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Phase 2 - MSK Flashcards

1
Q

Define Osteoarthritis

A

An AGE related, DYNAMIC REACTION PATTERN of a joint in response to INSULT and INJURY - also has a genetic component

(aka NON-INFLAM DEGENERATIVE MECHANINCAL SHEARING OF JOINTS, usually age related)

  • All tissues of joint involved but esp ARTICULAR CARTILAGE
  • Changes in underlying bone at joint margin

Multifactorial in origin

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2
Q

Subtypes of osteoarthritis

A
  • Nodal OA - strong genetic component
  • Inflammatory/erosive OA
  • Hip OA
  • Knee OA
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3
Q

OA Staging

A

1 = doubtful = ~10% cartilage loss
2 - osteophyte development starts (looks like little bony outpouchings)
3 - increased loss of joint space + osteophytes
4 - severe

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4
Q

Epidemiology of OA

A
  • Most common condition affecting synovial joints
  • Most important condition relating to disability as result of locomotor symptoms
  • 8.75 million people in the UK have sought treatment for OA

Impact to UK economy ~1% GNP (2008):

  • Lost days of work
  • Incapacity benefit
  • Treatment strategies
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5
Q

Causes/risk factors of OA

A
  • AGE (cumulative effect + decline in neuromuscular function) - esp >50 y/o
  • FEMALE (post menopause)
  • GENETIC predisposition - esp if POLYARTICULAR (COL2A1)
  • OBESITY
    • thought to be due to the low grade inflam state
    • release of IL1, TNF, ADIPOKINES (Leptin. adiponectin)
  • Occupation
    • manual labour - small hand joints
    • farming hips
    • football - knees

Others:

  • Direct trauma
  • Inflam arthritis
  • Abnormal biomechanics (e.g. congenital hip dysplasia, hypermobility, NEUROPATHIC CONDITIONS)
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6
Q

Percentage of people over 65 with osteoarthritis

A

80-90% over 65 will have radiographic evidence of OA and 50% will have symptoms

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7
Q

Pathophysiology of osteoarthritis

A

Characterised by:

  • LOSS OF CARTILAGE due to shift in homeostatic balance of tissue (i.e. imbalance between the cartilage being worn down and the chondrocytes repairing so net loss)
    • Matrix metalloproteinases increase -> collagen degradation + cyst formation -> increased mechanical wear -> stiffness + pain
    • Nitric oxide further activates metalloproteinases
  • DISORDERED BONE REPAIR (attemt to overcome via T1 collagen -> formation of osteophytes)

A METABOLICALLY ACTIVE + DYNAMIC PROCESS - mediated by CYTOKINES:
- IL-1
- TNFa
- NO
and DRIVEN BY MECHANICAL FORCES

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8
Q

SIgns + symptoms of OA

A
  • PAIN (may not be present despite radiographic change)
  • Transient Morning stiffness <1 hr (some say < 30 mins)
    • stiffness gets worse over course of day/with more activity
  • FUNCTIONAL IMPAIRMENT:
    • Walking
    • Activities of daily living
      • Inability to do stuff -> muscle wasting -> make things worse

Signs:

  • Altered GAIT
  • JOINT SWELLING (usually asymmetrical, hard + non-inflamed)
    • Bony enlargement
      • Heberden’s (DIP) and Bouchard’s (PIP) nodes + esp used joints 1st MCP, MTP, hip/knees(in nodal)
    • Effusion
    • Synovitis (if inflammatory component)
  • Limited range of motion
  • Crepitus (crackling noises - esp in patellar OA)
  • Tenderness
  • Deformities

No extra-articular presentation

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9
Q

Investigations for OA

A

X-RAY - remember findings as JOSSA (like bone fossa)

  • Joint space narrowing
  • Osteophyte formation
  • Sub-chondral sclerosis
  • Sub-chondral cysts
  • Abnormalities of bone contour

Bloods normal

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10
Q

Diff diagnosis OA

A

Rheumatoid or Reactive Arthritis

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11
Q

Non-medical management of OA

A
  • Patient education/support
  • Activity/exercise
  • Weight loss (can be a pre-requisite for surgery)
  • Physiotherapy
  • Occupational therapy

Weight bearing supports:

  • Footwear/orthoses (can get wedge to improve weight bearing)
  • Walking aids: stick, frame
  • Splints
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12
Q

Pharm treatments of OA

A

Pain killers/anti-inflam

Topical

  • NSAIDs
  • Capsaicin cream

Oral

  • Paracetamol
  • NSAIDs (with caution - may be paired with PPIs)
  • Opioids (don’t work for chronic pain -> addiction)

Transdermal patches

  • Buprenorphine (strong opiod)
  • Lignocaine (local anaesthetic + antiarrhythmic)

Intra-articular steroid injections (not disease modifying and then get steroid side effects so not as commonly used if avoidable)

DMARDs for inflam OA

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13
Q

Surgical treatment of OA

A
  • Arthroscopy (only indicated for loose bodies)
    • camera into joint
  • Osteotomy (partial removal of bone)
  • Arthoplasty (complete replacement)
    • will eventually have to be replaced
  • Fusion of bones (if joint won’t tolerate replacement well e.g. ankle/foot)
    • stops pain but loss of mobility
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14
Q

Indications for Arthoplasty

A
  • Significant/uncontrolled pain (esp at night)
  • Sig loss of function

It may be discouraged in youger patients as they will inevitably need replacement

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15
Q

Complication of OA

A
  • pain, loss of function etc.
  • Loose bodies (bone/cartilage fragment) can get stuck within joints and can cause the joint to ‘lock’
    • esp in KNEE
    • only indication of ARTHROSCOPY in OA
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16
Q

Presentation of Nodal OA

A
  • affects hands -> reduced function
  • Heberden’s (DIP) and Bouchard’s (PIP) nodes
  • MCP esp of thumb affected
  • Initial inflam phase
  • BONY SWELLINGS + CYSTS
  • Relapse/remit over a few years
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17
Q

Presentation of Knee OA

A
  • Can affect 3 compartments (in isolation or a combination of these):
    • Medial (mc)
    • Lateral
    • Patellofemoral (request more views when imaging)
  • Slow evolution if no significant trauma
  • Oft stays stable for years once established (unless there is trauma)
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18
Q

Presentation of Hip OA

A
  • Pain in groin - may persist at night and wake people up
  • Difficulty walking
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19
Q

Presentation of Erosive/Inflam OA

A
  • Erosive element - can look like birds wings on scan
  • Inflammatory component
  • DMARD therapy oft used (ususally milder things like hydroxychloroquine)
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20
Q

When can a clinical diagnosis of OA be made without investigation

A

If patient is:

  • Over 45
  • Has typical activity related joint pain
  • No morning stiffness or morning stiffness that lasts less than 30 minutes
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21
Q

Advice to give regarding a prescription of alendronate

A
  • Take first thin in morning
  • On an empty stomach
  • Remain upright 30 mins after taking
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22
Q

Define fibromyalgia

A

A chronic pain syndrome diagnosed by presence of widespread MSK pain lasting >3 MONTHS with all other causes ruled out

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23
Q

DDx of Fibromyalgia

A

Polymyalgia Rheumatica also presents with widespread pain, more common in females

  • but presents almost exclusively OVER 50 Y/O
  • Also has raised ESR/CRP
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24
Q

Risk factors of Fibromyalgia

A
  • FEMALE
  • Poor socieconomic status
  • Depression/stress
  • 20-50 Y/O
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25
Q

Pathophys of fibromyalgia

A

Unknown
Possibly hyper excitability of pain fibre

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26
Q

Presentation of Fibromyalgia

A
  • Increased sensitivity to pain
  • Fatigue
  • Sleep disturbance
  • Fibro-fog (problems with memory + conc)
  • Morning stiffness esp back + neck
  • Headaches
  • IBS
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27
Q

Investigations for Fibromyalgia

A

Clinically diagnosed:
- Issues with widespread pain in combination with fatigue, memory, sleep difficulties
- need to feel pain in 11+ out of 18 regions palpated all over body

No serological markers; NO raised ESR/CRP

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28
Q

Management of Fibromyalgia

A
  • Educating patient on the condition
  • Exercise/physiotherapy
  • Relaxation
  • Analgesia (paracetamol, tramadol/codeine)
  • CBT, counselling, low dose tricyclic antidepressants
    • for SEVERE NEUROPATHIC PAIN
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29
Q

Complications of Fibromyalgia

A
  • affects quality of life
  • anxiety, depression, insomina
  • opiate addiction
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30
Q

Define Antiphospholipid syndrome

A

An autoimmune disorder which causes a hypercoaguable state due to increasing the tendancy of blood to clot
- characterised by thrombosis, recurrent miscarriages + aPL Abs

Can be primary or secondary to other AI e.g. SLE

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31
Q

Epidemiology of APS

A

Mostly in YOUNG FEMALES

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32
Q

RFx of APS

A
  • FEMALE
  • DIABETES
  • HTN
  • OBESITY
  • Smoking
  • Oestrogen therapy (at menopause)
  • other AI e.g. SLE
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33
Q

Pathophys of APS

A

In APS abnormal antiphospholipid antibodies are produced and present in blood. These attack the phospholipids on the surface of blood constituent cells + vessel walls -> impaired blood flow. Can lead to arterial and venous clots.

Particularly problematic in pregnancy with a risk of miscarriage.

