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PHASE 2A MEDICINE - ANJALI createdd > Rheumatology and Bone Disease > Flashcards

Rheumatology and Bone Disease Flashcards

1
Q

Cathy age 63, 6month history of increasing joint pain and stiffness, mainly across knuckles and wrists, Lasts an hour or so in mornings, eases off as uses hands, possible some swelling, ibuprofen helped a little, getting her down. Is this inflammatory or degenerative?

A

Inflammatory

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2
Q

History taking and presentation- what are the difference in inflammatory and degenerative disease?

A

Inflammatory: - pain eases with use - Stiffness (significant >60mins, early morning/ at rest (evening) -Swelling synovial+/-bony -Hot and red? -Pt demographics: young, psoriasis, FHx -Joint distribution: hands and feet -Respond to NSAIDs Degenerative: - pain increases with use, clicks/clunks -Stiffness not prolonged <30mins, morning/evening -No swelling or bony swelling -Not clinically inflamed -Pt demographics: older, prior occupation/sport -Joint distribution: 1st CMCJ, DIPJ, knees -Less convincing response to NSAIDs

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3
Q

What should you ask in MSK history taking (pain and stiffness)?

A

-Where is the pain -What is the nature of the pain -Is there any stiffness -Is there any swelling -What is the history of these symptoms -How has this affected function

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4
Q

WHat are the signs that bone pain is due to underlying tumour/infection?

A

Pain at rest and at night, unremitting pain.

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5
Q

Where does RA usually present?

A

Small joints of hands and feet, particularly history of swelling. But can affect any synovial joint inc joints in cervical spine and temporomandibular joint - Small joints in hands and feet - Wrist - Shoulder - TMJ - Temporomandibular joint - Knees - Ankles

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6
Q

Where does Osteoarthritis usually present?

A
  • First carpometacarpal joint -Base of thumb (typically one of the first joints involved) - Hips - Spine - Knees - Big toe
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7
Q

If a patient has symptoms in their hands only / only the big toe of their feet, what could be?

A

Osteoarthritis

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8
Q

Where does Psoriatic arthritis usually present?

A

Widespread joint distribution + Enthesitis + Dactylitis

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9
Q

What is enthesitis?

A

Inflammation and pain where a tendon joins bone

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10
Q

What is dactylitis?

A

Swelling of a whole digit – whole finger/ toe

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11
Q

Describe the chronicity and natural history of gout?

A
  • Acute phase: discrete episodes, completely fine in between - Chronic phase: occurs if left untreated, many years – constant inflammation and pain
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12
Q

Describe the chronicity and natural history of RA?

A

Escalation of symptoms over weeks (6-8 weeks), relatively rapid in onset and then stays at a level

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13
Q

Describe the chronicity and natural history of reactive arthritis?

A

Extremely bad at beginning (around 10 days after instigating infection), then symptoms tend to get better.

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14
Q

What is the cause of reactive arthritis?

A
  • Classic reactive arthritis: triggered by bacterial gastroenteritis or STIs - Less classical: post viral
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15
Q

What is palindromic RA?

A

Inflammatory symptoms that abate either completelet/ nearly completely but then come back in episodes over a period of time. - Some patients evolve into having full blown RA - Some patients continue with palindromic RA

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16
Q

What is the wrist joint?

A

Radio-carpal joint: scaphoid and lunate articulate to form this

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17
Q

What do the carpal bones articulate with?

A

Metacarpals and also form the wrist joint

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18
Q

What is the Carpal tunnel?

A

Carpal bones form an arch in the coronal plane and a membranous band – flexor retinaculum spans between the medial and lateral edges of the arch  carpel tunnel. Median nerve goes through the carpal tunnel

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19
Q

What muscles attach to the metacarpals?

A

Interossei muscles via the medial and lateral surfaces (which are concave)

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20
Q

Name the metacarpals in order

A

Metacarpal I = thumb Metacarpal II = index finger Metacarpal III = middle finger Metacarpal IV = ring finger Metacarpal V = little finger

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21
Q

What are the 3 important joints in the hand/ fingers?

A
  • MCP: Metacarpophalangeal joints (knuckles)
  • PIP: Proximal interphalangeal joint (one closes to the MCP)
  • DIP: Distal interphalangeal joint (one at the end of the finger)
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22
Q

What is the clinical picture of RA?

A
  1. Symmetrical, polyarthritis, if untreated  deformity
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23
Q

What features may RA hands show?

A
  • -Ulnar deviation
  • Subluxation of MCP
  • Swan neck deformity
  • Erosion on X ray
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24
Q

What is ulnar deviation?

A

patients fingers are drifting towards the ulnar border of the hand – caused by the extensor tendons at the metacarpalpharyngeal joints slipping of their normal anchorage point –> puls the fingers round to ulnar border

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25
Q

What is subluxation of MCP?

A

– swollen and prominent due to synovial thickening + MCP joint itself is sitting higher than the level of the fingers (fingers have subluxed down) bc of the destructive nature of the arthritis

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26
Q

What is a swan neck deformity?

A

Proximal interpharyngeal joint is distended and the distal interpharyngeal joint is flexed due to a tendon issue

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27
Q

What is the typical RA picture on X ray?

A

Erosions of the bone – chunk of bone disssapears bc of inflammatory cytokines in joints

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28
Q

How can Osteoarthritis affect the hands - name the specific terms?

A

Nodal OA hands:

  • Bouchard’s node: PIP
  • Heberden’s node: DIP
  • these terms are specific to OA
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29
Q

How can OA affect the knees?

