type of drugs are:

Methotrexate

Cyclosporin

Azathioprine

A

Methotrexate and azathioprine: inhibitors of DNA synthesis

Azathioprine: lymphocyte signalling inhibitor

140
Q

What is the use of methotrexate at a high and low dose?

A

High dose: cytotoxic chemotherapeutic agent

Lose dose: immunosuppressant

141
Q

Outline the mechanism of action of methotrexate

A
  • Disrupts DNA synthesis
  • Stops the action of the enzyme dihydrofolate needed for DNA production
  • Folate antagonist
142
Q

Identify 3 side effects of methotrexate

A
  • bone marrow suppression
  • risk of infection
  • nephrotoxicity
  • hepatotoxicity
  • seizures
143
Q

Name three indications for methotrexate

A
  • post transplantation immunosuppression
  • inflammatory bowel disease
  • rheumatoid arthritis
  • renal vasculitis
  • paediatric leukaemia
  • psoriasis
144
Q

Outline the mechanism of action of azathioprine

A
  • disrupts DNA synthesis
  • blocks purine synthesis mainly in lymphocytes
145
Q

List 3 side effects of azathioprine

A
  • Bone marrow suppression
  • Risk of infection
  • Nephrotoxicity
  • Hepatotoxicity
  • Seizures
146
Q

Name three indications for azathioprine

A
  • post-transplantation immunosuppression
  • inflammatory bowel disease (Crohn’s or UC)
  • renal valculitis
147
Q

Outline the mechanism of action of cyclosporin

A
  • small molecule inhibitor of calcineurin
  • effect of inhibiting signal transduction from the activated TCR complex
  • profound inhibition of T-cell activation
148
Q

List 3 side effects of cyclosporin

A
  • nephrotoxicity
  • hypertension
  • hepatotoxicity
  • anorexia and legarthy
149
Q

List 2 indications for cyclosporin

A
  • usually given for organ transplantation (liver, heart, kidney, lung)
  • sometimes used for inflammatory conditions
150
Q

Outline 2 disadvantages of non-steroidal immunosupprant drugs

A

Effectiveness

  • often insufficient to control inflammatory disease with subsequent progression
  • usually have a slow rate of onset, limiting usefulness in acute severe disease

Toxicity

  • even at a low dose, immunosupprants have significant toxicities
  • eg. bone marrow suppression, frequent infection, nephro/hepatotoxicity
151
Q

List 2 biologic therapies for immunosuppression

A
  • Infliximab
  • Rituximab
152
Q

State the nature of agent and target for the following

  • infliximab
  • rituximab
  • etanercept
A

Infliximab:

  • Nature of agent: monoclonal antibody, anti-TNF therapy
  • Target: soluble cytokine

Rituximab: anti-CD20

  • Nature of agent: monoclonal antibody
  • Target: surface market

Etanercept:

  • Nature of agent: soluble receptor
  • Target: soluble cytokine
153
Q

List 3 indications for infliximab

A
  • anklyosing spondylitis
  • psoriatic arthritis
  • rheumatoid arthritis
  • psoriasis
  • Crohn’s disease
  • juvenile arthritis
154
Q

Outline the mechanism of action of infliximab and etanercept

A
  • anti TNF-a and TNF-b
  • blocks it’s interactions with TNF cell receptors
  • TNF-a and -b produced from macrophages and T cells
  • stimulates IL-1,-8 and -6
  • reduces inflammation
155
Q

State 3 side effects of biologics

A
  • injection site reaction
  • flu-like symptoms eg. fever, chills, headache, runny nose
  • immune deficiency (particularly legionella, listeria and reactivation of TB)
156
Q

State 3 side effects of immunosuppressants

A
  • bone marrow suppression
  • risk of infection
  • nephrotoxicity
  • hepatotoxicity
  • seizures
157
Q

What infections are individuals on infliximab and rituximab more susceptible to?

A

Infliximab:

  • TB (especially disseminated TB): need to screen for TB before prescribing
  • Salmonella and listeria

Rituximab:

  • Generalised increased risk of serious infection
  • High risk of Hep. B reactivation (need to screen and give prophylaxis if necessary)
158
Q

What is the biggest risk with anti-TNF therapy?

A
  • High risk of TB
  • Patients often have defective gramuloma formation and disseminated disease
  • need to screen for latent TB infection prior to treatment
159
Q

How is chronic back pain defined and how is it usually caused?