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34
Q

Presentation of APS

A

Remember CLOTS:

  • Coagulopathy:
    • Thrombosis -> DVT, PE or Stroke/MI/Renal infarct (or antiphospholipid nephropathy)/Raynaud’s
  • Livedo reticularis
  • Obstetric issues
    • Recurrent miscarriages or early/severe pre-eclampsia
  • Thrombocytopenia

Balance problems, headaches, double vision etc.

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35
Q

Diagnosis of APS

A
  • Hx of thrombosis/pregnancy complications
  • FBC: may show THROMBOCYTOPENIA
  • Ab screen:
    • +VE ANTICARDIOLIPIN Ab (IgG/M)
    • +VE LUPUS ANTICOAG
    • +VE ANTI-BETA-2 GLYCOPROTEIN 1 Ab
      (not necessarily all together)

Diagnose after 2 abnormal blood tests 12 weeks apart

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36
Q

Management of APS

A
  • Low dose aspirin (or antiplatelets e.g. clopidogrel) if no history (prophylactic)
  • If history of clots + APS Ab: WARFERIN
    • contraindicated in pregnancy (birth defects + placenta bleeding)
  • Pregnant: LMWH + ASPIRIN
  • Lifestyle -> smoking cessation, reg exercise, healthy weight etc
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37
Q

Acronym to remember main parts of APS

A

CLOT:

-Coag defect
- Livedo reticularis
- Obstetric complications
- Thrombocytopenia (in some)

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38
Q

Red flags for Low Back Pain

A

TUNA FISH:

  • Trauma (suggests osteoporsis)
  • Unexplained weight loss (cancer)
  • Neurological symptoms (cauda equina syndrome)
  • Age >50 or <20 (secondary bone cancer, ank spond, herniated disk)
  • Fever (infection)
  • IV drug use (infection - esp pseudomonas aruginosa)
  • Steroid use (infection)
  • History of cancer (spine mets)
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39
Q

Diff diagnosis of mechanical lower back pain

A
  • Lumbosacral muscle strains/sprains
  • Lumbar spondylosis
  • Herniated disk (oft involves L5/S1 nerve root)
  • Spondylolysis (minor stress fracture in lumbar vertebra)
  • Vertebral compression factor
  • Spondylolisthesis (a vertebra moves foward straining disk + connections to other vertebrae)
    Spinal stenosis
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40
Q

Most common primary bone cancers

A
  • Chondrosarcoma
  • Osteosarcoma
  • Ewing sarcoma (mesenchymal stem cell in bone marrow) - v. rare (seen in teens - 15 y/o)

(also Fibrosarcoma - but is not a bone cancer)

Rarer; more common in children

Secondary tumours and MYELOMAS are most common

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41
Q

RFx for primary bone cancer

A
  • Previous RADIOTHERAPY
  • Previous CANCER
  • PAGET’S DISEASE
  • Benign bone LESIONS

More common in MALES

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42
Q

Presentation of Bone cancers

A
  • Bone PAIN
    • WORSE at NIGHT (wake up at night)
    • Constant or intermittant (not associated with movement) - may increase in intensity
    • Resistant to analgesia
  • Atypical bony/soft tissue swelling/masses
    • Easy bruising (if affecting bone marrow)
    • may have path. fractures
  • Mobility issues (unexplained limp, joint stiffness, reduced range of motion)
    • esp of LONG BONE/VERTEBRAE
  • Inflammation/tenderness over bone
  • Systemic symptoms (fever, weight loss, fatigue)
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43
Q

Investigations for bone cancer

A
  • 1st line: X-RAY
  • Gold: BIOPSY
  • Bloods:
    • FBC,
    • ESR/CRP, ALP, LDH, Ca all raised
    • U+E
  • CT chest/abdo/pelvis (staging)
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44
Q

Appearance of main bone cancers on X-ray

A
  • Osteosarcoma:
    -looks fluffy (bone destruction),
    • sun burst,
    • Codman’s triangle (periosteum lifted off bone - can’t lay down new bone)
    • can have LUNG METS
  • Chondrosarcoma:
    • Popcorn calcification
    • Endosteal scalloping
  • Ewing sarcoma:
    • Onion skin change
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45
Q

Management for bone cancer

A

Chemo/Radiotherapy
- Bisphosphonates if increased bone lysis

Surgery -> limb sparing or amputation

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46
Q

Complications of bone cancers

A

Hypercalcemia, bone pain, metastases, pathological fractures

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47
Q

Most common primary bone cancer in children

A

Osteosarcoma

  • is the most common primary bone balignancy in general
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48
Q

Define osteomalacia

A

Poor bone mineralisation leading to soft bone, usually due to vit D deficiency (in adults) AFTER EPIPHYSIAL FUSION

Rickets is specifically caused by inadequate mineralisation of bone and epiphyseal cartilage in a GROWING skeleton ie BEFORE EPIPHYSIAL FUSION (children)

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49
Q

Epidemiology of osteomalacia

A
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50
Q

Causes/Risk factors for Osteomalacia

A
  • Inherited
  • Hyper PTH (could be due to low vit D)
  • Low vit D
    • Malabsorptive disorders (IBD)
    • low sunlight exposure/live in colder climate + spend most of time indoors
    • darker skin
    • CKD (kidneys convert vit D to 1,25-dihydroxyvitamin D (Calcitriol))
    • Liver disease (decreased vit d hydroxylation - cholecalciferol -> 25-hydroxyvitamin D)
    • Anticonvulsant drugs (increased Cytochrome P450 metabolism of Vit D)
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51
Q

Pathophys of Osteomalacia

A

Poor bone mineralisation due to CALCIUM DEFICIENCY - usually due to vit D deficiency -> reduced Ca2+ and PO4^3- (forms hydroxyapitite - mineralises bones) -> soft bones

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52
Q

Presentation of Osteomalacia

A
  • Fatigue
  • Bone pain + tenderness
    • dull ache which is worse on weight-bearing exercises - difficulty weight-bearing
  • Fractures (esp in neck of femur); abnormal fractures
  • PROXIMAL weakness/muscle aches
  • Waddling gait; difficulty with stairs
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53
Q

Presentation of Rickets

A
  • Growth retardation
  • Hypotonia
  • Skeletal deformities:
    • Knock knees (valgus deformatiy)
    • Bow legs (varus deformity)
    • Wide epiphysis on imaging
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54
Q

Investigations for osetomalacia

A
  • X- ray: loss of cortical bone due to defective mineralisation
    • Looser zones (transverse lucencies w/ sclerotic borders) - basically partial fractures
    • osteopenia - more radiolucent bones
  • DEXA -> low bone mineral density
  • Bloods: low serum calcium + phosphate, PTH will be raised if vit D def; ALP raised
    • Serum 25-hydroxyvitamin D - low
  • Bone biopsy - incomplete mineralisation - DIAGNOSTIC
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55
Q

Ranges for 25-hydroxyvitamin D (-cholecalciferol)

A
  • < 25 nmol/L = vit D deficiency
  • 25-50 nmol/L = vit D insufficiency
  • > 75 nmol/L = optimal
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56
Q

Management of Osteomalacia

A
  • Vit D supplements (-> rapid mineralisation + reduce symptoms) - Colecalciferol (D3 tablets)/increase in diet e.g. eggs
    • for deficiency:
      • 50 000 IU 1/wk for 6wks
      • 20 000 IU 2/wk for 7wks
      • 4000 IU daily for 10wks
    • If dietary insufficiency/after initial treatment
      • 800 IU or more /day for life
    • If malabs - give IM calcitriol
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57
Q

Define Paget’s Disease

A

Focal disorder of excessive bone turnover/ remodelling that results in areas of sclerosis and lysis

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58
Q

Epidemiology of Paget’s disease

A
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59
Q

Risk factors for Paget’s disease

A
  • Age >50
  • MALE
  • European origin
  • FHx
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60
Q

Pathophysiology of Paget’s disease

A
  • Excessive Osteoblast/clast activity (resorption + disorganised new bone formation) -> excessive bone turnover
  • Patchy areas of sclerosis in some places and lysis in others
  • Enlarged + misshapen bones -> risk of fracture
  • Particularly affects axial skeleton (skull, spine), pelvis + long bones of limbs

Happens in 3 phases:
- lytic phase
- mixed phase
- blastic phase

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61
Q

Investigations for Paget’s disease

A

X-ray:

  • Bone enlargement + deformity
  • Osteoporosis circumscripta (well defined lytic lesions) in some places (esp skull)
  • Cotton wool appearance in skull (poorly defined areas of sclerosis + lysis)
  • V-shaped defects in long bones

Bloods: ALP RAISED, everything else normal

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62
Q

Management of Paget’s disease of bone

A
  • Bisphosphonates
  • Calcium + vit D supplements (esp while on bisphosphonates)
  • NSAIDs for bone pain
  • Surgery to correct deformaties
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63
Q

Complications of Paget’s disease of bone

A
  • OSTEOSARCOMA
  • Spinal stenosis (narrowing of spinal canal) -> cord compression -> potential neuro symps
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64
Q

Define polymyalgia rheumatica

A

Inflammatory condition that causes pain in shoulders, pelvic girdle and neck.

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65
Q

Epidemiology of Polymyalgia rheumatica

A
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66
Q

Risk factors/associations of Polymyalgia rheumatica

A

Strong association with GCV - oft occur together

  • Age > 50
  • FEMALE
  • Caucasian
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67
Q

Pathophys of Polymyalgia rheumatica

A

Cause unknown but believed to be multifactorial.

