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Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is osteoarthritis?

A
  • Degenerative change-> wear and tear of synovial joints

- Imbalance between cartilage wearing down + chondrocytes repairing

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2
Q

What are the risk factors for osteoarthritis?

A

Obesity, age, occupation, trauma, female, family history

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3
Q

What are the X-ray changes characteristic of osteoarthritis?

A

LOSS or no X-ray change

  • Loss of joint space
  • Osteophytes
  • Subchondral sclerosis-> increased density of bone along joint line
  • Subchondral cysts-> fluid filled holes in bone
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4
Q

How does osteoarthritis present?

A
  • Joint pain + stiffness-> worse on activity
  • Deformity, instability, reduced function
  • Joints affected-> MCP (thumb base), DIPJs, wrist, hips, knees, SIJs, cervical spine
  • Hands-> Heberden’s nodes (DIPJ), Bouchard’s (PIPJ), squaring of thumb base, weak grip, reduced ROM
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5
Q

What are Heberden’s nodes?

A

Deformity of DIPJs in osteoarthritis

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6
Q

What are Bouchard’s nodes?

A

Deformity of PIPJs in osteoarthritis

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7
Q

How is osteoarthritis diagnosed?

A
  • Can make without investigations in >45s

- Symptoms-> activity related pain, no morning stiffness, no stiffness lasting <30 mins

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8
Q

How is osteoarthritis managed?

A
  • Weight loss
  • Physio
  • OT
  • Analgesia-> paracetamol, NSAIDs (oral/topical), PPI, opiates
  • Intra-articular steroid injections
  • Joint replacement-> hip/knee
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9
Q

What is rheumatoid arthritis?

A
  • Autoimmune condition causing chronic inflammation of synovial lining, tendon sheaths and bursa
  • Symmetrical polyarthritis
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10
Q

What are the risk factors for rheumatoid arthritis?

A
  • Women
  • Any age but usually middle
  • FH
  • HLADR4 gene (in RF +ve patients)
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11
Q

What is rheumatoid factor?

A
  • Autoantibody-> usually IgM
  • Targets Fc portion of IgG antibody-> systemic inflammation
  • Present in 70% of RA patients
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12
Q

What is anti-CCP?

A
  • Antibody sometimes present in rheumatoid arthritis

- More sensitive than rheumatoid factor

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13
Q

How does rheumatoid arthritis present?

A
  • Pain, swelling + stiffness-> improves with activity
  • Joints-> hands + feet (eg wrist, ankle, MCP, PIP, MTPJs)
  • Can affect large joints-> knees, shoulders, elbows
  • DIPJs hardly affected
  • Atlantoaxial subluxation
  • Hand signs-> Z-shaped deformity of thumb, Swan neck deformity, Boutonniere’s
  • Extra-articular disease
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14
Q

What hand signs can patients get in rheumatoid arthritis?

A
  • Boggy inflammation + swelling
  • Z-shaped deformity of thumb
  • Swan neck deformity-> hyperextended PIPJ + flexed DIPJ
  • Boutonniere’s deformity-> hyperextended DIPJ + flexed PIPJ
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15
Q

What extra-articular disease can present in rheumatoid arthritis?

A
  • Caplan’s syndrome-> pulmonary fibrosis + nodules
  • Bronchiolitis obliterans
  • Felty’s syndrome-> rheumatoid arthritis + neutropaenia + splenomegaly
  • Sicca syndrome-> secondary Sjogren’s
  • Anaemia
  • CVD
  • Carpal tunnel
  • Episcleritis + scleritis
  • Rheumatoid nodules
  • Amyloidosis
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16
Q

What is Felty’s syndrome?

A

rheumatoid arthritis + neutropaenia + splenomegaly

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17
Q

How is rheumatoid arthritis investigated?

A
  • Clinical
  • Rheumatoid factor
  • Anti-CCP
  • CRP
  • ESR
  • X-rays-> joint destruction, bony erosions etc
  • US-> synovitis
  • Referral criteria
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18
Q

What X-ray changes might be present in rheumatoid arthritis?

A
  • Joint destruction + deformity
  • Soft tissue swelling
  • Periarticular osteopenia
  • Bony erosions
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19
Q

What is the referral criteria for suspected rheumatoid arthritis?

A
  • Adult with persistent synovitis regardless of markers

- Urgent-> small joints of hands + feet, multiple joints, symptoms for 3+ months

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20
Q

What is the diagnostic criteria for rheumatoid arthritis?

A

American College of Rheumatology + European League Against Rheumatism-> score added up and 6+ indicates

  • More joints-> higher
  • Small joints-> higher
  • RF and anti-CCP
  • ESR and CRP
  • Symptoms for 6+ weeks
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21
Q

What is the DAS28 score?