A

Loss of the medial/ lateral compartment joint space –>leg changes shape –>

  • bow legged / knock kneed - Varus (bowelegged deformity)
  • Valgus (knock kneed / lateral deformity
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30
Q

What is Ankylosing spondylitis?

A

Inflammatory arthritis of the spine that causes fusion of the spinal joints and a fixed rigid spine

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31
Q

Where does gout usually affect?

A

Big toe joint: 1st MTPJ arthritis , also midfoot, ankle knee, other joints

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32
Q

What is chronic polyarticular tophaceous gout?

A

Persistant polyarticular gout due to: renal disease (urate build up) or genetic defect in enzymes that process urate. White material = urate crystals that build up in the soft tissues

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33
Q

What are the 2 important inflammatory maker blood tests in rheumatology?

A
  • ESR
  • CRP
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34
Q

What is ESR?

A

Erythrocyte sedimentation rate , take a blood sample and centrifuge it, if there is inflammation the red cells get coated by fibrinogen + other inflammatory proteins –>red cells stick together in big clumps and will fall faster when centrifuged. Measure of the rate of which the red blood cells fall to the bottom of the test tube - Quicker they fall –>the more inflammation present (ESR high)

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35
Q

For how long will ESR stay high after the inflammatory trigger has gone?

A

It will stay high for quite a long time (120 day lifespan rbc) – useful in clinical practice bc you will see the time lag between some of the other markers. Rises and falls slowly (days to weeks)

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36
Q

When is ESR raised?

A

Inflammation and infection

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37
Q

What is a disadvantage of ESR?

A

Prone to false positives

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38
Q

Who is at risk of false positively high ESR?

A
  • Age, female, obesity, racial difference (South east asia have a naturally higher ESR), hypercholesterolaemia, high Immunoglobulins (inc myeloma), anaemia
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39
Q

What is a useful way of diagnosing SLE?

A

ESR will go up but other measures (like CRP) will not

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40
Q

What is CRP?

A

C reactive protein – acute phase protein (pentameric peptide) that is made in the liver

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41
Q

What is CRP made in response to?

A

Proinflammatory cytokines inc IL-6, IL-1, TNF (released in inflammation/infection)

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42
Q

What is the role of CRP?

A

Binds to damaged cells and activates the complement cascade

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43
Q

What happens to CRP during the course of an infection?

A

Rises and falls rapidly - High at 6hrs, peak at 48hrs after the onset of inflammatory/infective process - Come down again quite quickly

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44
Q

What are auto-antibodies?

A

Immunoglobulins that bind to self antigens –>cause inflammation in perfectly normal parts of the body

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45
Q

In RA what autoantibodies may be present?

A
  • RF: Rheumatoid factor
  • anti-CCP: Cyclic cittrulinated peptide
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46
Q

In SLE what autoantibodies may be present?

A
  • ANA: anti nuclear antibody (binds to antigens within cell nucleus)
  • dsDNA: double stranded DNA
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47
Q

What is Spondyloarthritis (SpA)?

A

describes a group of conditions that have common features :

  • affects spine and peripheral joints
  • familial clustering and links to certain type 1 HLA antigens (HLA B27)
  • Ankylosing spondylitis (axial SpA) - Enteropathic Arthritis - Psoriatic Arthritis - Reactive arthritis - Acute anterior uveitis (iritis) - JIA (enthesitis-related) - Undifferentiated SpA
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48
Q

What tissue type are these all SpA conditions associated with (to some extent)?

A

HLA B27

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49
Q

What is HLA B27

A

Human leucocyte antigen B27, Class 1 surface antigen (present on all cells except rbc), encoded by Major histocompativility comples (MHC) on Chr 6.

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50
Q

What is the function of HLA B27

A

Antigen presenting cell

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51
Q

In the UK, how many people are HLA B27 positive?

A

9%. Stand alone this is not important but if the patient has symptoms it is relevant

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52
Q

What is the global distribution of HLA B27 positivity like?

A
  • Higher in northern hemisphere: Scandanavia, northern states and also have higher incidences of spondyloarthritis - Lower near the equator
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53
Q

Why is HLA B27 linked with disease? 3 main theories:

A

3 main theories:

  • ‘molecular mimicry’ infection –> immune response–> infectious agent has peptides very similar to HLA B27 molecules–> auto immune response triggered against HLA B27
  • Misfolding theory: HLA has the propensity to misfold–> when it is unfolded it can joint together and accumulate inside the endoplasmic recticulum–> triggers and inflammatory response ‘the endoplasmic recticulum upr’–> cascade of inflammatory cytokines (IL-23,17)
  • HLA B27 heavy homodimer hypothesis: Under certain circumstances the B27 heavy chains can join together to form dimers–> accumulate in the endoplasmic reticulum–> triggers same erupr–> cascade of inflammatory cytokines. Dimers can also upregulate other components on the immune response like NK cells Incomplete and doesnt explain all the disease we see in SpA
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54
Q

How many patients with ankylosing spondylitis are HLA B27 positive?

A

85%

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55
Q

What are the clinical features of SpA?

A
  • Spinal disease: inflammatory back pain, over time–> restricted movement and change to spine – straight spine, neck forward , exaggerated kyphosis of the thoracic spine, patients often stand with knees bent to not lose centre of gravity
  • Ethesitis: inflammation of tendon. Achilles tendon, patellar tendon, elbow – tennis elbow
  • Oligoarthritis: 1 or 2 large joints that are inflamed. Knee joint
  • Iritis/acute anterior uveitis: eye is red, uncomfortable, photophobic and may have blurring of vision, if irregular iris/pupil –previous episodes of inflammation that have causes scarring inside the eye. Ask about history or red painful eye associated with blurring of vision and photophobia
  • Psoriasis: psoriatic plaques – red raised skin with scale on top, very itchy. Elbows, fronts of knees, other places
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56
Q

How is SpA arthritis different to RA?