Inflammation of muscles in shoulder, neck + pelvic girdle -> pain + stiffness

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68
Q

Presentation of Polymyalgia rheumatica

A

Symps must have been present for 2 weeks to be diagnosed

  • Bilateral shoulder pain (may radiate to elbow)
  • Bilateral pelvic girdle pain
  • Worse in morning (>30min)/with inactivity
  • Interferes with sleep
  • RESPONDS WELL TO STEROIDS (like GCV)

Systemic: weight loss, fatigue, low grade fever, low mood

  • upper arm tenderness
  • carpel tunnel syndrome
  • pitting oedema
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69
Q

DDx for Polymyalgia rheumatica

A
  • SLE
  • myositis
  • hyper/hypo thyroid
  • Osteomalacia
  • Osteoarthritis
  • Rheumatoid arthritis
  • Cervical spondylosis
  • Adhesive capsulitis
  • Fibromyalgia
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70
Q

Investigations for polymyalgia rheumatica

A

Diagnosis mainly based on clinical presentation + response to steroids

  • Bloods: Raised inflam markers
  • NORMAL CREATINE KINASE (diff from myositis - no muscle damage) and creatinine (rhabdomyolysis)

For diffs - check before starting steroids:
- FBC, U+E, urin dipstick, LFTs, Ca, TSH, CK, RF (-ve)
- Serum protein electrophoresis (for myeloma/other protein abnormalities)

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71
Q

Management of polymyalgia rheumatica

A

Initially: 15mg PREDNISOLONE per DAY - rapid improvement

If poor response to steroids after 1 week - probs not PMR - stop steroids + consider alt diagnosis

After 3 weeks:
- would expect 70% improvement in symps + normal inflam markers to diagnose PMR
-> reducing regime (15mg till fully controlled, 12.5mg for 3 wks, 10mg for 4-6wks, reduce by 1mg every 4-8 wks)

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72
Q

Things to consider when on long term steroids

A

Pt needs to be aware they will become steroid dependant after ~3 weeks and must not stop steroids as - risk of ADRENAL CRISIS

think STOP:

  • Sick day rules - if sick, increase dose
  • Treatment card - to inform others they are steroid dependant if they become unresponsive
  • Ostoporosis prevention (consider prophylactic bisphosphonates + calcium/vit d supplements)
  • PPIs (consider for gastric protection)
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73
Q

Define Rheumatoid arthritis

A

Autoimmune inflammation (and subsequent destruction) of joints (typically starting with small joints leading onto big joint inflammation) in a symmetrical pattern of involvement. No spinal involvement

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74
Q

Epidemiology of RA

A
  • 1-2% population
  • 2-3x more common in females
  • Middle age (but any age)
  • Increase risk of mortality esp CVD
  • Increasing damage + disability if left untreated (infalmmation treatable. Damage irreversible)
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75
Q

Risk factors for RA

A
  • Women 30-50 - 3x more likely than in men pre-menopause - equalises with men after menopause
  • FHx
    • HLA DRA/HLA DRB1 genetic link (same group as DM)
  • Smoking
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76
Q

Pathophys of RA

A
  • ARGININE -> CITRULINE mutation in T2 COLLAGEN
    • anti-CCP (cyclic citrulinated peptide) formation
  • Increased T cell mediated w/ neutrophil + monocyte involvement inflammation
    • releases cytokines -> SYNOVIAL LINING HYPERPLASIA -> PANNUS (inflam cells + cytokines)
  • Pannus releases metalloproteinase + grows past joint margins
    -> Erode into cartilage and then bone
  • After cartilage breakdown - bones rub against each other + degenerate
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77
Q

Which cytokines particularly linked to RA

A

IL-1 + TNFa

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78
Q

presentation of RA

A
  • Pain, hot swelling of:
    • Symmetrical, typically small joints: hands, wrists,
    • forefeet
    • DIP sparing
  • Hand deformaties:
    • **Boutonniere (like pushing button)
    • Swan neck
    • Z thumb
    • Ulnar finger deviation**
  • Prolonged early MORNING STIFFNESS (>1 hour) - improves as day progresses
    • Sudden change in function
  • Big joints involved later, bad prognostic sign if involved at presentation
    • BAKER’S CYST - popliteal synovial sac bulge

Can get Intermittent, Migratory or Additive involvement
- No spinal involvement

Extra-articular involvement

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79
Q

What are the Extra articular complications of RA

A
  • Lungs = pulm fibrosis
  • Heart = increased IHD risk
  • eyes = episcleritis, keratoconjunctivitis siccs (dry eyes)
  • Kidney = CKD
  • RHEUMATOID SKIN NODULES (most common - esp at elbows)
  • increased risk of vasculitis and Sjogren’s
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80
Q

Diagnosis of RA

A
  • Physical Exam
  • Bloods:
    • CRP (+/-ESR) - can be raised up to 100 in a flare
    • RF (70% with RA are RF +ve but non-specific)
    • Anti-CCP (cyclic citrullinated peptide) - 70-80% with RA are +ve (specific)
      • Selective for patients with most AGGRESSIVE disease (likelihood of damage, multisystem features - tells us additional treatment needed)
  • XR esp Hands + feet - DIAGNOSTIC + prognostic
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81
Q

Findings of physical exam of RA

A
  • Decreased grip strength / difficulty in fist formation
  • Often subtle synovitis – MCPs, PIPs, MTPs, ankles
  • DIPs are spared
  • Usually symmetrical
  • Deformity unusual at presentation
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82
Q

Findings of XR for RA

A

LESS

  • LOSS OF JOINT SPACE (narrowing)
  • EROSION OF BONE
  • Soft tissue swelling
  • Soft bone from PERIARTICULAR OSTEOPENIA (imbalanced remodelling)
83
Q

Treatment of RA

A
  • DMARDs - need to give quickly as 65-75% efficacy raised to 90% if started within 3 months
    • METHOTREXATE (Gold - contraindicated in preg - inhibits folate) - 10-25mg per week
    • Also Sulfasalazine, Leflunomide, Hydroxychloroquine (sulfasalzine + hydroxychloroquine ok in preg)
  • Physio, Ortho, Podiatry -> support + educate
  • Escalate to BIOLOGICS if RESISTANT (v expensive)
    • Anti- TNF = INFLIXIMAB (1ST LINE biologic - alongside MTX), ADALIMUMAB
    • Rituximab (anti CD20 - ie anti B cell) - 2nd line
    • Tocilizumab (IL-6 inhib)
    • Abatacept (anti-T cell)
    • JAK INHIBITORS (Baricitinib/Filgotonib)
  • NSAIDs
  • STEROIDS injections if v painful (can give oral too)
  • Ice
  • Splints/rest
84
Q

Define gout

A

Acute joint pain + swelling caused by inflammatory response to deposition of monosodium urate crystals intra-articularly

85
Q

Epidemiology of gout

A

Gout 6x more common in MEN (7.3% >75 y/o) + ELDERLY - esp OVERWEIGHT
- Overall male : female ratio 5:1
- Uncommon in females under 50 due to hormone

86
Q

RFx for gout

A

Hyperuricaemia

Intake:

  • ALCOHOL (beer, lager, stout) - rich in GUANOSINE
  • Diet – red meat, shellfish, offal
  • Sweetened soft drinks (fructose shares renal uric acid transporter so promotes uric acid pathway -> don’t get rid of uric acid -> hyperuricemia)

Output:

  • CKD (more common in elderly) -> lactic acid + ketones
  • Drugs - esp DIURETICS, aspirin, cyclosporin, TB drugs
  • Genetics
  • Fructose shares renal uric acid transporter

Uric acid also a product of DNA/RNA metabolism - high cell turnover -> increased urate

87
Q

What food is anti-gout

A

DAIRY

88
Q

Pathophys of gout

A

HYPERURICAEMIA (plasma supersaturated at 360mmol/L -> MONOSODIUM URATE crystal formation

  • deposit in joints -> affects synovial cells
  • immunological reaction initiated to try and remove them, leads to acute pain and swelling
89
Q

Presentation of gout

A
  • Acute episodes (will recover spontaneously within 7-10) - recurrent
    • typically predictable = MONOARTICULAR esp MTP big toe joint
      • also Mid-foot, ankle, knee, wrist, elbow, hand
    • esp at NIGHT
    • Swelling, Erythema, Shiny overlying skin
    • possible periarticular involvement - E.g. Olecranon bursitis - bursa fills with extra fluid due to irritation/inflam -> swollen
    • activates inate immune so sometimes get systemic
    • can’t put weight on it
  • Chronic = has Tophi (pathognomonic)
90
Q

DDx of inflamed joint

A

Septic arthritis
Trauma
Gout
Calcium Pyrophosphate Arthritis (pseudogout)
Rheumatoid Arthritis
(Osteoarthritis!) - also oft commonly involves toe

91
Q

Clinical phases of untreated gout

A

🡪 asymptomatic hyperuricemia,
🡪 acute/recurrent gout,
🡪 intercritical gout (recurrent flares - intercritical = time between flare, typically occurs within 2 years) - more + more frequent
🡪 chronic tophaceous gout (typically after 10yrs or more of recurrent polyarticular/poorly controlled gout
- Tophi can form in soft tissue, osseous tissues, ligaments and different organs and either in presence or absence of gouty arthritis) - tophi is just the name of the stone like monosodium urate deposits - esp undersurrounding skin

92
Q

Diagnosis of gout

A

Gold = JOINT ASPIRATION + POLARISED LIGHT MICROSCOPY

  • STRONGLY NEGATIVELY BIREFRINGENT NEEDLE SHAPED crystals - not seen in normal health