A

For rheumatoid arthritis

  • Disease activity-> assess 28 joints for swelling + tenderness
  • Use ESR + CRP too
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22
Q

What affects prognosis in rheumatoid arthritis?

A

Young, male, more joints, RF and anti-CCP positive, erosions on X-ray-> worse prognosis

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23
Q

What is used for rheumatoid arthritis treatment?

A
  • NSAIDS, COX-2 inhibitors, steroids (+PPI cover)
  • DMARDs-> methotrexate, leflunomide, sulfasalasine, hydroxychloroquinine
  • May use infliximab or etanercept or rituximab
  • CRP + DAS28 to monitor treatment success
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24
Q

What is the mechanism of action of methotrexate?

A

Interferes with folate metabolism + suppresses immune system-> use in rheumatoid arthritis

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25
Q

How is methotrexate taken?

A
  • 1 tablet/injection once weekly

- Folic acid 5mg on different day

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26
Q

What are the side effects of methotrexate?

A

Pulmonary fibrosis, teratogenic, liver toxicity, mouth ulcers, mucositis, low WBCs

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27
Q

What is leflunomide?

A

Interfered with pyrimidine production (RNA + DNA)-> used in rheumatoid arthritis

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28
Q

What are some side effects of leflunomide?

A

Hypertension and peripheral neuropathy

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29
Q

What is sulfasalazine?

A

Immunosuppressant + anti-inflammatory-> related to folate metabolism

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30
Q

What is a side effect of sulfasalazine?

A

Reduced sperm count

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31
Q

What is hydrochloroquine?

A

Antimalarial but immunosuppressant too-> use in rheumatoid arthritis

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32
Q

What are some side effects of hydrochloroquine?

A

Nightmares + reduced visual acuity

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33
Q

How do anti-TNF drugs (eg etanercept) work?

A

Block TNF cytokines + reduce inflammation

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34
Q

What are some side effects of anti-TNF drugs (eg etanercept)?

A

reactivation of TB + Hep B

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35
Q

What is rituximab?

A

Monoclonal antibody-> can use in RA

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36
Q

What are some side effects of rituximab?

A

Low platelets, night sweats

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37
Q

What is psoriatic arthritis?

A
  • Inflammatory arthritis associated with psoriasis

- Seronegative spondyloarthropathy

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38
Q

How many patients with psoriasis have psoriatic arthritis?

A

10-20%

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39
Q

What are the different patterns of psoriatic arthritis?

A
  • Symmetrical polyarthritis-> hands, wrists, ankles, DIPJ
  • Asymmetrical pauciarthritis-> digits + few joints
  • Spondylitis pattern-> back, sacroiliitis etc
  • Other-> spine, achilles, plantar fascia
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40
Q

What are the signs of psoriatic arthritis?

A
  • Nails-> psoriasis, nail pitting, onycholysis
  • Dactylitis-> full finger inflammation
  • Enthesitis-> tendon inserting to bone tender
  • Eyes-> conjunctivitis, anterior uveitis
  • Aortitis
  • Amyloidosis
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41
Q

What is the PEST screening tool?

A

Psoriasis Epidemiological Screening Tool-> if high score get rheum referral

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42
Q

What are the X-ray changes classical of psoriatic arthritis?

A
  • Pencil in cup-> central erosion to bone beside joint, one bone hollow + other narrow, in hands + feet
  • Periostitis-> periosteum inflammed
  • Ankylosis-> bones join + stiffen
  • Osteolysis-> destroy bone
  • Dactylitis-> soft tissue swelling
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43
Q

What is the ‘pencil in cup’ X-ray sign?

A

Sign of psoriatic arthritis

  • central erosion to bone beside joint
  • one bone hollow + other narrow
  • in hands + feet
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44
Q

What is arthritis mutilans?

A
  • Severe psoriatic arthritis
  • Osteolysis of phalanxes + progressive shortening
  • Telescopic finger
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45
Q

How is psoriatic arthritis managed?

A
  • NSAIDs
  • DMARDs
  • Anti-TNF
  • Ustekinumab-> monoclonal antibody
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46
Q

What is reactive arthritis (Reiter syndrome)?

A
  • Acute monoarthritis
  • Synovitis in reaction to recent infective trigger
  • Often GE or STI
  • Seronegative spondyloarthopathy
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47
Q

What usually triggers reactive arthritis (Reiter syndrome)?

A
  • Gastroenteritis

- STI-> chlamydia

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48
Q

What gene is seronegative spondyloarthropathy associated with?

A

HLAB27

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49
Q

What symptoms is reactive arthritis (Reiter syndrome) associated with?

A

Can’t pee, see or climb a tree

  • Bilateral conjunctivitis
  • Anterior uveitis
  • Circinate balantitis
  • Arthritis
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50
Q

How is reactive arthritis (Reiter syndrome) managed?