A

Defined: back pain lasting >3 months

  • Usually mechanical or wear and tear
160
Q

Outline the process of finding the cause of back pain

A

Back pain is a symptom, not a diagnosis

  • >85% isolated back pain is unexplained
  • source of pain is difficultt o determine eg. ligaments, facet joints, paravertebral muscles, discs, spinal nerve roots
161
Q

State the 3 main causes of back pain

A
  • Mechanical (97%): non-specific low back pain
  • Systemic: infection, malignancy, inflammatory
  • Referred ie. no back pathology
162
Q

Outline the features of non-specific lower back pain

A
  • onset: any age
  • generally worsens with movement or prolonged standing
  • better at rest
  • early morning stiffness lasting <30minutes
163
Q

Outline three causes of non-specific low back pain and their features

A

Lumbar strain/sprain

  • most common cause
  • muscle spasms usually settle after 24-48hrs
  • reassurance and symptomatic treatment (non-steroidal)

Degenerative disc disease (spondylosis)

  • usually asymptomatic, inc. pain with flexion, sitting, sneezing

Degenerative facet joint disease

  • more localised, increased pain with extension

Disc prolapse, spinal stenosis

Compression fractures

164
Q

How do you differentiate between pain due to a problem with a disc v facet joints

A

Disc: pain on leaning forward/coughing

Facet joint: pain on extension

165
Q

What the the mainstay of management for non-specific low back pain?

A
  • keep diagnosis under review

- Mainstay: exercise programme and physiotherapy

  • analgesics as appropriate (avoid opiates)
166
Q

Outline the clinical presentation as seen with a disc prolapse

A

ie. herniated nucleus pulposus
- may be acute
- inc. pain with cough
- leg > back pain
- sciatica, radiculopathy (pinched nerve)
- +ve straight leg raise test
- reduced reflexes
- most resolve spontaneously within 12 weeks

167
Q

Should imaging be used as a tool for investigating back pain?

A
  • Poor correlation of pain with imaging therefore no
168
Q

Define cauda equina syndrome

A

impairment of the nerves in the cauda equina, characterised by dull pain in the lower back and upper buttocks and lack of sensation in the buttocks, genitalia and thigh, together with bladder and bowel disturbances

  • Medical emergency
169
Q

Outline the clinical presentation with cauda equine syndrome

A

Neuropathic:

  • bilateral sciatica (usually unilateral)
  • saddle anaesthesia (loss of sensation of buttocks, inner thigh and genitalia)
  • dull pain

Bladder / bowel dysfunction

  • acute emergency
  • reduced anal tone
170
Q

What is the most common cause for cauda equina syndrome?

A

Large disc prolapse

171
Q

Define spinal stenosis

A

Anatomical narrowing of the spinal canal due to disc / osteophytes / congenital / combination of issues

  • ie. congenital and/or degenerative
172
Q

How does spinal stenosis typically present and how is it diagnosed?

A

Presentation:

  • Claudication in legs/calves
  • worse with walking
  • better with rest in flexed position
  • presents bilaterally

Investigations:

  • imaging if diagnosis is uncertain or will alter diagnosis
173
Q

Define spondylolisthesis

How would it present

A

A slip of one of the vertebra forward of backward on the vertebra below

Presentation:

  • asymptomatic in most
  • pain that may radiate to posterior thigh
  • inc. pain with extension (leaning backwards)
174
Q

How does a compression fracture typically present?

A
  • Elderly patient
  • sudden onset of severe pain

(elderly patient with new back pain - red flag)

  • more common in women
  • radiation in belt around the chest/abdomen (dermatomal pain)
  • usually settles within 3 months
175
Q

How would compression fractures be diagnosed and treatment?

A

Diagnossi:

  • X-Ray, DEXA scan, clinical

Treatment:

  • conservative (analgesics)
  • calcitonin
  • vertevroplasty (cement): risk of bleeding
176
Q

Outline 2 causes of referred back pain and the other associated features that could differentiate the cause

A

Aortic aneurysm

  • CVS features (BP, inc. HR), collapse, pulsating abdominal mass

Acute pancreatitis

  • epigastric pain, relief leaning forwards, unwell

Peptic ulcer disease (duodenal)

  • epigastric pain with meals, history of PUD, vomiting, melaena

Acute pyelonephritis / renal colic

  • history of UTI/stones, unwell, radiation, haematuria, frequency

Endometriosis/Gynae issue

177
Q

State the 3 broad systemic causes of back pain

A
  • infection
  • malignancy
  • inflammatory
178
Q

What features asscoiated with back pain would suggest infective discitis?

A
  • Infection of the discs*
  • fever
  • weight loss
  • unwell
  • constant back pain: even at rest, night pain
  • -* high risk groups: immunosuppressed, diabetes, IV drug users
179
Q

What is the most common causative agent of infective discitis?