A
  • RA mainly affects the small joints of hands and feet - Polyarthritis
  • SpA affects 1 or 2 large joints -Oligoarthritis
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57
Q

What are the clinical features of SpA?

A

SPINEACHE: S-Sausage digit (dactylitis) P-psoriasis I-inflammatory back pain N-nsaid good response E-enthesitis (heel) A-arthritis C-Crohns/Colitis/ Elevated CRP H-HLA B27 E-eye (uveitis)

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58
Q

What percentage of patients with spinal inflammation have a high CRP?

A

50%

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59
Q

What are the signs that it is Inflammatory back pain?

A
  • Young age of onset <40 yrs
  • Long duration – months or years
  • Better with excersize, worse with rest
  • Stiffness in the morning
  • Pain at nightime – often in the second half of night (as they stiffen up through night), can wake up with pain,
  • Thoracic spine, front of rib cage, alternating buttock pain
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60
Q

What is buttock pain a sign of?

A

Sacro-iliac joint pain

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61
Q

What is the sequence of damage in ankylosing spondylitis/axial spondylarthritis?

A
  • Repeated episodes of inflammation in the vertebral corners (bright white)
  • Over time the body repairs itself with fat cells, which replace the areas of inflammation
  • However: once there is fat cells within the bone –> triggers an automatic response whereby new bone (calcium) is formed along the lines of the ligaments –> fusion in the spine (syndesmophytes)
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62
Q

How is ankylosing spondylitis staged?

A
  • Non radiographic stage (back pain, sacroilitis on MRI may be present)
  • Radiographic stage (eventual progression to syndesmophytes)
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63
Q

How long will it take ankylosing spondylitis to progress to the radiographic stage?

A

May take up to 10yrs

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64
Q

How is diagnosis of ankylosing spondylitis made?

A

In patients with more than 3 months back pain and age of onset less than 45 yrs: • Sacroillitis on imaging (MRI) + atleast 1 SpA feature • HLA-B27 positive + atleast 2 SpA features (don’t need imaging)

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65
Q

What will MRI show in ankylosing spondylitis?

A

Bone marrow oedema – subchondral periarticular (bright white on a T2 MRI scan)

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66
Q

What are the features of ankylosing spondylitis on X ray?

A

Late stage - X ray is not diagnostic imaging - aim to pick up before it gets to this stage -

  • Syndesmophytes: calcium that grows on the front of the spine – they join together, eventually will happen in multiple levels of the spine.
  • Pic shows lumbar spine and bit of thoracic spine syndesmophytes - Sacroiliitis: fusion of the sacro-iliac joints
  • End stage: Bamboo spine – vertebrae seem all joined together as a block of bone and cant see the disc space
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67
Q

What is the final stage of AS?

A

Sever kyphosis of thoracic and cervical spine - makes forward vision v difficult/impossible

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68
Q

What is the management of AS?

A
  • Physiotherapy (excersize)
  • Anti-inflammatory NSAIDs- pain control
  • Biological drugs: anti TNF, IL-17 blockers, IL-23 blockers
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69
Q

What is psoriatic arthritis?

A
  • Can be just peripheral joint involvement
  • Can have it alongside spinal involvement
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70
Q

How can psoriatic arthritis present on hand?

A
  • Dactylitis – very painful, patient thinks they have broken their toes
  • DIP joint swelling
  • Nails extensive psoriasis changes: brittle, flaky, lifted away from nailbed, multiple dents
  • Skin psoriasis
  • Z thumb
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71
Q

What are hidden sites of psoriasis?

A
  • Behind and in the ear
  • Nail pitting >5 or 6
  • Psoriasis in umbilicus
  • Scalp
  • Back of bottom
  • Genital psoriasis
  • Onycholysis: nail is thickened and lifted away from nail bed – little finger has triangle across the corner of the nail
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72
Q

What is Arthritis mutilans?

A

Form of psoriatic arthritis, destructive arthritis affecting the small joints of the hands  erodes the joint away. Fingers deformed, not fixed joints very bendy

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73
Q

What is the managament of SpA?

A
  • If only spinal involvement (Ankylosing spondylitis) –> biological drugs
  • If spinal involvement + peripheral arthritis (Ankylosing spondylitis + psoriatic arthritis) –>combination of biological drugs + oral DMARDs (Methotraxate, sulphosalazine, leflunomide)
  • If only psoriatic arthritis –>oral DMARDs
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74
Q

What is reactive arthritis?

A

Describes a triad of: Arthritis, conjunctivitis and (sterile) urethritis. Can be a one off episode or recurrent epsidoes or the beginning of a lifelong SpA condition. Following an infection (bacterial gastroenteritis, STIs)

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75
Q

What is the aetiology of reactive arthritis?

A

Typical infection – bacterial gastroenteritis, STIs (Chlammydia most common , also gonorrhoeae)

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76
Q

What are the signs of Reactive arthritis?

A
  • Oligoarthritis (knee joint most common), conjunctivitis and urethritis
  • Keratoderma blenorrhagica: on soles of feet
  • Circinate balanitis: genitial inflammation
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77
Q

What is enteropathic arthritis?

A

Inflammatory arthritis associated with ulcerartive colitis or Crohns disease.

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78
Q

What is the clinical picture of enteropathic arthritis?

A

Has the exact same joints distribution as psoriatic arthritis: oligoarthritis of the large joints, often they don’t mirror the bowel inflammation

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79
Q

What is the Tx of enteropathic arthritis?