Also:

  • FBC (raised WCC)
  • U+E (checking kidney function - affects treatment)
  • LFT if concern re alcohol
  • Serum Uric Acid (often normal during acute attack as uric acid is in joint so less in blood)
  • CRP
  • Only use Xray if recurrent episodes or concern re sepsis
    • Punched out/Rat bite EROSIONS (joint space preserved but erosion away from/below articular border) - extensive in late disease
93
Q

Tx of acute gout

A
  • Rest, ice, hydrate, continue urate lowering therapy
  • NSAID (short course) but CONTRAINDICATED if:
    • Renal failure
    • Peptic Ulcer Disease
    • Some pts with asthma
  • COX-2 inhibitors (NSAID alt)
    • Elderly don’t tolerate NSAIDs well
  • Colchicine (alt to NSAIDs) - anti-mitotic - disrupts multiple inflam pathways
    • SE = Diarrhoea
  • Corticosteroids
    • Intra-articular injections
    • Oral - low dose (5-10mg short course)

Other analgesics don’t work! - they don’t deal with inflammation

EDUCATE PATIENT - explain the disease
-Advice about lifestyle, Alcohol, Diet, Weight loss
- reduce purines, increase dairy
- Adequate fluid intake (increased incidence in summer due to dehydration)

94
Q

Tx of long tem gout

A

URIC ACID LOWERING THERAPY:

Xanthine Oxidase Inhibitors:

    1. Allopurinol (1st line)
    1. Febuxostat (if allopurinol not tolerated/doesn’t work - e.g. CKD) – more potent Xanthine Oxidase Inhibitor

Increases urate excretion

    1. Benzbromarone / Probenecid – if allergic / intollerant
  • Losartan

Give Colchicine 500microg OD for 6 months alongside this as there is an increased risk of CV morbidity (lots of uric acid being moved around body)

95
Q

Indications for uric acid lowering therapy

A
  1. Recurrent attacks
  2. Evidence of tophi or chronic gouty arthritis
  3. Associated renal disease
  4. Normal serum Uric acid cannot be achieved by life-style modifications
96
Q

Aim of uric acid lowering therapy

A

REDUCE URIC ACID BELOW <300 umol/l

97
Q

complications of gout

A

Disability and misery
Tophi

Renal disease:

  • Calculi 10 -15%
  • Chronic urate nephropathy
  • Acute urate nephropathy (cytotoxics)
98
Q

Pathophys of pseudogout

A

Deposition of CALCIUM PYROPHOSPHATE crystals along joint capsule

99
Q

Epidemiology of pseudogout

A

3x more common in WOMEN - esp ELDERLY
- Typically on background for OA

100
Q

RFx of pseudogout

A
  • Diabetes
  • metabolic disease
  • OA
101
Q

Sx of pseudogout

A
  • oft POLYARTICULAR w/ KNEE commonly involved (also wrists, hands)
  • SWOLLEN, HOT, RED joint
102
Q

Diagnosis of pseudogout

A

JOINT ASPIRATION + POLARISED LIGHT MICROSCOPY

  • slightly positive birefringent rhomboid shaped crystals - can sometimes be found in normal health

Also:

  • FBC (raised WCC)
  • CRP
  • X RAY
    • CHONDROCALCINOSIS
    • May see subcondral cysts
103
Q

Tx of pseudogout

A

Only acute treatment

  • NSAIDs
  • then Colchicine
  • then Steroid injections
104
Q

Define osteoporosis

A

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

105
Q

Epidemiology of osteoporosis

A

% of people who will get an osteoporotic fracture:
- 50% of females over 50 (POST MENOPAUSAL CAUCASIAN WOMEN)
- 20% of males over 50

106
Q

RFx for osteoporosis

A

SHATTERED

  • Steroids or RAISED CORTISOL (Cushings)
    • increase resorption + induce osteoblast apoptosis
  • Hyperthyroid/Hyper PTH
  • Alcohol + smoking (poisons osteoblasts)
  • Thin (low BMI)/reduced skeletal loading
  • Testosterone LOW
  • EARLY MENOPAUSE (low oestrogen)
  • Renal/Liver failure
  • Erosive/Inflam disease
    • cytokines increase resorption
  • DMT1 or Malabsorption

Older age, any type of hypogonadism, previous fractures

  • FAMILY HISTORY (50% bone structure inherited)

Drugs:
Depo-provera (in young women)
Aromatose inhibitors (breast cancer)
GnRH analogues
Androgen deprivation

107
Q

Pathophys of osteoporosis

A

Fractures triggered by some sort of force greater than strength of bone

Bone strength affected by:

  • Bone mineral density (standard measure of osteoporosis)
  • Bone size
  • Bone quality (depends on Turnover, Architecture + Mineralisation)

Oestrogen keeps bone turnover damped down - Post menopausal -> loss of restraining effects
Increased bone turnover (more and more left in partially resorped state) → net loss of bone

Trabecular architecture becomes poorer with age:
-> loss of cross connecter trabeculae which prevent buckling -> ~16x weaker bone

Remodelling unit activation frequency increases with age - damage more likely so remodelling needed more

108
Q

Sx of osteoporosis

A

FRACTURES

  • Wrist (Colles) - fall on outstreatched wrist - more common in 50-60 y/o
  • Hip/Proximal femur - older ppl fall + can’t catch themselves
  • Compression vertebral crush (may cause kyphosis)
109
Q

Dx of osteoporosis

A

Bone densitometry - DEXA scan - Duel energy XR absorptionometry but low radiation dose

  • For risk assessment + diagnosis
  • Sites:
    • LUMBAR SPINE
    • PROXIMAL FEMUR
    • DISTAL RADIUS
  • Gives a T-SCORE - a standard deviation score:
    • Number used for DIAGNOSIS
    • Compares with a GENDER-MATCHED YOUNG ADULT mean

Also FRAX score (Fracture Risk Assesment Tool)
- assess 10y fracture risk in osteoporotic patients

110
Q

Diagnostic criteria for osteoporosis + osteopenia

A

T-score

  • Osteoporosis = < -2.5
  • Osteopenia = -1 - -2.5

severe osteoporosis os <-2.5 + a fracture

111
Q

Tx for osteoporosis

A

Anti-resorptive:

  • BISPHOSPHONATES - inhibit osteoclasts by inhibiting RANK-L signelling
    • Oral: ALENDRONATE (daily/weekly), Risedronate, Ibadronate
    • IV: Ibadronate, Zolendronate (once yearly)
  • Denosumab - rapid acting RANK-RANKL inhibitor (potential rebound turnover increase if stopped)

Anabolic: Teriparatide (PTH analogue) - expensive

Also:
- HRT
- oestrogen receptor modulator - raloxifere

112
Q

Define septic arthritis

A

Direct bacterial infection of a joint
- direct access or haematogenou spread

113
Q

Epidemiology of septic arthritis

A

45% > 65 y/o
Prosthetic joint infection > native
- Risk of infections in prosthetic joints increasing
- Septic revision = X2 cost of non-septic and >3x cost of primary replacement
M = F

114
Q

Presentation of septic arthritis

A
  • V Painful, red, swollen, hot joint w/ joint in previously fit person
    • Children may just not use it so you may not notice at first
  • 90% monoarthritis (don’t rule out if polyarticular)
  • KNEE > Hip > shoulder

MEDICLA EMERGENCY - can destroy knee in 24hrs or less!

115
Q

RFx for septic arthritis

A
  • Any cause for bacteraemia
  • Direct/penetrating TRAUMA
  • Local skin BREAKS/ULCERS
  • DAMAGED joints
    • PROSTHETIC JOINTS
  • IMMUNOSUPPRESSION (including just steroids)
  • ELDERLY (>65 Y/O)
  • RA or other immune diseases
  • DIABETES
116
Q

Common pathogens affecting adult native joints

A
  • Staph Aureus (esp consider if have RA/DM) - mc
  • Strep
    • Group A (pyogenes) - b haemolytic
    • Group B
    • Strep pneumoniae
  • Neisseria gonorrhoea (consider in young, sexually active, MSM)
  • Gram -ve bacilli (consider in extremes of age, if systemically unwell or IVDU)
    • E coli
    • Pseudomonas Aeruginosa
  • Anaerobes (diabetes)
    • Clostridium
    • Bacterioides
  • Mycobacterium - typically TB (immunocomp)
  • Fungi (immunocomp)
117
Q

Most common pathogens affecting native joints in children

A

<2 y/o:

  • S AUREUS
  • Strep esp Gp A
  • Gram -ve bacilli (e.g. Kingella Kingae - a oropharyngeal commensal)
    • Historically most common were HAEMOPHILUS INFLUENZA, s aureus and strep (Gp A) but H influenza is no longer a common infection due to the vaccination program

> 2 y/o:

  • S AUREUS
  • Strep
  • Gram -ve bacilli
    -Historically H influenza was more common than gram -ve
118
Q

Common pathogens affecting prosthetic joints

A
  • STAPH AUREUS (most common)
  • Enterococci
  • MRSA
  • Enterobacter
  • Pseudomonas
  • Diphtheriodes
  • Haemolytic strep
  • Anaerobes
119
Q

Dx of septic native joint

A
  • FBC: high WCC (neutrophilia)
  • CRP raised (esp if over 100 - up to 100 could indicate a RA flare)
    • ESR can be normal
  • Blood cultures (sepsis)
  • sexual health review to check for gonorrhoea
  • Joint aspirate (usually seeded by bacteraemia) - GOLD, always do
    • Turbid fluid (ie more opaque/cloudy/thick+gloopy)
    • Leukocyte positive
    • Gram stain for microbes
    • polarised light microscopy to rule out gout/pseudogout
120
Q