How is it treated?

A

Causative: Staph. aureus

Treatment:

  • IV antibiotics and surgical debridement
  • Look for source
180
Q

What features alongside back pain would suggest malignancy?

A
  • history of malignancy (lung, prostate, thyroid, kidney, breast)
  • onset >50yrs
  • constant pain, often worse at night
  • systemic features, primary tumour signs (weight loss etc.)
181
Q

What features alongside back pain would suggest it’s due to inflammation

A
  • onset <45yrs (young teens and early adulthood)
  • early morning stiffness lasting >30mins
  • pain improves with movement
  • buttock pain
  • worse at rest, better with activity, NSAIDs help
182
Q

State what ‘red flags’ for low back pain mean and identify 5

A

Fxn: to aid further investigations

  • new age onset <16 or >50
  • following significant trauma
  • previous malignancy
  • systemic symptoms (weight loss, fever)
  • previous steroid use
  • IV drug abuse, HIV or immunosuppressed
  • recent significant infection
  • urinary retention
  • non-mechanical pain (worse at rest)
  • thoracic spine pain
  • saddle anaesthesia
  • reduced anal tone
  • hip or knee weakness
  • generalised neurological deficit
  • progressive spinal deformity
183
Q

What are ‘yellow flags’ for back pain and list 5

A

Yellow flags: psychosocial factors indicative of long-term chronicity and disability

Attitudes toward current problem

Beliefs: misguided belief that they have something serious

Compensation: awaiting payment for an accident

Diagnosis: inappropriate communication, misunderstanding

Emotions: other emotional difficulties eg. depression, anxiety

Family: either overbearing or undersupportive

Work: relationship

184
Q

Compare mechanical and inflammatory back pain under the following

Age onset

Onset

Morning stiffness

Exercise

Rest

Night

A

Age onset

M: any age

I: <40yrs

Onset

M: variable, may be acute

I: insidious

Morning stiffness

M: <30mins

I: >30 mins

Exercise

  • M: may worsen pain
  • I: improves pain and stiffness

Rest

  • M: often improves
  • I: no improvement

Night

  • M: may improve
  • I: may wake during night
185
Q

Differentiate ankylosing spondylitis (AS) and axial spondyloarthritis (axSpA)

A

Spondyloarthritis: inflammatory rheumatic disease (arthritis) of the spine, sometimes also the joints of the arms and legs

Axial spondyloarthritis: affects mainly the spine and sacroiliac joints that connect the lower spine to the pelvis

  • have inflammation causing stiffness and pain

Ankylosing spondylitis: fusion of vertebra in the spinal cord

  • destruction causing deformities of the spine

Many with axial spondyloarthritis will go on to developing a degree of ankylosing spondylitis

186
Q

How is ankylosing spondylitis diagnosed?

A

Criteria: radiological criteria associated with at least 1 clinical criteria

Radiological:

  • Sacroiliitis grade >2 bilaterally or grade 3-4 unilaterally

Clinical:

  • low bak pain and stiffness for >3 months which improves with exercise, not relieved by rest
  • limitation of motion of the lumbar spine in both sagittal and frontal planes
  • limitation of chest expansion relative to normal values correlated for age and sex
187
Q

What are the classification of axSpA

A

Classification with >3 months back pain and age of onset >45 years

  • sacroiliitis on imaging with >1 SpA feature

OR

  • HLA-B27 with >2 other SpA features

SpA features:

  • inflammatory back pain
  • arthritis, enthesitis, uveitis, dacylitis
  • psoriasis
  • Crohn’s
  • good response to NSAIDs
  • family history for SpA
  • HLA-B27
  • Elevated CRP
188
Q

How axSpA diagnosed?

A

Clinical diagnosis

  • classification does not equate diagnostic criteria
189
Q

Outline the clinical presentation of axial spondyloarthritis

A
  • inflammatory back pain
  • fatigue
  • arthritis in other joints eg. hips, fascitis
  • enthesitis: achilles tendon, plantar dasciitis
  • inflammation outside of joints (extra-articular): eyes (uveitis), skin (psoriasis), bowel (Crohn’s/UC)
  • family history of the above
190
Q

What are the treatment options for axial spondylarthritis

A

Modifications:

  • exercise

- education

  • physical therapy, rehabillitation
  • patient associations, self-help groups
  • stop smoking (cessation)

NSAIDs

Biologics

  • TNF inhibitors (infliximab)

Surgery

191
Q

Outline the typical patient to develop AxSpA and AS

A
  • onset <45yrs
  • mainly late teens - early adulthood (15-35)
  • AS: mainly male
  • AxSpA: 50:50 split
192
Q

How is AxSpA and AS diagnosed?