A
  • Methotrexate is good for both
  • Azathiproine(good for bowels) but not for arthritis
  • Anti-TNF is good for both
  • Newer biological drugs -vedolizumab (good for bowels) but can be bad and trigger inflammatory arthritis
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80
Q

Definition of osteoporosis

A

Systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture

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81
Q

What are the common fractures in osteoporosis?

A
  • Vertebral fracture (sudden onset back pain, 2/3 asympomtatic)
  • Colle’s fracture (wrist broken end of radius bent backwards following fall on outstretched arm)
  • Hip-Proximal femur
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82
Q

What is the prevalence of fracture due to osteoporosis?

A

VERY COMMON - Women>50: 50% - Men >50: 20%

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83
Q

fracture in Osteoporosis commonly occur due to?

A
  • Trauma (can be minor – changing duvet, lifting heavy if osteoporosis)
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84
Q

What determines risk of fracture?

A

BONE STRENGHT

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85
Q

What determines bone strength?

A
  • BMD (combo of peak bone mass and rate of bone loss)
  • Bone size (bigger, thicker = stronger)
  • Bone quality (bone turnover, architecture, mineralisation)
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86
Q

When is peak bone mass reached?

A

Around 30

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87
Q

How do bones grow throughout age?

A

Long bones during childhood, spine grows fast during puberty, after longitudinal growth – grow width (cortical apposition) still grow that way - Women who got period early have shorter legs and longer backs

88
Q

When does bone loss really start to progress?

A

50 ,especially in women during menopause

89
Q

What resorbs bone?

A

Osteoclasts

90
Q

What builds bone?

A

Osteoblasts

91
Q

What is normal bone turnover called?

A

Quiescence

92
Q

What happens in postmenopasual osteoporosis?

A

Loss of restraining effects of oestrogen on bone turnover: - High bone turnover - Predominantly cancellous bone loss - Microarchitectural disruption -loss of resistance to fracture that is NOT FULLY REFLECTED IN THE BONE DENSITY MEASUREMENT

93
Q

Why can ageing cause osteoporosis?

A
  • Increased tunrnover at the bone/bvascular interface within cortical bone –> results in structural weakness (trabecularization of cortical vone) - bones preferentialy preserve the vertical trabeculae and sacrifice the horizontal ones -Eular Buckling theory (horizontal trabeculae removed and 16x less strong)
94
Q

What happens to resorbtion space with ageing?

A

Increases - Lots more points of weakness in the bone –>increase fracture risk

95
Q

How is osteoporosis diagnosed and classified?

A

Bone densitometry - BDM - DEXA scan :

  • T score ->-1.0 = normal
  • -1.0 to -2.5 = osteopenia
  • < -2.5 = Osteoporosis
  • < -2.5 plus fracture = severe osteoporosis
96
Q

What sites does DEXA measure?

A
  • Lumbar spine
  • proximal femur
  • distal radius
97
Q

What are the measures that DEXA outputs?

A
  • BMD
  • T score
98
Q

What is the T-score?

A

Standard deviation score in DEXA scan. Compared with gender matched young adult average (peak bone mass). To diagnose osteoporosis

99
Q

Who is susceptible to osteoporosis (risk factors)?

A
  • Ppl with Inflammatory diseases – RA, seronegative arthiritis, connective tissue diseases also IBS
  • Endocrine disease: Hyperthyroidism , primary hyperparathyroidism, Cushings, menopause early or iatrogenic, male hypogonadism, anorexia/ athletes
  • Anorexia
  • Athletes who overtrain
  • Reduced skeletal loading: low body weight, immobility
  • Medications: glucocoritcoids, depo-provera (contraception), aromatase inhibitors (BCR tx), GnRH analogues (BRC, endometriosis), androgen deprivation
  • Previous fracture
  • FHx
  • Alcohol
  • Smoking
100
Q

Why do inflammatory diseases increase the risk of osteoporosis?

A

IL-6,1 etc stimulate osteoclastic activity

101
Q

What is heritable about osteoporosis risk?

A
  • Bone density
  • angle and lenght of femoral neck
102
Q

How do you predict the risk of fracture?

A

FRAX

103
Q

What are the classes of Tx for Osteoporosis?

A
  • Anti resorptive (bisphosphonates, HRT, Denosumab)
  • Anabolic(Teriparatide)
104
Q

What are the Txs of osteoporosis?

A
  • First line Tx: Oral bisphosphonates (alendronate, risedronate) daily or weekly. Can also be IV Ibadronate/Zoledronate
  • Denusomab
  • Teriparatide (multiple vertebral fractyres/very low BMD)
105
Q

What is Tx in osteoporosis guided by?

A

Risk of fracture !!!! not BMD alone

106
Q

Bisphosphonates mode of action

A

Synthetic analogues of bone pyrophosphate –> adhere to hydroxyapatite and inhibit osteoclasts (by inhibiting an enzyme in the cholesterol synthesis pathway - Farnesyl Pyrophosphate Synthase)

107
Q

What is denosumab?

A

Monoclonal antibody to RANK ligand. Administered as single subcut injection every 6 months . Tx of osteoporosis, Anti-resorpbtive agent –> increased BDM, increases fractures at spine

108
Q

How effective is denosumab?

A
  • Rapid acting and very potent anti-resorptive
  • Good fracture risk reduction
  • REBOUND INCREASE OF BONE TURNOVER WHEN STOPPED
109
Q

Disadvantage of Denosumab?

A

REBOUND INCREASE OF BONE TURNOVER WHEN STOPPED

110
Q

What is Teripartide?