A
  • Hot joint policy-> antibiotics until septic excluded
  • Aspirate-> MC&S to exclude septic + crystal exam (gout or pseudogout)
  • NSAIDs
  • Steroid injections
  • Systemic steroids in multiple joints
  • Most resolve in 6 months
  • Recurrent-> DMARDs or anti-TNF
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51
Q

What is ankylosing spondylitis?

A
  • Seronegative spondyloarthropathy
  • Progressive stiffness + pain in spine-> SIJ + vertebral column joints
  • Fusion in joints
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52
Q

What is the classic X-ray finding in ankylosing spondylitis?

A

Bamboo spine

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53
Q

How does ankylosing spondylitis present?

A
  • Typically young male with symptoms for 3 months
  • Lower back pain + stiffness in buttocks
  • Improves with movement
  • Worse at night + morning (may wake)
  • Takes 30 minutes to improve on a morning
  • Vertebral fractures
  • Lots of systemic associations eg weight loss, chest pain, dactylitis
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54
Q

What other systemic/extra-articular symptoms can ankylosing spondylitis present with?

A
  • Weight loss
  • Fatigue
  • Chest pain-> costovertebral + costosternal joints
  • Enthesitis
  • Dactylitis
  • Anaemia
  • Anterior uveitis
  • Aortitis
  • Heart block
  • Restrictive lung disease
  • Pulmonary fibrosis
  • IBD
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55
Q

What is Schober’s test?

A
  • Stand straight + find L5 vertebrae
  • Mark 10cm above + 5cm below joint
  • Ask to bend forwards + measure distance
  • Different of <20cm-> restriction of lumbar movements
  • Supports diagnosis of ankylosing spondylitis
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56
Q

What investigations are done in ankylosing spondylitis?

A
  • CRP + ESR
  • HLAB27 genetics
  • X ray of spine and sacrum-> bamboo spine
  • MRI-> bone marrow oedema
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57
Q

What X-ray findings might be present in ankylosing spondylitis?

A
  • Bamboo spine
  • Squaring of vertebral bodies
  • Subchondral sclerosis + erosions
  • Syndesmophytes-> bone growth where ligaments insert
  • Ossification-> ligaments/discs turn to bone
  • Fusion-> SI, facet or costovertebral joints
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58
Q

How is ankylosing spondylitis managed?

A
  • NSAIDs
  • Steroids in flares
  • Anti-TNF-> etanercept or infliximab
  • Secukinumab
  • Physio
  • Exercise
  • Avoid smoking
  • Bisphosphonates for osteoporosis
  • Surgery
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59
Q

What is Systemic Lupus Erythematosus (SLE)?

A
  • Inflammatory autoimmune connective tissue disease
  • Affects multiple organs + systems (systemic)
  • Red malar rash (erythematosus)
  • Relapsing remitting course
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60
Q

Who is Systemic Lupus Erythematosus (SLE) more common in?

A
  • Women
  • Asians
  • Young to middle ages adults
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61
Q

What is the pathophysiology of Systemic Lupus Erythematosus (SLE)?

A
  • Anti-nuclear antibodies-> to cell nuclei
  • Immune response to target proteins-> inflammatory response
  • Chronic + against body tissues
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62
Q

How does Systemic Lupus Erythematosus (SLE) present?

A
  • Photosensitive malar rash-> butterfly rash on nose + cheeks worsened by sunlight
  • Fatigue
  • Weight loss
  • Arthralgia
  • Myalgia
  • Fever
  • SOB
  • Pleuritic chest pain
  • Mouth ulcers
  • Hair loss
  • Raynaud’s
  • Lymphadenopathy
  • Splenomegaly
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63
Q

How is Systemic Lupus Erythematosus (SLE) investigated?

A
  • Autoantibodies-> anti-nuclear (ANA), anti-double stranded DNA (anti-dsDNA), antiphospholipid (secondary)
  • FBC-> normocytic anaemia
  • CRP + ESR
  • C3 + C4 decreased
  • Urine protein:creatinine + renal biopsy-> nephritis
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64
Q

What diagnostic criteria can be used in Systemic Lupus Erythematosus (SLE)?

A

SLICC or ACR-> ANA + clinical features

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65
Q

What auto-antibodies are usually present in Systemic Lupus Erythematosus (SLE)?

A
  • anti-nuclear (ANA)
  • anti-double stranded DNA (anti-dsDNA)
  • antiphospholipid (secondary)
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66
Q

What are the complications of Systemic Lupus Erythematosus (SLE)?

A

Chronic inflammation…

  • CVD-> often cause death
  • Infection
  • Anaemia of chronic disease
  • Pericarditis
  • Pleurisy
  • Interstitial lung disease
  • Lupus nephritis
  • Neuropsychiatric
  • Recurrent miscarriage
  • IUGR
  • Pre-eclampsia
  • Preterm
  • Anti-phospholipid syndrome
  • VTE
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67
Q

How is Systemic Lupus Erythematosus (SLE) managed?