Dx of prosthetic joint

A
  • History
    • Oft present with just pain (not hot/swollen)
    • Local: wound healed slowly; always been sore (means infection was always there since prosthesis put in - presents faster)
    • Haematogenous: became painful after recent infection/dental work
  • Examination
  • X-rays
  • FBC (usually unfelpful - high WCC uncommon as usually chronic)
  • ESR, CRP
    • Single CRP >10 and ESR >30 = 50% chance of infection (if normal 90% chance not infected)
    • Multiple raised = 80% chance of infection (if multiple normal = 95% chance not infected)

If other tests inconclusive: Alpha defensin (antimicrobial peptide secreted by neutrophils) - sensitivity/specificity ~95% but v expensive

ASPIRATION -> Microbio culture (aerobic + anaerobic)
- Patient needs to be off antibiotics for at least 2 weeks

121
Q

Tx of native septic joint

A
  • Stop immunosuppression
    • If on long term steroids - DOUBLE DOSE as they may be unable to naturally increase steroid levels
  • Analgesia (NSAIDs)
  • JOINT ASPIRATION (repeatedly if needed) + washout until no recurrent effusion
  • empirical ANTIBIOTICS - long course: 6 WEEKS MIN
    • flucloxacillin for g-ve,
    • vancomycin for MRSA,
    • ceftriaxone + azithromycin (gonorrhoea)
  • Splinting/rest/off-load with crutches/physio
122
Q

Tx of prosthetic septic joint

A
  • Analgesia
  • Stop immunosuppression, increase steroids etc

Potential options:

  • after determining specific bacteria -> ANTIBIOTIC SUPPRESSION
    • will not eliminate sepsis but used if unfit for surgery/if they have multiple prosthetic infections
  • DEBRIDEMENT + retention of prosthetic
    • NOT FOR CHRONIC, retains infection
    • only if prosthesis not loose
  • EXCISION ARTHOPLASTY (remove only infected section, let it fill in with scar tissue)
    • if HIGH RISK
  • One stage arthroplasty - RADICAL DEBRIDEMENT
    • avoid bone graft - will reinfect
    • 85% success
  • Two stage arthroplasty - radical debridement
    • can put in local antibiotic spacer/give systemic Abx in waiting period
    • 90-95% success
  • Amputation
123
Q

Characteristic presentation of gonococcal arthritis

A

Occurs from disseminated gonococcal infection

  • Fever (potentially), arthritis, tenosynovitis (inflammation of tendon sheath/synovial membrane around tendons - harder to aspirate)
    • Polyarticular - multiple joint, small + large
  • Maculopapular (grey base - pustular lesions)
    • Esp in Peripheries (palms, soles)
    • Painful before it is visible
    • Usually >5 lesions
124
Q

Define osteomyelitis

A

Acute inflamed infected BM

125
Q

Epidemiology of Osteomyelitis

A

Increasing incidence of chronic osteomyelitis
- increased prevalence of predisposing conditions such as diabetes mellitus and peripheral vascular disease.
- Ageing population

**Bimodal age distribution **

  • Children 80% of acute, haematogenous osteomyelitis
  • Adults >50 y/o
  • Adolescents and adults get contiguous osteomyelitis/direct inoculation (often associated with direct trauma)
  • Older patients: oft contigous linked to Diabetes mellitus/Peripheral Vascular disease/Arthroplasties
126
Q

Causes/RFx for osteomyelitis

A
  • Behavioural factors
    -Ie risk of trauma - e.g. if they enjoy extreme sports etc
  • Vascular supply (poor)
    • Arterial disease
    • DM
    • Sickle cell disease
  • Pre-existing bone/joint problem
    • Inflammatory arthritis
    • Prosthetic material including arthroplasty
  • Immune deficiency
    • Immunosuppressive drugs
    • Primary immunodeficiency
  • Similar RFx to IE
    • IVDU
    • Central lines; on dialysis
    • Catheter
  • UTI/other infection
127
Q

Common pathogens associated with osteomyelitis

A

Common microbes:

  • STAPH AUREUS (mc)
  • coagulase-negative staphylococci,
  • aerobic gram-negative bacilli (30%)

Others:

  • Streptococci (skin, oral)
  • Enterococci (bladder, bowel)
  • Anaerobes (bowel)
  • Fungi, (immunocomp)
  • Mycobacterium tuberculosis (immunocomp)

In SCD:

  • SALMONELLA

In IVDU:

  • PSEUDOMONAS AERUGINOSA
  • Serratia marcescens
128
Q

Routes of how pathogens can cause osteomyelitis

A
  • Direct innoculation - trauma/surgery (poly/monomicrobial)
  • Contigous spread - from adjacent soft tissue/joints (poly/monomicrobial)
  • Haematogenous seeding (monomicrobial)
129
Q

Haematogenous seeding osteomyelitis - which bones commonly affected + pathophys

A

Children = LONG BONES

  • High but slow blood flow to metaphysis of growing long bones (high metabolic activity)
  • Endothelial basement membranes absent (easier to get into bone)
  • Capillaries lack/have inactive phagocytic lining cells (less immune defence)
  • Predisposes to infection

Adults = VERTEBRAE + clavicle/pelvis

  • Vertebrae become more vascular with AGE
  • Bacterial seeding of vertebral endplate more likely
  • Also: lumbar vertebral veins communicate with pelvic veins with valveless anastemoses. Can get infection via retrograde flow from lower GU infections

IV Drug Users = CLAVICLE + PELVIS (oft younger so vertebrae less vascular)

130
Q

Pathophys of osteomyelitis

A

Microbial surface components adhere to matrix molecules

  • Acutely -> inflammation + bone oedema
  • Chronic -> SEQUESTRUM INVOLUCRUM
    • Infalm exudate in marrow
    • Causes increased intramedullary pressue
    • Causing extension of exudate into bone cortex
    • It ruptures through periosteum
    • Interrupts periosteal blood supply -> NECROSIS
    • Leaves separated pieces of dead bone
    • NEW BONE forms
    • necrotic bone embedded in pus + thick sclerotic bone placed around sequestra to compensate + support abnormal
131
Q

Presentation of osteomyelitis

A
  • Onset over SEVERAL DAYS
  • DULL BONY PAIN + HOT + SWOLLEN + ERYTHEMA
  • May be aggravated by MOVEMENT
  • Systemic: FEVER, RIGORS, sweats, malaise

If Vertebral OM: lumbar most common

  • May extend posteriorly -> epidural/subdural abscess or meningitis
  • Anterior/lateral extension -> abscesses in surrounding structures e.g. retroperitoneum, psoas

If chronic: typical signs + any of below

  • DEEP ULCERS (sequestrae) that fail to heal despite several weeks of treatment
  • Non-healing fractures
  • Draining sinus tract

Can also occur close to joint and pus can discharge into joint when infection breaks through cortex (more common in infants)

132
Q

DDx for osteomyelitis

A
  • Soft tissue infection (Cellulitis (deep dermis + subcut) and erysipelas (dermis +/- superficial cutaneous lympatics))
  • Bursitis (swelling of joint soft tissue)
  • CHARCOT JOINT
    • Progressive degeneration of weight bearing joint + bony destruction due to sensory nerve damage e.g. in DIABETIC NEUROPATHY
    • Oft affects foot -> presents w/ Diabetic feet
  • Gout
  • Avascular necrosis of bone (from steroids, radiation, bisphosphonates)
  • Fracture
  • Malig
133
Q

Investigations for osteomyelitis

A
  • History (symptoms)
  • Examination (signs)
  • Lab tests: CRP + WCC (FBC)
    • Acute - HIGH WCC
    • Chronic - can have NORMAL WCC
    • CRP raised but can be normal
  • Imaging:
    • PLAIN XR
      • Poor sensitivity/specificty esp in EARLY OM
        • Only osteopenia initially
        • >1-2 weeks before bone changes
    • MRI (more senstitive)
      • marrow oedema from 3-5 days
      • Delineates cortical, bone marrow and soft tissue inflammation
    • CT (alternative to MRI)
    • Nuclear Bone scan if metalwork makes CT/MRI impossible
  • BLOOD CULTURES (can be diagnostic)
    • may not need invasive diagnostic testing if organism isolated from blood is a pathogen likely to cause osteomyelitis.
    • +ve in 50% of Acute OM
  • BIOPSY (diagnostic)
    • Open bx&raquo_space;> needle bx
    • 2 specimens better than 1
    • Culture
    • 16sRNA PCR may be necessary (to get enough to culture)
  • Histology showing inflammation and osteonecrosis
134
Q

What are the XR changes seen in chronic osteomyelitis

A
  • cortical erosion,
    - periosteal reaction, (edge raised)
    - mixed lucency,
    - Sclerosis
    - sequestra
    - soft tissue swelling
135
Q

Tx of osteomyelitis

A
  • Immobilise
  • ANTIMICROBIAL THERAPY - 6 weeks IV minimum
    • first broad spectrum empirical then tailor to specific
      • Vanc/Teicoplanin (MRSA + s aureus)
      • Fusidic acid (s aureus)
      • Flucoxacillin (salmonella)
    • poor penetration to bone if vascular disease
    • stop based on CRP response - failure to respond -> re-image (but bone changes may persist even with infection resolution)
    • faster resolution if TOTAL SURGICAL DEBRIDEMENT
136
Q