A

PTH analogue – the first 34 aa of PTH

  • Rebuild and reconnect trabeculae- cortex gets thicker
111
Q

When is Teripartide indicated?

A

Severe Osteoporosis - very expensive

112
Q
  1. What is the most severe form of joint inflammation?
A

Gout

113
Q

What is inflammatory arthritis?

A

New onset joint swelling: - Synovial - Often red - Warm to touch Inc: RA, SpA, Crystal arthritis and Septic Arthritis

114
Q
  1. What is synovial swelling?
A

Compressible, tender, soft and squishy NOT BONY

115
Q
  1. What are the symptoms of inflammatory arthritis?
A
  • Starts abruptly – new onset joint swelling
  • Worse in the morning/ inactivity
  • Stiffness >30mins USUALLY LONGER
  • Constant or intermittent
  • Joint swelling: synovial, often red and warm to touch
116
Q
  1. What will CRP be in inflammatory arthritis?
A

Most cases CRP will go up (sometimes not with psoritatic)

117
Q
  1. What are types of Inflammatory arthritis?
A
  • Rheumatoid Arthritis
  • Seronegative spondyloarthritis (Psoriatic, ank spond, reactive arthritis, enterohepatic – crohns and ulcerative colitis related)
  • Crystal arthritis – gout(uric acid crystals) and pseudogout (calcium pyrophosphate crystals)
  • Septic arthritis
118
Q
  1. What is septic arthirits?
A

Infection within the joint itself. ALWAYS THINK ABOUT THIS, make firm diagnosis by fluid culture from joint . VERY PAINFUL PRESENTATION

119
Q
  1. How common is septic arthritis?
A

Uncommon, rare

120
Q
  1. Who is susceptible to septic arthritis?
A
  • IV drug use
  • immunosuppressed
121
Q

Prevalance of Rheumatoid arthritis?

A

1% of population, more common in females (2-3x)

122
Q
  1. What are the risk factors for RA?
A

2 BIGGEST:

  • FHx
  • Smoking
    • Middle age (but any age)
  • Female gender
123
Q
  1. What is the clinical picture of RA?
A
  • Symmetrical polyarthritis: small joints – hands, wrists, feet (PIP,MCP)
  • Big joints involved later (bad prognostic sign if involved at presentation)
  • NO SPINAL INVOLVEMENT (apart from some ligamental involvement at start of neck)
124
Q
  1. What does seronegative mean?
A

Not associated with autoantibody production. SpA is a seronegative inflammatory arthritis

125
Q
  1. What is the clinical picture of SpA?
A
  • Assymetric big joints, with spinal involvement
  • Associated symptoms: inflammatory bowel, GI infection, eye inflammation an psoriasis
126
Q

Is SpA is more commen in men or women?

A

Men

127
Q

What is the clinical picture of Psoriatic arthritis?

A

Several diff patterns:

  • RA like
  • DIP joint involvement (this is more common in OA)
  • Mutilans – rare
  • Dactylitis – sausage digit/toe
  • Assymetrical large joints + spine
128
Q
  1. What does nail involvement in psoriasis predict?
A

Arthritis developing – psoriatic arthritis (pitting, oncolysis, dactylitis)

129
Q
  1. What is dactylitis characteristic of?
A

PSORIATIC ARTHRITIS

130
Q

What will CRP be like in Psoriatic arthritis?

A

May not be significantly raised

131
Q
  1. What is the clinical picture of Crystal arthritis?
A

Typically acute intermittent episodes of joint inflammation.

  • Gout: feet, ankles, knees, elbows, hands. Hyperuricaemia (high levels of uric acid in blood)
  • Pseudogout: wrists, knees, hands, chondrocalcinosis on X ray
132
Q
  1. What is the most common cause of crystal arthritis?
A

Gout

133
Q
  1. What are the crystals in gout?
A

Urate

134
Q
  1. What are the crystals in pseudogout?
A

Calcium pyrophosphate

135
Q
  1. What are the risk factors for gout?
A
  • 6x more common in men
  • beer (purine)
  • renal impairment diuretics(increase conc of uric acid)
  • aspirin (reduces renal excretion of uric acid)
  • FHx
136
Q
  1. What are the risk factors for pseudogout?
A
  • 3x more common in women
  • typically on background of OA
137
Q
  1. What form of crystal arthritis can you see on an X ray?
A

Pseudogout – chondrocalcinosis on X ray (calcification of cartilage – see cartilage you shouldn’t be able to see – knees, around thumb base) -diagnostic

138
Q
  1. What is the clinical picture/ symptoms of osteoarthritis?
A
  • Usually slow onset – months to years
  • Typically weight bearing joints, DIP, PIPs, thumb bases, big toes
  • Minimal early morning stiffness (gelling)
  • No variability to joint swelling
  • Clear changes on X ray
139
Q

What is the CRP in degenerative disease -OA?

A

Normal

140
Q

How would the joint feel in OA?

A

ROCK HARD

141
Q

What is gelling a sign of?

A

Osteoarthritis

142
Q

What is gelling?

A

Osteoarthritis - degenerative disease: Patients describe like the fluid in joints is set to jelly, when you first stand up from sitting you have to unset it and get it moving but within a few minutes you are fineee – NO PROLONGED STIFFNESS.

143
Q

What is the onset of OA compared to the onset of inflammatory arthritis?

A
  • OA: slow - over years
  • Inflammatory: rapid - weeks to months
144
Q

When making a diagnosis of an inflammatory arthritis - what questions should you ask patient + consider?