A

CLinical diagnosis

  • suggestive symptoms
  • imaging
  • associated features eg. family history, extra-articular
  • HLA-B27 status, CRP/ESR
193
Q

Outline the pathology of osteoarthritis

A
  • Proteolytic breakdown of the cartilage matrix from an increased production fo enzymes
  • the proteoglycan and collagen fragments are released into the synovial fluid as the disease progresses
  • erosion of the cartilage roughens the surface and fibrillation which narrows the joint space
  • there is inc. production of synovial metalloproteinases, cytokines and TNF which diffuse back into the cartilage and destroy soft tissue around the joint

Result:

  • joint gets destroyed
  • surface of joint erodes and cartilage wears away
  • osteophytes may form
  • subchondral changes occur
  • joint stops functioning as normal
  • surrounding tissues mobility are affects (capsule, ligaments, tendons, muscles, adjacent joints)
194
Q

Outline the clinical presentation of osteoarthritis

A
  • pain, stiffness and swelling
  • clicks / crepitus
  • deformity, reduced mobility
  • walking support, instability

Commonly affects: hands, feet, hip, knee

195
Q

Differentiate between primary and secondary osteoarthritis

A

Primary OA: no known cause

Secondary OA: known cause eg. post traumatic, post infection, post inflammation, post avascular necrosis, developmental/genetic/environmental/nutritional

196
Q

What are the stages of osteoarthritis on X-Ray?

A

Grade 0: no radiographic features of OA present

Grade 1: doubtful joint space narrowing (JSN) and possible osteophytic lipping

Grade 2: definite osteophytes and possible JSN on anteroposterior weight-bearing radiograph

Grade 3: multiple osteophytes, definite JSN, sclerosis, possible bony deformity

Grade 4: large osteophytes, marked JSN, severe sclerosis and definite bony deformity

197
Q

Outline the management for minor (grade 1) osteoarthritis

A
  • if pt. not predisposed to OA, no special therapeutic treatment as symptoms are minimal/ non-existent
  • lifestyle considerations eg. regular exercise, weight loss
  • supplements eg. chondroitin
  • surgery not recommended
198
Q

Outline the management for mild (grade 2) osteoarthritis

A
  • physiotherapy: different non-pharmacological therapies to help relieve the pain and discomfort caused in the mild stage
  • exercise and strength training for increased joint stability and weight loss
  • braces, knee supports, shoe inserts
  • analgesia as required
199
Q

Outline the management for moderate (stage 3) osteoarthritis

A

OTC NSAIDs or pain-relief therapies prescribed

  • if these don’t work, can use stronger pain medication eg. codeine

If no response to physical therapy, weight loss, use of NSAIDs, braces, local anti-inflam gels

  • May require intra-articular injections of steroid/hyaluronic acid in the joint: non-curative byt give short-term relief in symptoms

Some may consider prophylactic realignment surgery

200
Q

Outline the management for severe (Grade 4) osteoarthritis

A
  • no response to analgesia, physical therapy, weight loss, NSAIDs, brace, local anti-inflam cells

Surgery

  • Replacement
  • Realignment
  • Excision
  • Fusion
201
Q

Outline the basic principles of a joint replacement

A
  • take away diseased surafce
  • replace with artifical material the needs to stick to bone
  • materials: titanium, cobalt chrome alloys, ceramics, coated implants
202
Q

Outline the early recovery programme following a joint replacement

A
  • pre-op education and exercise
  • physiotherapist, occupational therapist, discharge planning
  • minal soft tissue dissection surgery
  • reduces recovery from 2 seeks to 1-4 days
203
Q

State 3 advnatages of a total hip replacement

A
  • cup orientation
  • stem orientation
  • assessment
  • more insight
  • may be a better surgical technique
  • better anatomical positioning (long-term results)
  • reduces the ceramic on ceramic noise
204
Q

State 3 complications of a hip replacement

A
  • dislocation
  • fracture
  • leg length discrepancy
  • hip noise
  • implant breakage / failure
  • general: DVT/PE, infection, swelling, stiffness, anaesthesia problems, failure of procedure, death
205
Q

State 3 complications of a knee replacement

A
  • stiffness
  • fracture
  • ligament or tendon damage
  • kneeling difficulty
  • failure
  • general: DVT/PE, infection, swelling, stiffness, anaesthesia problems, failure of procedure, death
206
Q
A

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