A
  • Symptom control not sure
  • NSAIDs, prednisolone, hydroxychloroquinine, suncream + sun avoidance
  • Immunosuppressants when severe-> MTX, azathioprine etc
  • Biological when severe/resistance-> rituximab etc
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68
Q

What is Discoid Lupus Erythematosus?

A

Non-cancerous skin condition associated with risk of SLE + squamous cell cancers

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69
Q

Who is Discoid Lupus Erythematosus more common in?

A
  • Women
  • Age 20-40
  • Darker skinned
  • Smokers
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70
Q

How does Discoid Lupus Erythematosus present?

A
  • Lesions on face/ears/scalp-> inflamed, dry, erythematous, patchy, crusty/scaling, photosensitive
  • Scarring alopecia-> hair doesn’t grow back
  • Hyper/hypopigmented scars
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71
Q

How is Discoid Lupus Erythematosus managed?

A
  • Skin biopsy to confirm
  • Sun protection
  • Topical steroids
  • Intralesion steroid injections
  • Hydroxychloroquine
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72
Q

What is systemic sclerosis?

A
  • Autoimmune inflammatory + fibrotic connective tissue disease
  • Affects skin + internal organs
  • Scleroderma-> hardening of skin
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73
Q

What are the different types of systemic sclerosis?

A
  • Limited cutaneous systemic sclerosis-> CREST syndrome

- Diffuse cutaneous systemic sclerosis-> CREST features + internal organ problems

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74
Q

What are the features of limited cutaneous systemic sclerosis (CREST syndrome)?

A
  • Calcinosis
  • Raynaud’s
  • Oesophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
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75
Q

What are the features of Diffuse cutaneous systemic sclerosis?

A
  • Calcinosis
  • Raynaud’s
  • Oesophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
  • HTN + CAD
  • Pulmonary HTN + fibrosis
  • Glomerulonephritis
  • Scleroderma renal crisis
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76
Q

What are the features of systemic sclerosis?

A
  • Scleroderma-> tight + shiny skin
  • Calcinosis-> deposits under skin
  • Raynaud’s
  • Oesophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
  • Systemic and pulmonary HTN
  • Pulmonary fibrosis
  • Scleroderma renal crisis
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77
Q

What is Raynaud’s phenomenon?

A
  • Fingers completely white/blue in response to cold
  • Vasoconstriction of vessels
  • Common without underlying disease but may indicate systemic sclerosis
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78
Q

What auto-antibodies may be present in systemic sclerosis?

A
  • ANA
  • Anti-centromere
  • Anti-Scl-70
79
Q

What is nailfold capillaroscopy?

A
  • Examine where skin meets fingernails at base
  • Peripheral capillaries-> abnormal, avascular, microhaemorrhages etc
  • Look for systemic sclerosis in Raynaud’s
80
Q

What is used to investigate for systemic sclerosis?

A

Nailfold capillaroscopy

  • Examine where skin meets fingernails at base
  • Peripheral capillaries-> abnormal, avascular, microhaemorrhages etc
  • Look for systemic sclerosis in Raynaud’s
81
Q

How is systemic sclerosis diagnosed?

A

American College of Rheumatology + European League Against Rheumatism criteria-> clinical + antibodies + nailfold capillaroscopy

82
Q

How is systemic sclerosis managed?

A
  • Steroids + immunosuppressants
  • Skin stretching
  • Emollients
  • Cold avoidance
  • PT + OT
  • Nifedipine-> Raynaud’s
  • PPIs
  • Analgesia
  • Anti-HTNs
83
Q

What is polymyalgia rheumatica?

A

Inflammatory condition causing pain and stiffness in the shoulders, pelvic girdle and neck

84
Q

What is polymyalgia rheumatica strongly associated with?

A

Giant cell arteritis

85
Q

Who is polymyalgia rheumatica most common in?

A
  • Women
  • Caucasians
  • 50+
86
Q

What are the core features of polymyalgia rheumatica?

A
  • Symptoms for 2+ weeks
  • Bilateral shoulder pain + can radiate to elbow
  • Bilateral pelvic girdle pain
  • Worsened-> movement
  • Interferes with sleep
  • 45 min+ of morning stiffness
  • Systemic-> weight loss, low mood
  • Upper arm tenderness
  • Carpal tunnel
  • Pitting oedema
87
Q

What the the differentials for polymyalgia rheumatica?

A
  • OA
  • RA
  • SLE
  • Myositis
  • Cervical spondylosis
  • Adhesive capsulitis
  • Hyper or hypothyroidism
  • Osteomalacia
  • Fibromyalgia
88
Q

How is polymyalgia rheumatica diagnosed?