A
  1. Is it inflammatory (visible joint swelling +feel, Elevated CRP, Variable symptoms with flares)
  2. Which joint pattern?
  3. Associated symptoms/risks (psoriasis, inflammatory eye/bowel, FHx,smoking)
  4. Tests (RF/CCPA for RA, uric acid for gout, X rays)
145
Q
  1. What are specific markers for RA?
A

RF ,CCP+

146
Q
  1. What are specific marker for gout?
A

Uric acid blood test – in between attacks. (if someone has an attack of gout the uric acid has partly left the blood to deposit in the joint)

147
Q
  1. What will inflammatory arthritis affecting joints look like on X ray?
A

Will take a year to see the damage on an x ray (MRI, ultrasound more sensitive). Don’t relay on X ray for early stage in diagnosis

148
Q

Case presentation: Involvement of MCP, PIP joints, wrists, elbows, knees and feet, symmetrical distribution - what is it?

A

Rheumatoid arthritis: symmetrical, involves small joints dominated, large joints later

149
Q

Case presentation: - Asymmetric, some little joints, some big joints and spine - what is it?

A

Psoriatic arthritis

150
Q

Case presentation: DIP, thumb bases, weight bearing joints, big toes - what is it?

A

Osteoarthritis

151
Q

Case: Mrs Green 58, pain in hands, worsening over 12-18 months, decreased grip strenght, stiff in morning - 15mins, worst in end of fingers, thumbs. Paracetamol and occasional ibuprofen helps a bit. Tests: CRP 1.3 (1-5) RF 24 (0-20) X ray- degenerative changes in DIP joints of both hands and first CMC joints, no erosions what is the diagnosis?

A

Osteoarthritis

152
Q

Does a positive RF indicate Rheumatoid arthritis?

A

NO

  • RF at a low level of positivity does not mean patient has RA
  • RF IS VERY NON SPECIFIC
  • 10x more people with a positive RF than have RA
153
Q

Case: Mrs Jones 43, 4 week history of pain and definite swelling across MCPs and PIPs of both hands, started suddenly, struggling to use hands, stiffness 1-2hrs in morning, tingling in hands at night, started with pain under toes in last week. On examination: swelling MCPs, decreased fist tender MCP and MTP squeeze Tests: CRP 12.7 RF 38 CCP 150 (0-10) ANA - weak positive X rays: normal What is the diagnosis?

A

Rheumatoid Arthritis

154
Q

Describe the pathology of joint inflammation in RA?

A

Synovitis:

  • Synovial cells proliferate
  • Increase in synovial cells and immune cells creates a - Pannus (thick, swollen synovial membrane with granulation tissue made up of fibroblasts, myofibroblasts and inflamatory cells)
  • Over time–> pannus damages cartilage and other soft tissues, can also erode bone - also increased osteoclastic acitivity due to increased RANKL -Chronic inflammation –> angiogenesis - allows more inflammatory cells to arrive
155
Q

Describe the pathophysiology of RA?

A

Autoimmune disease:

  • Genetic factors: HLA-DR4, HLA-DR1 +Environmental factors: Smoking, bronchial stress, pathogens
  • Cause citrullination of self antigens
  • Inflammatory cell recruitment into joint space(cytokines – IL-6,TNF-alpha) due to macrophages and T and B cells
  • Synovitis and Joint destruction
156
Q
  1. What is citrullination?
A

Amino acid arginine in T1 collagen and vimentin –>converted to Citrulline. Now body doesn’t recognise this and produces autoantibodies. Occurs in RA pathophysiology

157
Q

What autoantibodies in RA?

A
  • RF: autoantibodies to the Fc portion of IgG: 75-80% of RA patients
  • Anti-CCP: targets citrullinated proteins. More specific and sensitive to RA
158
Q

What happens when these autoantibodies bind to their targets in RA?

A

Form immune complexes which accumulate in the synovial fluid–> activate complement system–>promotes joint inflammation

159
Q
  1. What is the clinical presentation of RA?
A
  • Pain and swelling of joints: small joints, hands, wrists, forefeet
  • Prolonged early morning stiffness
  • Sudden change in function
  • Intermittent, migratory or additive involvement
160
Q

What joint does RA NOT INVOLVE?

A

DIP joint (that is OA typically)

161
Q

On physical examination of patient with RA, what will be found?

A
  • decreased grip strength/ fist formation
  • Often subtle synovitis: MCPs, PIPs, MTPs, ankles
  • DIPs spared
  • Usually symmetrical
  • Deformity is unusual at presentation
162
Q

What investigations/ tests for RA and their typical result?

A
  • FBC: may show a norochromic/normocytic anaemia
  • ESR and CRP: raised
  • Serology(autoantibodies): anti-CCP 70%, RF in 70%
  • X rays: may be normal in early disease, may see soft tissue swelling
  • MRI and Ultrasound more useful
  • Aspiration of joint: may be necessary if effusion present
  • MSK ultrasound: demonstrates persistant synovitis
163
Q

What is a much more specific test for RA?

A

Anti-CCP: almost never false positive. Also selects subset of patients with the most aggresive disease

164
Q

How specific is RF?

A

Not very, false positive in 10-15% of population

165
Q

What are useful ways of monitoring Tx in RA?

A
  • CRP/ESR - bc their raised in proportion to the inflammation
  • MSK ultrasound: deciding on the need for DMARDs/ assesing their efficacy
  • X ray
166
Q

When can the X ray be normal in RA?

A

Early stages

167
Q
  1. What are the X ray findings associated with RA?
A
  • Early stage= normal x ray
  • Soft tissue swelling ,periarticular osteopenia ,Joint space narrowing ,Bone erosion
168
Q
  1. When does bone erosion occur in RA?
A

Had disease for long time many months (6-12months)

169
Q

Why can periarticular osteopenia occur around the inflamed joints?

