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Take 2: Electric Boogaloo > Phase 2 - MSK > Flashcards

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 loss2 - osteophyte development starts (looks like little bony outpouchings)3 - increased loss of joint space + osteophytes4 - 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 OAImpact 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 - kneesOthers:- 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- NOand 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 worseSigns:- 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- DeformitiesNo 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 contourBloods 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 therapyWeight 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-inflamTopical- NSAIDs- Capsaicin creamOral- 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 functionIt 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

UnknownPossibly 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 bodyNo 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- ThrombocytopeniaBalance 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 childrenSecondary 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 LESIONSMore 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 lysisSurgery -> 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 FUSIONRickets 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

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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50
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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51
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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52
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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53
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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54
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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55
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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56
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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57
Q

Risk factors for Paget’s disease

A
  • Age >50- MALE- European origin- FHx
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58
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 limbsHappens in 3 phases:- lytic phase- mixed phase- blastic phase
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59
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 bonesBloods: ALP RAISED, everything else normal

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60
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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61
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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62
Q

Define polymyalgia rheumatica

A

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

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63
Q

Risk factors/associations of Polymyalgia rheumatica

A

Strong association with GCV - oft occur together- Age > 50- FEMALE- Caucasian

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64
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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65
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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66
Q

DDx for Polymyalgia rheumatica

A
  • SLE- myositis- hyper/hypo thyroid- Osteomalacia- Osteoarthritis- Rheumatoid arthritis- Cervical spondylosis- Adhesive capsulitis- Fibromyalgia
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67
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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68
Q

Management of polymyalgia rheumatica

A

Initially: 15mg PREDNISOLONE per DAY - rapid improvementIf poor response to steroids after 1 week - probs not PMR - stop steroids + consider alt diagnosisAfter 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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69
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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70
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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71
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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72
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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73
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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74
Q

Which cytokines particularly linked to RA

A

IL-1 + TNFa

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75
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 bulgeCan get Intermittent, Migratory or Additive involvement- No spinal involvementExtra-articular involvement
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76
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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77
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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78
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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79
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)

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80
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
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81
Q

Define gout

A

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

82
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

83
Q

RFx for gout

A

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

84
Q

What food is anti-gout

A

DAIRY

85
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

86
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)
87
Q

DDx of inflamed joint

A

Septic arthritisTraumaGoutCalcium Pyrophosphate Arthritis (pseudogout)Rheumatoid Arthritis(Osteoarthritis!) - also oft commonly involves toe

88
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

89
Q

Diagnosis of gout

A

Gold = JOINT ASPIRATION + POLARISED LIGHT MICROSCOPY - STRONGLY NEGATIVELY BIREFRINGENT NEEDLE SHAPED crystals - not seen in normal healthAlso:- 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

90
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 inflammationEDUCATE 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)
91
Q

Tx of long tem gout

A

URIC ACID LOWERING THERAPY:Xanthine Oxidase Inhibitors: - 1. Allopurinol (1st line)- 2. Febuxostat (if allopurinol not tolerated/doesn’t work - e.g. CKD) – more potent Xanthine Oxidase InhibitorIncreases urate excretion- 3. Benzbromarone / Probenecid – if allergic / intollerant- LosartanGive 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)

92
Q

Indications for uric acid lowering therapy

A
  1. Recurrent attacks2. Evidence of tophi or chronic gouty arthritis3. Associated renal disease4. Normal serum Uric acid cannot be achieved by life-style modifications
93
Q

Aim of uric acid lowering therapy

A

REDUCE URIC ACID BELOW <300 umol/l

94
Q

complications of gout

A

Disability and miseryTophiRenal disease:- Calculi 10 -15%- Chronic urate nephropathy- Acute urate nephropathy (cytotoxics)

95
Q

Pathophys of pseudogout

A

Deposition of CALCIUM PYROPHOSPHATE crystals along joint capsule

96
Q

Epidemiology of pseudogout

A

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

97
Q

RFx of pseudogout

A
  • Diabetes- metabolic disease- OA
98
Q

Sx of pseudogout

A
  • oft POLYARTICULAR w/ KNEE commonly involved (also wrists, hands)- SWOLLEN, HOT, RED joint
99
Q

Diagnosis of pseudogout

A

JOINT ASPIRATION + POLARISED LIGHT MICROSCOPY - slightly positive birefringent rhomboid shaped crystals - can sometimes be found in normal healthAlso:- FBC (raised WCC)- CRP- X RAY - CHONDROCALCINOSIS - May see subcondral cysts