A
  • Clinical + response to steroids
  • Inflammatory-> CRP + ESR
  • FBC, U+Es, LFTs, TFTs, CK (raised)
  • RF
  • Calcium-> other causes
  • Urine dip
  • Rule out-> ANA (SLE), anti-CCP (RA), Bence-Jones (myeloma), CXR
89
Q

How is polymyalgia rheumatica managed?

A
  • Oral prednisolone-> 15mg OD
  • Assess after 1 week + stop if no response
  • Assess after 3-4 weeks-> should improve
  • Good response-> reducing regime long term
  • Recurrence-> increase dose + can take 1-2 years
  • Rheumatology referral-> if need steroids for 2+ years
90
Q

How long does it take for someone to become dependent on steroids?

A

3 weeks

91
Q

What extra precautions should be done when someone is on long-term steroid therapy?

A
  • Sick day rules-> increase dose when unwell
  • Treatment card-> alert when unresponsive
  • Osteoporosis prevention-> bisphosphonates + calcium + vitamin D
  • PPI
92
Q

What is giant cell arteritis?

A

Systemic vasculitis of medium + large arteries-> commonly temporal arteritis

93
Q

What is giant cell arteritis associated with?

A

Polymyalgia rheumatica-> high risk when female + 50+

94
Q

What is a key complication of temporal arteritis?

A

Irreversible vision loss

95
Q

What are the symptoms of temporal arteritis?

A
  • Headache-> severe, unilateral, temple/forehead
  • Scalp tenderness-> when brush hair etc
  • Jaw claudication
  • Blurred/double vision-> can get rapid complete painless sight loss
  • Systemic-> fever, muscle ache, fatigue, weight loss, loss of appetite, peripheral oedema
96
Q

How is temporal arteritis diagnosed?

A
  • Raised ESR
  • Temporal artery biopsy-> multinucleated giant cells + beware of skip lesions
  • FBC, LFTs, CRP
  • Duplex US of temporal artery-> hypoechoic halo sign
97
Q

How is temporal arteritis managed?

A
  • Steroids immediately-> 40-60mg prednisolone a day + review response in 48 hours
  • Steroids till symptoms resolve-> can take few years
  • Aspirin 75mg OD-> if suspect visual loss + stroke
  • PPI + osteoporosis prevention
98
Q

What are the complications of temporal arteritis?

A
  • Neuro-opthalmic-> visual loss + stroke
  • Relapses
  • Steroid related SEs
  • CVA
  • Aortitis-> aneurysm + dissection
99
Q

What is polymyositis?

A

Chronic inflammation of muscles

100
Q

What is dermatomyositis?

A

Connective tissue disorder in which skin + muscles are chronically inflamed

101
Q

What is the key investigation for polymyositis & dermatomyositis?

A

Creatinine kinase-> can be >1000u/L (normal- <300)

102
Q

What can cause polymyositis & dermatomyositis?

A

Malignancy-> paraneoplastic syndrome of lung, breast, ovarian or gastric cancers

103
Q

How does polymyositis present?

A
  • Muscle pain + weakness-> bilateral, proximal, shoulders, pelvic girdle, over a few weeks
  • No skin involvement
  • Fatigue
104
Q

How does dermatomyositis present?

A
  • Muscle pain + weakness-> bilateral, proximal, shoulders, pelvic girdle, over a few weeks
  • Fatigue
  • Photosensitive erythematous rash-> back, shoulders, neck
  • Purple rash on face + eyelids
  • Periorbital oedema
  • Subcutaenous calcinosis
  • Gottron lesions-> scaly + erythematous
105
Q

How is polymyositis diagnosed?

A
  • Clinical
  • High CK
  • Autoantibodies-> anti-Jo-1
  • Electromyography (EMG)
  • Muscle biopsy
106
Q

How is dermatomyositis diagnosed?

A
  • Clinical
  • High CK
  • Autoantibodies-> anti-Mi-2, ANA
  • Electromyography (EMG)
  • Muscle biopsy
107
Q

How is polymyositis managed?

A
  • Assess for underlying cancers
  • PT + OT
  • Corticosteroids, azathioprine, IV Igs, biologicals
108
Q

How is dermatomyositis managed?

A
  • Assess for underlying cancers
  • PT + OT
  • Corticosteroids, azathioprine, IV Igs, biologicals
109
Q

What is the pathophysiology if antiphospholipid syndrome?

A
  • Antiphospholipid antibodies
  • Interfere with coagulation + make more prone-> hypercoagulable
  • Primary or secondary (eg SLE)
110
Q

What are the associations/complications of antiphospholipid syndrome?