Why may Teicoplanin be prefered over vancomycin in osteomyelitis and what are its SE

A

it’s longer lasting

  • GI upset
  • Pruritis
137
Q

Complicated osteomyelitis

A

TB OM

  • May be slower onset
  • Systemic symptoms
  • Epidemiology different from pyogenic OM
  • Blood Culture less useful
  • Biopsy essential
    • prolonged mycobacterial culture
    • Caseating Granolumata on histology
    • Induced sputum may help (sometimes occult pulmonary TB)
  • Longer treatment 6 months
138
Q

Define Seronegative spondyloarthropathies + epidemiology

A
  • Asymmetrical inflammation of BIG joints with SPINAL involvement (excluding psoriatic arthritis which can be Symmetrical)
  • Seronegative = RF negative
  • More common in MEN
  • ASSOCIATED w/ HLA B27 (MHC-1) - link to IBD
139
Q

General features of Spondylathropathies

A

SPINE ACHE

  • Sausage digits (dactylitis)
  • Psoritis
  • Inflam back pain
  • NSAID GOOD RESPONSE
  • Enthesitis (inflam of enthesis - site where ligaments insert into bone - esp heel)
  • Arthritis
  • Crohn’s/Colitis/raised CRP (can have normal CRP in AnkSpond)
  • HLA B27
  • Eye (anterior uveitis)
140
Q

Pathophys Ankylosing Spondylitis

A

Abnormal stiffening of joints - primarily sacrioiliac + axial skeleton - due to new bony formation

  • Prolonged Inflam/oedema -> fatty change -> calcium deposists along tendon
    • SYNDESMOPHYTES (vertical abnormal growth) esp at corners of vertebrae
    • make spine less mobile
141
Q

RFx for Ank Spond

A
  • HLA-B27 ASSOCIATED - class 1 so in all cells (possible to have without HLA-B27 tho)
    • Molecular mimicry (e.g. if pathogenic molecule has compound similar to HLA-B27 -> )
    • Misfolding theory (sets of inflam due to diff shape)
      • IL23, IL17, 16, TNFa - KEY
    • Heavy chain homodimer hypothesis
  • MALE - usually <40 y/o
  • Smokers
142
Q

Presentation of Ank Spond + 1 key complication

A
  • Progressively worsening (in flares) LOWER BACK PAIN + STIFFNESS
    • Worse in morning/after inactivity; better with movement
    • alternating nagging sacroileac/BUTTOCK pain
  • EMPHASITIS (esp achiles tendon) - swollen, thick, increased blood flow
  • Anterior uvitis
    • photophobia, possible vision blurring, iris scarring if recurrent
  • Psorisis (elbows + knees - extensor surfaces)
    • red base, white scale, itchy
  • clear synovial fluid accumulation
  • End-stage: fusion of spine + SI joint
    • Severe kyphosis (question mark posture)
  • can get costovertebral + costosternal inflammation -> potenitally eventual restrictive lung disease

Complication: vertebral fractures

143
Q

Classic presentation of inflam spine disease

A
  • Youngish patient (teens/20s)
  • Gradual onset over >3 months
  • Can go to sleep fine but wake up in middle of night due to (usually thoracic) back pain
    • Improves with movement
  • Significant morning stiffness (>30 mins)
  • Alternating, nagging buttock pain - radiating down back of thigh (sacroileac joint pain)
144
Q

Diagnosis of Ank Spond

A
  • CRP + ESR - raised (1st LINE)
  • HLA B27 genetic test - oft positive
  • MRI spine
    • Subchondral periarticular bone marrow oedema (early changes) breaking out of cortical bone - over time heals with fatty change
  • XR spine/pelvis (takes 8-10 years to show up usually)
    • bamboo spine (END STAGE) due to ossification of ligaments, discs + joints (calcium has grown along ligaments, fused spine together) -> radiographic stage (ankylosing spondilitis)
    • Syndesmophytes (bony growth originating from spinal ligament - like stalactites) - more common in men; more likely if elevated CRP
    • Squaring of vertebral bodies
    • Subchondral sclerosis + erosions
    • Can get ribcage involvement (fusion of facet + costovertebral joints)
    • Sacroiliitis (sacrum + hips) - have fused together - stops being painful but reduced mobility
145
Q

Test to check lumbar flexion ability

A

SCHOBER TEST
- they make marks 10cm above and 5cm below the ileac crest or L5 (around 15 cm apart)
- When they bend over with the legs fully extended (and feet 30 cm apart) - the marked area should extend by around 5cm or more (at least ~20cm)

  • <5cm increased length on flexion = indicative of ank spond
  • <2 = severe
146
Q

Treatment of ank spond

A
  • Exercise, Physiotherapy, lifestyle advice (smoking ceaseation)
  • NSAIDs
  • Biologics (disease modifying)
    • Anti-TNF, - etanercept (not an Ab), infliximab, adalimumab
    • Anti-IL17 - Secukinumab
    • JAK inhib (good for whole spectrum) - works inside cells

SULFAZALASINE DOESN’T WORK on SPINAL INFLAM

147
Q

Epidemiology of psoritic arthritis

A
  • 10-40% w/ psorisis develop within 10 y
  • 1 in 5 with psoriasis have psoriatic artheritis
  • 40-60% have HLA B27
148
Q

Presentation of psoritic arthritis

A
  • Symmetrical or Asym
    • INVOLVES DIPs
    • ATLANTA-AXIAL joint involvement
    • ENTHESITIS - Achiles tendon, plantar fascia
  • DACTYLITIS
  • NAIL PITTING (>5-10 pits across both hands = indicative)
    • ONYCHOLYSIS - lifiting of nail from nail bed
  • End-stage = bone fusion
149
Q

V severe presentation of psoritic arthritis

A

ARTHRITIS MUTILANS (v rare)

  • Occurs in phalanxes
  • Osteolysis of bones around joints in digits → progressive shortening
  • Skin then folds as digit shortens → telescopic finger

PENCIL IN CUP DEFORMITY

150
Q

Investigation of psoritic arthritis

A
  • Bloods: ESR + CRP - normal or raised; RF -ve; ant-CCP -ve
  • HLA-B27 genetic test - may be positive
  • X RAY:
    • DIP EROSION
    • Periarticular NEW BONE formation (looks DARKER)
    • Osteolysis (destruction)
    • Dactylitis (diffuse inflam appears as soft tissue swelling - may be more visible on MRI)
    • Pencil-in-cup deformity (in MUTILANS)
151
Q

Treatment of psoariatic arthritis

A
  • NSAIDs for symps
    • steroid injection if severe
  • Physio
  • DMARDS esp METHOTREXATE
    • try avoid sulfasalazine - CVD issues
  • if fails then ANTI-TNF (INFLUXIMAB, ETANERCEPT, adalimumab)
  • if that fails: IL12/23 BLOCKERS - USTEKINUMAB
    • works best for peripheries
  • IL17 blockers
152
Q

Define reactive arthritis

A

Sterile inflammation of synovial membranes + tendons triggered by infection at DISTANT site
- usually GI or genital/STI

153
Q

Common triggering pathogens of reactive arthritis

A
  • C trachomatis
  • Campy jejuni
  • Salm enteritidis
  • Shigella

Also:
- yersinia
- ureaplasma urealyticum

154
Q

Presentation of Reactive arthritis

A

Usually 2 days - 2 weeks post infection

  • Asymmetrical Oligoarthritis (affects 4 or less joints) - esp knees, ankles, feet
    • hot, swollen, painful, red + stiff joint
  • Dactylitis
  • REITER’S TRIAD: can’t see, can’t pee, can’t climb a tree
    • Conjunctivitis (discharge, burning, photophobia) - typically bilateral
      • may have anterior uveitis
    • Urethritis/Circinate balanitis (inflam of penile head with lesions)
    • Reactive arthritis + Enthesistis
  • Keratoderma blennorrhagica - palmo-plantar browny pustular rash
155
Q

Diagnosis of reactive arthritis

A
  • Bloods: ESR + CRP raised
  • HLA B27 may be +ve
  • ANA - negative
  • RF - negative
  • X-RAY
    • Sacroiliitis (pain in SI joints)
    • Enthesitis
  • Joint aspirate (MC+S) - negative (to exclude septic)
    • Can confirm not gout if sent for crystal examination

Sexual health review + stool culture

156
Q

Treatment of reactive arthritis

A
  • NSAIDs
  • Steroid injections (systemic steroids if polyarticular)
  • Prophylactic Abx till septic excluded

> 6 consequtively = CHRONIC
- DMARDs (MTX) then anti-TNF if MTX doesn’t work

157
Q

What is enteric arthritis

A

Inflam arthritis that flares up alongside IBD. Oft has inflam pain without overt arthritis. Oft involves SACROILIITIS.