A

Bc inflammation increased bone turnover rate–> stimulates osteoclastic activity

170
Q

Describe what this X rays shows and suggest a diagnosis

A

RA for atleast 10yrs, not well controlled:

  • Sparring of DIP
  • PIP Joints: erosions
  • MCP joints: complete destruction, cant see in any joint space
171
Q

What is the aim of Tx in RA?

A

Suppress inflammation as completely and quickly as poss once diagnosis Is confirmed.

Below shows without Tx the disease course:

172
Q

Tx pathway of RA?

A
  • Initial Tx: csDMARD monotherapy using oral methotrexate, leflunomide of sulfasalazine as soon as poss, ideally within 3 months of onset of persistant symptoms. Escalate dose as tolerated
  • Inadequate response to conventional DMARD: bDMARDS (Biological therapies -Upadacitinib then Rituximab
  • Symptomatic control: NSAIDs
  • Flare ups: Corticosteroid injections or tables
  • Ice - reduce heat
  • Splints and rest

173
Q

What is the management of Gout?

A

Acute attack:

  • Colchicine or High dose NSAID (excluding Aspirin)
  • After 24-48hrs reduced doses are given for a further week
  • PPIs co-prescribed in patients using NSAIDs

Long term:

  • Patient should be offered urate lowering therapy (severe gout, frequent attacks etc)
  • Xanthine oxidase inhibitors: Allopurinol or Febuxostat
174
Q

What is the most common type of arthritis?

A

Osteoarthritis

175
Q

How common is OA?

A
  • Most common type of arthritis
  • 1 in 5 women and 1 in 10 men >60 globally - 80% limitations in movement, 25% cannot perform daily activities of life
176
Q

What is the economic cost of OA?

A
177
Q

Describe the pathophysiology of Osteoarthritis?

A

NOT WEAR AND TEAR- COMPLEX DISEASE, some overlap with inflammatory:

  • Mediated by cytokines: IL-1,TNF-alpha, NO
  • Driven by mechanical forces: abnormal stress and loading, obesity
  • Main pathological features: Loss of cartilage, disordered bone repair
178
Q

What is osteoarthritis?

A

Results from damage to articular cartilage induced by genetic, metabolic and biochemical factors. Leads to an inflammatory response affecting cartilage, subchondral bone, ligaments, menisci, synovium and capsule

179
Q

What is the histology of a synovial joint?

A
180
Q

What are the pathological changes in OA?

A
  • Progressive loss of Articular Cartilage –> friction between the bones –> inflammation –> triggers pain through nerve endings in joint space
  • Decreased elasticity of cartilage
  • Osteophytes: bone grows outwards on the edges –> makes the joints look wider : Heberden nodes (PIP), Bouchard nodes (DIP)
181
Q

What cells produce and maintain the articular cartilage

A

Chondrocytes - embedded in an extracellular matrix containin T2 collagen

182
Q

What is the function of articular cartilage?

A
  • No friction between bones (along with synovial fluid)
  • Elastisity and high tensile strenght –> help weight bearing joints distribute weight so the underlying bone absorbs the shock an the weight
183
Q

What are the weight bearing joints?

A
  • Knees
  • Hips
  • Lower lumbar spine
  • Ankles
184
Q

Risk factors for OA?

A
  • Age: rare in <45, common >65
  • Gender: more common in females, after menopause
  • Genetics: OA hip Less common in afro-carribean and Asian populations, OA in hand rare in black and malayasian
  • Obesity
  • Occupation: manual labour (hand and small joints), farmers (hip), footballers (knees)
  • Local trauma – OA affects damaged joints more rapidly than healthy joints
  • Inflammatory arthritis e.g RA
  • Abnormal biomechanics e.g joint hypermobility (flexible ppl), congential hip dysplasia, neuropathic conditions( T2DM, syringomyelia)
185
Q

Why does age increase risk of OA?

A
186
Q

Why does obesity increase the risk of OA?

A
  • Fat tissue is pro-inflammatory
  • Mechanical factors for weightbearing joints-hip and knees
187
Q

Symptoms of OA?

A
  • Joint Pain with movement +/- weightbearing: often reason patient seeks advice medially,
  • Short lived morning joint stiffness
  • Functional impairment: walking, daily activities
188
Q

What are the signs of OA?

A
  • Alteration in gait
  • Restricted movement
  • Joint swelling (especially small joints)- bony enlargement, effusion, synovitis (if inflammatory component)
  • Crepitus
  • Tenderness
  • Deformities
  • Bony instability and muscle wasting
189
Q

What are the radiological features of OA?

A

MOST IMPORTANT - only when damage is advanced

  • Joint space narrowing (not specific to OA, may see in erosive inflammatory arthritis)
  • Osteophyte formation - bone tries to repair to compensate for loss of cartilage
  • Subchondral sclerosis
  • Subchondral cysts
  • Abnormalities of bone contour (not specific to OA)
190
Q

Case: A 70 yr old man attends with painful, swollen finger joints, pain is worse when he uses his hands and towards the end of the day. Mornign stiffness in the joints lasting 10-15mins. On examination there is bony swelling of all of the PIP and DIP joints bilaterally.

WHat is the diagnosis?

.

A

Osteoarthritis - nodal OA

191
Q

Primary prevention of MSK disease?

A

Reduce prevalence of risk factors (inc role of physical activity and nutrition, pregnancy, early years, children, older people,)

Modifiable risk factors: Vit D/calcium deficiency, obesity, physical activity, injury prevention

192
Q

What are the types of OA?