A
  • VTE, stroke, MI
  • Pregnancy-> recurrent miscarriage, stillbirth, pre-eclampsia
  • Thrombocytopaenia
  • Livedo reticularis-> purple rash + mottled
  • Libmann-Sacks endocarditis
111
Q

How is antiphospholipid syndrome diagnosed?

A

History of thrombosis or pregnancy complications + antibodies (antiphospholipid)

112
Q

How is antiphospholipid syndrome managed?

A
  • Rheumatology, haematology + ostatrics involvement
  • Warfarin-> INR range 2-3
  • LMWH + aspirin in pregnancy
113
Q

What is Sjogren’s syndrome?

A
  • Autoimmune disease of exocrine glands
  • Dry mucous membranes-> mouth, eyes, vagina
  • Primary or secondary (eg SLE)
114
Q

What antibodies are present in Sjogren’s syndrome?

A

Anti-ro + anti-la

115
Q

What is the Schirmer test?

A
  • Folded filter paper under lower lid + strip hand out over eyelid
  • 5 mins-> measure distance along strip
  • Normal-> >15mm
  • Sjogren’s syndrome-> <10mm
116
Q

How is Sjogren’s syndrome managed?

A
  • Artificial tears and saliva
  • Vaginal lubricants
  • Hydroxychloroquine
117
Q

What are the common complications of Sjogren’s syndrome?

A
  • Conjunctivitis
  • Corneal ulcers
  • Dental cavities
  • Candida infections
  • Sexual dysfunction
118
Q

What is vasculitis?

A

Inflammation of blood vessels-> can be small, medium or large

119
Q

What are some types of small vessel vasculitis?

A
  • Henoch-Schoenlein Purpura
  • Churg-Strauss
  • Wegener’s granulomatosis
  • Microscopic polyangiitis
120
Q

What are some types of medium vessel vasculitis?

A
  • Polyarteris nodosa
  • Churg-Strauss
  • Kawasaki’s disease
121
Q

What are some types of large vessel vasculitis?

A
  • Giant cell arteritis

- Takayasu’s arteritis

122
Q

How does vasculitis present (in general)?

A
  • Systemic-> fatigue, weight loss, anaemia, fever
  • Purpura-> purple + non-blanching
  • Joint + muscle pain
  • Peripheral neuropathy
  • Renal impairment
  • Uveitis + scleritis
  • HTN
123
Q

What investigations are done in vasculitis?

A
  • CRP
  • ESR
  • Anti-neurophil cytoplasmis (ANCA)
  • P-ANCA + C-ANCA
124
Q

How is vasculitis managed?

A
  • Depends on type
  • Rheum referral
  • Steroids-> oral, IV, nasal, inhaled
  • Cyclophosphamide
  • MTX
  • Azathioprine
125
Q

What is Henoch-Schonlein Purpura?

A
  • IgA vasculitis-> deposits in blood vessels

- Small vessel vasculitis

126
Q

How does Henoch-Schonlein Purpura present?

A
  • Purpuric rash on legs/bum
  • Joint pain
  • Abdominal pain
  • Renal involvement
  • Often kids <10 years
127
Q

What can trigger Henoch-Schonlein Purpura?

A
  • Upper airway infection

- GE

128
Q

How is Henoch-Schonlein Purpura managed?

A

Supportive-> simple analgesia

129
Q

How often does Henoch-Schonlein Purpura recur?

A

In 1/3 patients within 6 months

130
Q

What is Churg-Strauss?

A
  • Eosinophilic Granulomatosis with Polyangiitis

- Type of vasculitis-> small + medium vessel

131
Q

How does Churg-Strauss present?

A
  • Severe asthma in late teens/adults

- High eosinophils on RBC

132
Q

How does microscopic polyangiitis present?

A
  • Renal failure
  • SOB
  • Haemoptysis
133
Q

How does Wegener’s granulomatosis present?

A
  • Upper resp-> epistaxis, crusty secretions, saddle nise
  • Hearing loss
  • Cough, wheeze, haemoptysis
  • Glomerulonephritis
134
Q

What is polyarteritis nodosa associated with?

A

Hep B/C or HIV

135
Q

How does polyarteritis nodosa present?

A
  • MI
  • Renal impairment
  • Livedo reticularis-> mottles purple lace-like rash
136
Q

What is Kawasaki disease?

A

Medium vessel vasculitis

137
Q

What are the features of Kawasaki disease?

A
  • High fever for 5+ days
  • Erythematous rash
  • Bilateral conjunctivitis
  • Erythema + desquamation of palms + soles
  • Strawberry tongue
138
Q

What is the main complication of Kawasaki disease?

A

Coronary artery aneurysm

139
Q

How is Kawasaki disease managed?

A
  • Aspirin

- IV Igs

140
Q

How does Takayasu’s arteritis present?

A
  • Age <40
  • Fever
  • Malaise
  • Claudication
  • Syncope
141
Q

What is Takayasu’s arteritis?