100
Q

Tx of pseudogout

A

Only acute treatment- NSAIDs- then Colchicine- then Steroid injections

101
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

102
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

103
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 MalabsorptionOlder age, any type of hypogonadism, previous fractures- FAMILY HISTORY (50% bone structure inherited)Drugs: Depo-provera (in young women)Aromatose inhibitors (breast cancer)GnRH analoguesAndrogen deprivation

104
Q

Pathophys of osteoporosis

A

Fractures triggered by some sort of force greater than strength of boneBone 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 effectsIncreased bone turnover (more and more left in partially resorped state) → net loss of boneTrabecular architecture becomes poorer with age:-> loss of cross connecter trabeculae which prevent buckling -> ~16x weaker boneRemodelling unit activation frequency increases with age - damage more likely so remodelling needed more

105
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)

106
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 meanAlso FRAX score (Fracture Risk Assesment Tool)- assess 10y fracture risk in osteoporotic patients

107
Q

Diagnostic criteria for osteoporosis + osteopenia

A

T-score- Osteoporosis = < -2.5- Osteopenia = -1 - -2.5severe osteoporosis os <-2.5 + a fracture

108
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) - expensiveAlso:- HRT- oestrogen receptor modulator - raloxifere

109
Q

Define septic arthritis

A

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

110
Q

Epidemiology of septic arthritis

A

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

111
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 > shoulderMEDICLA EMERGENCY - can destroy knee in 24hrs or less!
112
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
113
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)
114
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

115
Q

Common pathogens affecting prosthetic joints

A
  • STAPH AUREUS (most common)- Enterococci- MRSA- Enterobacter- Pseudomonas- Diphtheriodes- Haemolytic strep- Anaerobes
116
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
117
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 expensiveASPIRATION -> Microbio culture (aerobic + anaerobic)- Patient needs to be off antibiotics for at least 2 weeks
118
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
119
Q

Tx of prosthetic septic joint

A
  • Analgesia- Stop immunosuppression, increase steroids etcPotential 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
120
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

121
Q

Define osteomyelitis

A

Acute inflamed infected BM

122
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

123
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
124
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:- SALMONELLAIn IVDU:- PSEUDOMONAS AERUGINOSA- Serratia marcescens

125
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)
126
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 infectionAdults = 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 infectionsIV Drug Users = CLAVICLE + PELVIS (oft younger so vertebrae less vascular)

127
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

128
Q

Presentation of osteomyelitis

A
  • Onset over SEVERAL DAYS- DULL BONY PAIN + HOT + SWOLLEN + ERYTHEMA- May be aggravated by MOVEMENT- Systemic: FEVER, RIGORS, sweats, malaiseIf 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 tractCan also occur close to joint and pus can discharge into joint when infection breaks through cortex (more common in infants)
129
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
130
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
131
Q

What are the XR changes seen in chronic osteomyelitis

A
  • cortical erosion, - periosteal reaction, (edge raised) - mixed lucency, - Sclerosis - sequestra - soft tissue swelling
132
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
133
Q

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

A

it’s longer lasting- GI upset- Pruritis

134
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

135
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
136
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)

137
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

138
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
139
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 diseaseComplication: vertebral fractures
140
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)
141
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
142
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

143
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 cellsSULFAZALASINE DOESN’T WORK on SPINAL INFLAM
144
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
145
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
146
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 fingerPENCIL IN CUP DEFORMITY

147
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)
148
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
149
Q

Define reactive arthritis

A

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

150
Q

Common triggering pathogens of reactive arthritis

A
  • C trachomatis- Campy jejuni- Salm enteritidis- ShigellaAlso:- yersinia- ureaplasma urealyticum
151
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

152
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 examinationSexual health review + stool culture
153
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
154
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

155
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

156
Q

Epidemiology of SLE

A

Most common in FEMALES- more common in Afro-Caribbean premenopausal women (20-40)

157
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
158
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 alopeciaJoints:- Symmetrical + non-errosive- Deformaties can be corrected- Less proliferative than RACan 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

159
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
160
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)

161
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 toolsPrimary:- Fairly benign- No digital ulcersSecondary - related to connective tissue diseases esp Systemic sclerosis, SLE and mixed- Can develop later in life- Can get digital ulcers
162
Q

Define Sjogren’s syndrome

A

Multisystem autoimmune EXOCRINE DYSFUNCTIONCan be primary or secondary (Associated with other AI conditions)

163
Q

Presentation of Sjogren’s

A

Dry, dry, dry- Dry eyes (keratoconjunctivitis sicca)- Dry mouth (xerostomia) - Parotid swelling- Dry vaginaAlso:- Arthritis- Rash- Vasculitis- Neurological- Interstitial lung disease- Association with pericarditis- Renal tubular acidosis (type 1)