A
  • Localised OA: nodal, hip, knee
  • Crystal associated OA
  • Primary generalised OA (RARE)
  • Erosive OA(RARE)
193
Q

What is nodal OA?

A

Involved hand joints, usually afffected one at a time over several years, relapsing remitting course over a few years. Bony swelling and cyst formation, reduction in hand function

  • Heberdern’s nodes - DIPs
  • Bouchards nodes - PIPs
194
Q

What are the risk factors for the ‘nodal’ form of OA?

A
  • Female predominance
  • Around female menopause
  • FMHx
195
Q

What does this X ray show, suggest diagnosis

A
  • Heberdens and Bouchards nodes: marginal osteophytes
  • Joint space loss (DIP,PIP)
  • MCP is sparred

Nodal form of OA

196
Q

What is secondary prevention in MSK disease?

A

Screening for asymptomatic:

  • Congenital hip dislocation
  • Osteoporosis
197
Q

WHO definition of MSK health

A
  • Healthy disease free muscles, joints,bones.
  • Ability to carry out a wide range of physical acitivities/ functions both effectively and symptom free
198
Q

Classification of MSK conditions

A
  • Inflammatory
  • MSK pain (Osteoarthritis, back pain)
  • Osteoporosis and fragility fractures
199
Q

What is tertiary prevention in MSK disease?

A

Management of conditions to reduce impact

  • Back pain
  • Joint pain
  • Minor injuries
200
Q

Case: 70 yr old lady presents with progressive pain in knees, pain is worse on exertion particulalrly using the stairs, she struggles with tasks around the house and had to move in with daughter, pain frequently wakes her up from sleep.

Suggest a diagnosis

A

Knee OA

201
Q

What is the life course approach to prevention of MSK disease?

A

202
Q

What is Knee OA?

A

Characteristics

  • Generally bilateral
  • Strongly associated with nodal OA in elderly women
  • Medial compartment of the knee is most commonly affected –> Varus (bowlegged deformity)

Disease course

  • Without significant trauma, evolution is very slow
  • Once established, often remains stable for years
203
Q

What compartment of the knee is most commonly affected in knee OA?

A

Medial

(often retropatellar OA is also present)

204
Q

What does this X ray show? Suggest Diagnosis

A
  • joint space narrowing in the medial compartment of knee
  • Sclerosis
  • osteophytes

OA of knee

205
Q

What does this X ray show (abnormal is right), suggest diagnosis

A

Skyline view of the knee –> shows lots of cartilage loss in the patellofemoral joint

OA of knee

206
Q

Case: 65 yr old lady presents with increasingly severe pain in the right groin, it is becoming difficult to walk, the pain wakes her up from sleep several times a night. Suggest a diagnosis? What should you do?

A

Hip OA

  • Groin pain

Refer to orthopoedics

207
Q

What is Hip OA?

A

2 types:

  • Superior-pole Hip OA: MOST COMMON. Joint space narrowing and scleoriss affects weight bearing upper surface of the femoral head and adjacent acetabulumn. most common in men, unilateral in presentation, both hips can become involved
  • Medial cartilage loss: more common in women, associated with nodal OA, usually bilateral, more rapidly disabling
208
Q

Case: 55 yr old woman presents with pain and swelling of the small joints of the hands, pain is worse on exertion but also worse after prolonged rest, morning stiffness lasting an hour each day.

On examination: bony swelling of the joints-in keeping with nodal OA but there is also some additional soft tissue swelling over the joints with associated tenderness

Her RF and anti-CCP are negative

What is the diagnosis?

A

Erosive/inflammatory OA

  • rare subgroup
  • DIPs and PIPs are inflamed and equally affected with poor functional outcome
  • Radiology shows marked osteolysis - erosion
  • Destructive phases are followed by phases of remodelling
208
Q
A
209
Q

What is Erosive OA?

A

Rare subgroup of OA:

  • bony erosions seen radiologically
  • DIPs and PIPs inflammed and equally afected
  • Poor functional outcome
  • Consider DMARD therapy
210
Q

In what subset of OA would you consider using DMARD therapy?

A

Erosive OA, as there is an inflammatory component

211
Q

Case:A 64 yr old woman with known OA of the knee complains that her left knee frequently ‘locks’ in a flexed position. What is this? what is the Tx?

A

Loose body (intra-articular body)

Classical symptom is LOCKING

Tx: Arthroscopy - refer for orthopoedics for them to remove it. THIS IS THE ONLY INDICATION FOR ARTHROSCOPY IN OA

212
Q

What is the only indication for arthroscopy in OA?

A

Loose body (intra-articular body)

Patient will complain of locking

213
Q

What is the non-medical management of OA?

A
  • Patient education
  • Activity and excersize
  • Weight loss
  • Physiotherapy
  • occupational therapy
  • Footwear
  • Orthoses
  • Walking aids: stick - can unload hip by up to 60%, frame
214
Q

What is the management of OA?

A

1-Non medical: self management, excersize, weight loss

2-Medical/Pharmacological:

  • Paracetamol/topical NSAIDs(preffered over oral NSAIDs), topical capsaicin
  • Transdermal patches: Byprenorphine, lignocaine
  • If insufficient pain relief consider opiod analgeisics - risk v benefit, wary in elderly
  • Intra-articular steroid injections - role remains unclear

3-Surgical: Consider for referral when:

  • Joint symptoms have a substantial impact on their QoL
  • Should have been offered at least 3 core Tx’s for OA
215
Q
A

PHASE 2A MEDICINE - ANJALI createdd (9 decks)

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