A
  • Large vessel vasculitis
  • Aorta, branches + pulmonary arteries
  • Aneurysms + blockages
142
Q

How is Takayasu’s arteritis diagnosed?

A

CT, MRI angiography, carotid doppler US

143
Q

What is Bechet’s syndrome?

A

Complex inflammatory condition causing recurrent oral + genital ulcers

144
Q

What gene is Bechet’s syndrome associated with?

A

HLA B51

145
Q

What are the features of Bechet’s syndrome?

A
  • 3+ ulcers a year taking 2-4 weeks to heal-> genital + oral
  • Erythema nodosum
  • Uveitis
  • Morning stiffness + arthralgia
  • CNS-> headaches + memory problems
  • Pulmonary artery aneurysms
  • DVT
146
Q

How is Bechet’s syndrome investigated?

A

Pathergy test-> subcut abrasion + measure size in 24-48 hours

147
Q

How is Bechet’s syndrome managed?

A
  • Steroid tablets
  • Colchicine
  • Lidocaine ointment
  • Immunosuppressants
148
Q

What is gout?

A
  • Crystal arthropathy

- High uric acid causes urate crystals in joints

149
Q

What are gouty tophi?

A
  • Subcutaneous deposits of uric acid
  • Often in hands, elbows, ears and DIPJs
  • Need to rule out septic arthritis if hot + swollen
150
Q

What differential for gout is important to rule out?

A

Septic arthritis

151
Q

What are the risk factors for gout?

A
  • Male
  • Obese
  • High purine-> meat + seafood
  • Alcohol
  • Diuretics
  • CVD
  • Kidney disease
  • Family history
152
Q

What joints are typically affected in gout?

A
  • MTPJ
  • Wrists
  • Base of thumb (CMJs)
153
Q

How is gout diagnosed?

A
  • Clinical + exclude septic joint
  • Aspirate-> needle shaped negatively birefringent crystals (monosodium urate)
  • Joint X ray-> lytic lesions, punched out erosions, sclerotic borders, overhanging edges to erosions
154
Q

What will be found on a joint aspirate in gout?

A

needle shaped negatively birefringent crystals (monosodium urate)

155
Q

How is gout managed acutely?

A
  • NSAIDs 1st line
  • Colchicine
  • Steroids considered
156
Q

How is gout managed long term?

A
  • Allopurinol after acute attack settled
  • Weight loss
  • Minimise seafood + alcohol
157
Q

What is allopurinol?

A
  • Xanthine oxidase inhibitor

- Used in gout (long term)

158
Q

What is pseudogout?

A
  • Crystal arthropathy
  • Calcium pyrophosphate crystals in joints
  • AKA chondrocalcinosis
159
Q

How does pseudogout present?

A
  • Hot, swollen, stiff, painful joint(s)
  • Affects knee, shoulders, wrists, hips
  • Can be chronic
160
Q

How is pseudogout diagnosed?

A
  • Rule out septic
  • Aspiration-> no bacteria, rhomboid shaped positive birefringent crystals (calcium pyrophosphate)
  • X ray shows LOSS + chondrocalcinosis-> thin white line in middle of joint space (calcium deposits)
161
Q

What does LOSS stand for (in X-ray signs)?

A
  • Loss of joint space
  • Osteophyte formation
  • Subchondral sclerosis
  • Subarticular sclerosis
162
Q

What will be found on joint aspiration in pseudogout?

A

rhomboid shaped positive birefringent crystals (calcium pyrophosphate)

163
Q

What X-ray sign is pathognomonic for pseudogout?

A

chondrocalcinosis-> thin white line in middle of joint space (calcium deposits)

164
Q

How is pseudogout managed?

A
  • Nothing if chronic + asymptomatic
  • May spontaneously resolve over few weeks
  • NSAIDs
  • Colchicine
  • Joint aspiration
  • Steroids
  • Arthrocentesis (washout)
165
Q

What is osteoporosis?

A

Reduction in bone density leading to weakness and fractures

166
Q

What is osteopenia?

A

Less severe than osteoporosis-> reduction in bone density

167
Q

What are the risk factors for developing osteoporosis?

A
  • Older
  • Female
  • Reduced mobility/activity
  • Low BMI
  • RA
  • Alcohol
  • Smoking
  • Long term steroids
  • Other meds-> SSRIs, PPIs, anti-epileptics, anti-oestrogens
  • Post-menopausal (as oestrogen protective)
  • Previous fracture
  • Falls
  • Endocrine disorders
168
Q

What can protect against osteoporosis?

A
  • Oestrogen therapies-> HRT

- Pre-menopausal

169
Q

What is the FRAX scoring tool?