164
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 glandsUncommonly a lip biopsy may be done -> Sialadenitis (salivary gland infection)
165
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
166
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 therapyDirectly confers Increased risk of LYMPHOMA- Eye infections (conjunctivitis, corneal ulcers)- Oral problems (dental cavities, candida infections)- Vaginal problems (candidiasis, sexual dysfunction)

167
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

168
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 stageCan get iron deficiency anaemia - can see ‘watermelon stomach’ on endoscopy

169
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
170
Q

Dx of scleroderma

A

Limited:- ANTI CENTROMERE Ab - 70%Diffuse = Scl-70 (topoisomerase) Ab- Oft ANA +VE- may be RNA polymerase Ab pos

171
Q

Tx for scleroderma

A

No cure - treat sympsRaynauds:- 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-IEarly detection of pulm arterial HTN:- Annual echos + pulm function testsTreat pulm fibrosis - Cyclophosphamide- NintedanibTreat skin oedema:- No treatment (mild)- Mycophenolate (more severe)- Autologous stem cell transplantation (widespread + severe)

172
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 skinCan be caused as part of paraneoplastic syndrome

173
Q

Epidemiology of Dermato/Polymyositis

A

POLYMYOSITIS: more common in WOMEN; esp 30-60 Y/ODERMATOMYOSITIS: more common in WOMEN; can also affect CHILDREN (juvenile dermatomyositis)HLA B8/DR3 genetic link

174
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 DISEASEDerm:- GOTTRON’S PAPULES - rashes on backs of knuckles (DIPs, PIPs)- HELIOTROPE eyelid rash- Photosensitive shawl sign- may get Malar rash- may get calcinosis cutis
175
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 lungsScreen for malig (PET-CT)
176
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
177
Q

Define vasculitis + sub types

A

Heterogenous, multisystem inflammation of blood vesselsLarge 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)

178
Q

Types of classification of vasculitis

A
  • Vessel size- Chappel Hill Consensus classification - Hybrid of vessel size, pathophys + underlying
179
Q

Pathophys of GCA

A

Affects branches of EXTERNAL CAROTIDHistologically:- 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 = headachesOpthalmological = visionFacial = jaw claudication

180
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
181
Q

RFx for GCA

A
  • Associated with polymyalgia rheumatica and ANCA associated vasculitis- Associated with CANCER- More common in FEMALE
182
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 lossExtra cranial - e.g. Aortitis- May mimic infection/cancer-CONSTITUTIONAL SYMPTOMS/B SYMPTOMS: - Weight loss, low-grade fever, Anaemia, Malasise- POLYMYALGIA- Limb CLAUDICATION

183
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)

184
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
185
Q

US vs biopsy

A

US:- Non invasive- Can check multiple sites/vessels (including extracranial) in one visit- Better sensitivity than TA biopsyBUT- 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

186
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 symptomsFor Relapse:- METHOTREXATE +/- TOCILIZUMAB (IL6 inhib - can be a steroid weaning measure)
187
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
188
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
189
Q

Epidemiology/RFx of Polyarteritis nodosa

A
  • MALES > 50 Y/O- Associated with HEP B (hep C + HIV)- more common in developing countries
190
Q

Pathophys of Polyarteritis Nodosa (PN)

A

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

191
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
192
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
193
Q

Tx of PN

A
  • CORTICOSTEROIDS (+ cyclophosphamide if needed)- Control HTN -> ACE-I- If Hep B +ve = +antiviral + plasma exchange if needed
194
Q

Complications of Polyarteritis Nodosa

A

GI perforation + haemorrhagesArthritisRenal infarctsStrokesMI

195
Q

Epidemiology of granulomatosis w/ polyangitis (GPA)

A

Late teens/early adulthood- most commonly seen in caucasians but could be any ethnicityStaph aureus nasal carriage - associated with relapse in established disease

196
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)

197
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.
198
Q

Tx of GPA

A
  • Nasal corticosteroid- Cyclophosphamide
199
Q

Epidemiology of mechanical lower backpain

A
  • v common, oft self limiting- May be normal esp in ppl 20-55 - Trauma/work related
200
Q

Signs of serious pathology in lower back pain

A
  • ELDERLY (may be myeloma)- NEuropathic pain (spinal cord compression)
201
Q

Lumbar spondylosis

A

Degeneration of IV disc -> loss of compliance + thins over time- seen in ELDERLYInitialy asymp -> progressive- MC = L4/L5 or L5/S1Give analgesia + physio if simple mechanical painIf serious pathology suspected -> XR + MRI

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