Peripheral arthritis that subsides with remission of IBD.
- same extra-articular manifestations as IBD

158
Q

Define/Pathophys of Systemic Lupus Erythamatosus

A

Autoimmune systemic inflammation caused by a Type 3 hypersensitivity reaction (antigen-antibody complex deposition)

Impaired apoptotic debris is pressented to TH2 cells -> B cell activation -> immune complex formation + deposition -> inflammation + tissue damage

159
Q

Epidemiology of SLE

A

Most common in FEMALES

  • more common in Afro-Caribbean premenopausal women (20-40)
160
Q

RFx for SLE

A
  • FEMALE (12x higher risk) (16-64 - of child bearing age)
  • HLA B8/ DR2/DR3
  • Low C4 (due to null allele)
  • Drugs (e.g. isoniazid - anti-TB)

Strong association with Antiphospholipid syndrome + thrombosis

161
Q

Presentation of SLE

A

Specific skin changes:

  • Acute:
    • Malar (butterfly) rash (photosensitive) - sparing of nasolabial folds (crease from nose to mouth)
    • Generalised erythema
    • Bullous LE (blistering)
  • Subacute
    • Annular (ring around lesions)
    • Psoriasiform
  • Chronic
    • Discoid (scarring)
    • Scarring alopecia (no hair regrowth)
    • Lupus profundus (tender, deep, subcutaneous nodules/plaques - localised on esp lateral aspects of arms/shoulders, breast, trunk, buttocks; also scalp, face, proximal extremities)

Non-specific skin changes:

  • Panniculitis (inflammation of subcut fat - red + tender)
  • Urticarial lesions (raised, v itchy rash e.g. hives/welts)
  • Vasculitis
  • Livedo reticularis (mottled appearance)
  • Oral lesions
  • Non-scarring alopecia

Joints:

  • Symmetrical + non-errosive
  • Deformaties can be corrected
  • Less proliferative than RA

Can affect any system:

  • GLOMERULONEPHRITIS (nephrItic)
  • Seizures + Psychosis
  • Serositis (pleural/peritoneal/pericardial inflam)
    • Pleural effusion
  • ANAEMIA (AHA - Coombs pos)
  • RAYNAUD’S
  • Potential Pyrexia
  • Recurrent miscarriages - Antiphospholipid syndrome
162
Q

Dx of SLE

A
  • FBC - CYTOPENIAS (Hb, WCC, plts)
    • RAISED ESR - CRP may be NORMAL
    • Creatinine raised
  • Urine dipstick - haematuria + proteinuria (Nephritic syndrome)
  • Serology:
    • 99% ANA +VE (sensitive)
    • Anti-dsDNA Ab (specific - monitor progression)
    • Anti-Ro, La, SM (smooth muscle)
    • may have ribonucleoprotein Ab
  • LOW C3 + C4
  • CXR - potential PLEURAL EFFUSION
163
Q

Tx of SLE

A

No treatment if mild:
- Educate + support (avoid triggers esp sunlight)
- Assess any major organ damage
- IF ANTIPHOSPHOLIPID AB +VE - AFFECTS TREATMENT DURING PREG
- Control atherosclerosis risk factors

  • Topical
    • Sunscreen
    • Corticosteroids
  • Oral/IV steroids if evidence of active disease (not long term)
  • Topical/oral Cytotoxic if SEVERE (careful in pregnancy)
    - Azathioprine, Mycophenolate, Ciclosporin, Methotrexate, Cyclophosphamide (most powerful)
  • NSAIDs (for joints)
  • Hydroxychloroquine if DMARD needed
  • Anticoags
  • Biologics
    • Rituximab (if severe)
    • Belinumab
  • Autologous stem cell transplant (last resort)
164
Q

Raynaud’s phenomenon

A
  • Pale + cyanotic changes esp in peripheries
  • Can be precipitated by drugs
  • Can get vascular damage e.g. Atherosclerosis, frostbite, secondary to vibrating tools

Primary:
- Fairly benign
- No digital ulcers

Secondary - related to connective tissue diseases esp Systemic sclerosis, SLE and mixed

  • Can develop later in life
  • Can get digital ulcers
165
Q

Define Sjogren’s syndrome

A

Multisystem autoimmune EXOCRINE DYSFUNCTION

Can be primary or secondary (Associated with other AI conditions)

166
Q

Presentation of Sjogren’s

A

Dry, dry, dry

  • Dry eyes (keratoconjunctivitis sicca)
  • Dry mouth (xerostomia)
    • Parotid swelling
  • Dry vagina

Also:

  • Arthritis
  • Rash
  • Vasculitis
  • Neurological
  • Interstitial lung disease
  • Association with pericarditis
  • Renal tubular acidosis (type 1)
167
Q

Investigations for Sjogren’s

A
  • Serology:
    • Anti-Ro + Anti La (for PRIMARY sjogren’s)
    • ANA oft +ve; RF may be +ve
  • SCHIRMER TEST - induce tears + place filter paper in/under eyes
    • <10mm significant (healthy should travel at least 15mm)
  • US - abnormal salivary glands

Uncommonly a lip biopsy may be done -> Sialadenitis (salivary gland infection)

168
Q

Tx of Sjogren’s

A
  • Tear + saliva replacement
  • Vaginal lubrication
  • Hydroxychloroquine - if history of fatigue, mayalgia, arthralgia or rashes - can stop progression
  • Corticosteroids (if organ-threatening involvement)
  • Immunosuppression if lung/kidney involvement
169
Q

Complications of Sjogrens’s

A

Risk of RENAL TUBULAR ACIDOSIS - type 1:

  • Syndrome characterised by hyperchloremic metabolic acidosis (ie acidosis caused by bicarb loss) with a normal anion gap
  • (type 1 = problem at distal part of tubules; type 2 = problem at proximal part of tubules, type 3 = carbonic anhydrase 2 def + carbonic anhydrase inhib block metabolism of bicarbonate + carbonic acid (rare); type 4 = hyperkaelemic distal)
  • Treat with alkali therapy

Directly confers Increased risk of LYMPHOMA

  • Eye infections (conjunctivitis, corneal ulcers)
  • Oral problems (dental cavities, candida infections)
  • Vaginal problems (candidiasis, sexual dysfunction)
170
Q

Define Systemic sclerosis + types

A

A vasculopathy related to excessive collagen deposition. There is inflammation and often autoantibodies are produced.

  • Most common type is LIMITED CUTANEOUS SCLERODERMA
  • Diffuse cutaneous
  • Sine scleroderma (no skin changes)
  • Mixed connective tissue disease
171
Q

Presentation of Limited cutaneous scleroderma

A

CREST

  • Calcinosis (deposits subcutaneously) - can feel chalky if they break through skin-> RENAL FAILURE
  • Raynaud’s (long history) -> digital ulcers
  • Esophageat dysmotility/STRICTURES (swallowing difficulty)
  • SCLERODACTYLY (local skin thickening/tightening on digits) -> restricted movement (similar skin tightening can occur on the face -> small mouth)
  • Telangiectasia (spider veins - skin/mucous membranes - sometimes just look like erythamatous points) - whiten when pressed
    -> risk of pulm HTN at late stage

Can get iron deficiency anaemia - can see ‘watermelon stomach’ on endoscopy

172
Q

Presentation of diffuse scleroderma

A
  • Proximal scleroderma (skin tightening) with trunk involvement
  • Shorter history of raynaud’s
  • Increased risk of renal crisis,
  • Increased risk of cardiac involvement, (e.g. myocarditis, pericarditis)
  • Increased risk of interstitial lung fibrosis
173
Q

Dx of scleroderma

A

Limited:
- ANTI CENTROMERE Ab - 70%

Diffuse = Scl-70 (topoisomerase) Ab

  • Oft ANA +VE
  • may be RNA polymerase Ab pos
174
Q

Tx for scleroderma

A

No cure - treat symps

Raynauds:
- Physical protection e.g. gloves
- Vasodilators - issue if hypotensive
- Nifedipine, Iloprost (IV for digital ulcers), Sildenafil, Bosentan
- Fluoxitine (SSRI)
- Sympathectomy (strip away adventitia from affected vessels)

  • Gastro-oesophageal reflux = PPIs for life
  • Prevent renal crisis -> ACE-I

Early detection of pulm arterial HTN:
- Annual echos + pulm function tests

Treat pulm fibrosis - Cyclophosphamide
- Nintedanib

Treat skin oedema:
- No treatment (mild)
- Mycophenolate (more severe)
- Autologous stem cell transplantation (widespread + severe)

175
Q

Define Dermatomyositis/Polymyositis

A

Included in a group of autoimmune conditions characterised by progressive muscle weakness, aching or pain. Causes inflam + necrossi of skeletal muscle

  • Dermatomyositis also affects skin

Can be caused as part of paraneoplastic syndrome

176
Q

Epidemiology of Dermato/Polymyositis

A

POLYMYOSITIS: more common in WOMEN; esp 30-60 Y/O

DERMATOMYOSITIS: more common in WOMEN; can also affect CHILDREN (juvenile dermatomyositis)

HLA B8/DR3 genetic link

177
Q

Presentation of Poly/Dermatomyositis

A
  • Symmetrical wasting of muscles of shoulder + pelvic girdle -> stiffness worse in morning, improves with activity
    • oft complains: trouble raising arms/raising from chairs or squatting
  • may involve resp muscles - linked to INTERSTITIAL LUNG DISEASE

Derm:

  • GOTTRON’S PAPULES - rashes on backs of knuckles (DIPs, PIPs)
  • HELIOTROPE eyelid rash
  • Photosensitive shawl sign
  • may get Malar rash
  • may get calcinosis cutis
178
Q

Dx of Myositis

A
  • Bloods: LDH + Creatine Kinase RAISED
  • Serology: Anti Jo1
    • Dermatomyositis only = Anti Mi2
  • Electromyography (EMG) - muscle inflam
  • MUSCLE FIBRE/skin BIOPSY -> Inflam/NECROSIS (DIAGNOSTIC)
  • CXR, pulm function tests, high res CT - check lungs

Screen for malig (PET-CT)

179
Q

Tx of Myositis

A
  • 1st line = steroids: PREDNISOLONE
    • 1 m then titre down dose
  • If inadequate response -> Immunosuppression
    • MYCOPHENOLATE, AZATHIOPRINE
    • IV Rituximab if needed
180
Q

Define vasculitis + sub types

A

Heterogenous, multisystem inflammation of blood vessels

Large vessel:

  • Giant cell arteritis
  • Takayatsu (same as GCA but specifically affects aortic arch of east asian, mainly women)

Medium vessel:

  • POLYARTERITIS NODOSA
  • Buerger’s disease (male smokers 20-40, peripheral skin necrosis)
  • Kawaski disease (Coronary artery aneurysm in KIDS)

Small vessel:

  • pANCA ASSOCIATED (Eosiniophilic granulomatosis w/ polyangitis)
  • cANCA ASSOCIATED - GRANULOMATOSIS w/ POLYANGITIS (GPA)
  • Henloch Schonlen Purpura/IgA vasculitis (Immune complex mediated)
181
Q

Types of classification of vasculitis

A
  • Vessel size
  • Chappel Hill Consensus classification
    • Hybrid of vessel size, pathophys + underlying
182
Q

Pathophys of GCA

A

Affects branches of EXTERNAL CAROTID

Histologically:

  • Activated immune cell (lymphocytes/macrophages) infiltration of vessel wall -> DIRECT damage + stimulates smooth muscle cell remodelling
  • Blurred margin between media and adventitia
  • Intima proliferated into lumen -> narrowed
  • Vessel wall infiltration, proliferation + damage -> weakening + occlusion of vessel
    -> Ischaemia, infarction + ANEURYSM
    -> clinical manifestation

Temporal = headaches
Opthalmological = vision
Facial = jaw claudication

183
Q

Epidemiology of GCA

A
  • UK prevalence - 0.41% - most common vasculitis
  • Peak incidence 70-80 y/o; rare below 50 y/o
  • Most common in white esp Scandinavian
184
Q

RFx for GCA

A
  • Associated with polymyalgia rheumatica and ANCA associated vasculitis
  • Associated with CANCER
  • More common in FEMALE
185
Q

Presentation of GCA

A

Cranial GCA:

  • Temporal artery
    • NEW ABRUPT LOCALISED (oft TEMPORAL) HEADACHE
    • Changes to temporal artery: Tenderness, Thickening, REDUCED/ABSENT PULSATION
    • Granulomatous -> Skip lesions
    • SCALP TENDERNESS (classic - pain when brushing hair)
  • Lingual or facial artery
    • Tongue/JAW CLAUDICATION (less common) - builds up with chewing
  • Vision affected:
    • BLURRING
    • Amaurosis fugax (like veil over vision)
    • Diplopia (double vision)
    • Photopsia (flashing lights)
    • Visual loss

Extra cranial - e.g. Aortitis

  • May mimic infection/cancer-CONSTITUTIONAL SYMPTOMS/B SYMPTOMS:
    • Weight loss, low-grade fever, Anaemia, Malasise
  • POLYMYALGIA
  • Limb CLAUDICATION
186
Q

Important negative features differentiating GCA from serious headache

A

GCA has no:

  • Vomiting (related to raised intracranial pressure - NOT GCA)
  • Acute localising clinical signs (can indicate Acute intercranial bleeding, Encephalitis, Meningitis)
  • Fever (indicates infection - unusual in acute ischaemic cranial headache but may sometimes get fever in large vessel vasculitis if many extra-cranial vessels inflamed)
187
Q

Dx of GCA

A
  • 1st line = FBC -> RAISED ESR +/- CRP
    • anaemia of chronic disease
    • Thrombocytosis
  • Diagnostic:
    • TEMPORAL ARTERY US (colour doppler) -> HALO SIGN (non-compressable)
    • TEMPORAL ARTERY BIOPSY (large samples - granulomatous inflam of media + intima in skip lesions)
  • PET-CT + Axillary US - check extra-cranial (+ check for cancer)
  • If vision loss -> ophthalmology review - Pal optic disc
188
Q

US vs biopsy

A

US:

  • Non invasive
  • Can check multiple sites/vessels (including extracranial) in one visit
  • Better sensitivity than TA biopsy

BUT
- Must be done quickly + OPERATOR DEPENDANT (variability in reliability based on experience)

Biopsy:

  • Invasive
  • Only check 1 area at a time
  • 100% specific but 39% sensitive
189
Q

Tx of GCA

A
  • 40-60mg ORAL PREDNISOLONE (higher up to 60mg if Hx of ischaemic symptoms e.g. visual loss, limb/jaw claudication)
    • responds V. WELL
  • IV METYLPREDNISOLONE if EVOLVING visual loss
  • Reduce to zero over 12-18 months provided no return in symptoms

For Relapse:

  • METHOTREXATE +/- TOCILIZUMAB (IL6 inhib - can be a steroid weaning measure)
190
Q

Complications of high dose steroids + counter measures

A
  • Steroid induced diabetes/worsens pre-existing DIABETES
  • OSTEOPOROSIS (assess to prevent fractures; give calcium + vitD (Adcal-D3)/bisphosphonates (Alendronic acid - 70mg))
  • INFECTION
  • GI TOXICITY (peptic ulcers)

Can give PPIs + BISPHOSPHONATES

191
Q

Complications of GCA

A
  • Strokes if untreated (1%)
  • SUDDEN PAINLESS VISION LOSS (can be bilateral)
    • temporary Amaurosis Fugax (seen in TIA)
    • if not treated asap -> PERMENANT
      -> HIGH DOSE IV METHYLPREDNISOLONE
192
Q

Epidemiology/RFx of Polyarteritis nodosa

A
  • MALES > 50 Y/O
  • Associated with HEP B (hep C + HIV)
  • more common in developing countries
193
Q

Pathophys of Polyarteritis Nodosa (PN)

A

Affects muscles, skin, GI, kidneys + heart, nervous system (systemic)
- particularly affects branching points

194
Q

Presentation of PN

A
  • Unilateral orchitis (characteristic)
  • Peripheral neuropathy -> mononeuritis multiplex (damage to at least 2 diff areas of PNS)
  • GI
    • Abdo pain
    • Malabsorption
  • Skin involvement:
    • Livedo reticularis - mottled, purpleish, lace like appearance
    • Ulcers
    • Cutaneous/subcutaneous nodules (hallmark)
    • Gangrene
  • Kidneys:
    • PRE RENAL AKI/CKD -> HTN
  • Heart:
    • HF, Coronary A obs
195
Q

Diagnosis of PN

A
  • CRP/ESR raised
    • HBsAg may be present
  • CT angiogram -> beads-on-string appearance (microaneurysms)
  • BIOPSY (in e.g. kidney): transmural fibrinoid necrosis/NECROTISING VASCULITIS due to HTN
196
Q

Tx of PN

A
  • CORTICOSTEROIDS (+ cyclophosphamide if needed)
  • Control HTN -> ACE-I
  • If Hep B +ve = +antiviral + plasma exchange if needed
197
Q

Complications of Polyarteritis Nodosa

A

GI perforation + haemorrhages
Arthritis
Renal infarcts
Strokes
MI

198
Q

Epidemiology of granulomatosis w/ polyangitis (GPA)

A

Late teens/early adulthood
- most commonly seen in caucasians but could be any ethnicity

Staph aureus nasal carriage - associated with relapse in established disease

199
Q

Presentation of GPA

A

Triad of ENT, lung and kidney signs.

  • SADDLE SHAPED NOSE (due to perforated nasal septum)
  • Epistaxis
  • Crusty nasal/ear secretions - otorrhoea -> HEARING LOSS
  • Sinusitis
  • Cough, wheeze
    • Haemoptysis (may mistake for pneumonia on CXR)
  • GLOMERULONEPHRITIS (more advanced)

+ constitutional symps (fatigue, fever, malaise, night sweats, weight loss etc.)

May also have:
- ocular, rashes/ulcers, myalgia/arthralgia, neuropathy (esp mononeuritis multiplex) + thromboembolism (esp during active disease - but usually asymp)

200
Q

Dx of GPA

A
  • FBC: Anaemia (Eosniophilia??)
    • CRP +/- ESR elevated
  • CT chest (lung involvement oft present but asymp) - nodules; infiltrates
    • may do pulm function test -> elevated diffusion capacity = haemorrhage
  • Immunoassay -
    (proteinase 3) PR3-ANCA +ve
    • if -ve but still suspecious -> Immunoflouresence = c-ANCA POSITIVE (not p-ANCA)
    • If still -ve -> Renal/skin biopsy: GRANULOMAS, necrosis, vasculitis
  • Urinealysis + microscopy - check renal involvement
    • elevated creatinine shows up after haematuria etc.
201
Q

Tx of GPA

A
  • Nasal corticosteroid
  • Cyclophosphamide
202
Q

Epidemiology of mechanical lower backpain

A
  • v common, oft self limiting
  • May be normal esp in ppl 20-55
    • Trauma/work related
203
Q

Signs of serious pathology in lower back pain

A
  • ELDERLY (may be myeloma)
  • NEuropathic pain (spinal cord compression)
204
Q

Lumbar spondylosis

A

Degeneration of IV disc -> loss of compliance + thins over time

  • seen in ELDERLY

Initialy asymp -> progressive

  • MC = L4/L5 or L5/S1

Give analgesia + physio if simple mechanical pain

If serious pathology suspected -> XR + MRI

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