A

Risk of fragility fracture (major osteoporotic and hip fractures) over the next 10 years

  • Age
  • Sex
  • BMI
  • Co-morbidities-> RA, secondary osteoporosis, glucocorticoids
  • History of fracture
  • Smoking
  • Alcohol (>3 units/day)
  • Family history
  • BMD
170
Q

How is bone mineral density measured?

A
  • DEXA scan
  • Measure how much radiation absorbed by bones + indicate how dense
  • Measured at hip
  • T-score-> number of std devs below mean for healthy young adult
171
Q

What is a normal BMD score?

A

-1 or more

172
Q

What BMD score indicates osteopaenia?

A

-1 to -2.5

173
Q

What BMD score indicates osteoporosis?

A

-2.5 or less

174
Q

What BMD score + features indicate severe osteoporosis?

A

-2.5 or less + fracture

175
Q

When is FRAX score measured?

A
  • When at risk
  • Women >65
  • Men >75
  • Younger with risk factors
176
Q

How is osteoporosis managed?

A
  • Activity
  • Stop smoking
  • Fall avoidance
  • Calcium + Vitamin D
  • Bisphosphonates eg alendronate
  • Denosumab-> monoclonal antibody
  • HRT
  • Follow up-> repeat FRAX + DEXA every 3-5 years
  • Can have ‘treatment holiday’ if no fractures for 18 months to 3 years
177
Q

How do bisphosphonates work?

A

Interfere with osteoclast activity-> prevent resorption of bone (not replace lost bone)

178
Q

What are some examples of bisphosphonates and how are they taken?

A
  • Alendronate + risondronate-> PO + need to take on empty stomach then sit upright for 30 mins before moving or eating
  • Zolendronic acid-> IV once yearly
179
Q

What are the side effects of bisphosphonates?

A
  • Reflux + oesophageal erosions
  • Atypical fractures
  • Osteonecrosis of the jaw + external auditory canal
180
Q

What is osteomalacia?

A

Vitamin D deficiency leading to defective bone mineralisation and ‘soft’ bones

181
Q

What is Rickets?

A

Vitamin D deficiency leading to defective bone mineralisation and ‘soft’ bones-> in kids + before growth plates close

182
Q

What can cause Vitamin D deficiency + osteomalacia?

A
  • Poor dietary intake
  • Darker skin-> need longer sun exposure to get same level
  • Malabsorption disorder (eg IBD)
  • CKD as less metabolised in kidneys
183
Q

What is the normal physiology and role of Vitamin D?

A
  • Created from cholesterol by skin in response to UV radiation
  • Metabolised in kidneys
  • Needed to absorb calcium + phosphate from intestines + kidneys
  • Regulates bone turnover + promotes bone reabsorption to boost serum calcium
184
Q

What are the effects of low Vitamin D on blood components and bones?

A
  • Low calcium and phosphate-> defective bone mineralisation
  • Secondary hyperparathyroidism-> response to low calcium so tries to stimulate increased reabsorption from bones-> further mineralisation problems
185
Q

How does osteomalacia present?

A
  • Asymptomatic
  • Fatigue
  • Bone pain
  • Muscle weakness + aches
  • Pathological fractures
186
Q

How is osteomalacia investigated?

A
  • Serum 25-hydroxyvitamin D-> <25nmol/L counts as diagnostic (25-50nmol/L is insufficiency)
  • Low calcium, low phosphate, high ALP, high PTH
  • X-ray-> osteopenia
  • DEXA-> may have low BMD
187
Q

How is osteomalacia treated?

A
  • Vitamin D supplements-> high dose short term (eg 4000IU daily for 10 weeks) then maintenance of 800IU+ for life
  • Insufficiency-> maintenance regime only
188
Q

What is Paget’s disease of the bone?

A

Bone turnover excessive and unco-ordinated due to osteoclast and osteoblast activity balance

189
Q

What is the pathophysiology of Paget’s disease of the bone?

A
  • Bone turnover excessive and unco-ordinated due to osteoclast and osteoblast activity balance
  • High (sclerosis) + low (lysis) density areas in patches
  • Causes enlarged, misshapen bones that easily fracture
  • Particularly axial skeleton (head + spine)
190
Q

How does Paget’s disease of the bone present?

A
  • Older adults
  • Bone pain + deformity
  • Fractures
  • Hearing loss
191
Q

What are the biochemical findings in Paget’s disease of the bone?

A
  • Raised ALP
  • Other LFTs normal
  • Normal calcium + phosphate
192
Q

What are the X-ray findings in Paget’s disease of the bone?

A
  • Bone enlargement and deformity
  • Osteoporosis circumscripta-> lytic lesions + well definted
  • Cotton wool skull appearance-> sclerosis + lysis
  • V-shaped defects in long bones-> osteolytic
193
Q

How is Paget’s disease of the bone managed?

A
  • Bisphosphonates
  • NSAIDs for pain
  • Calcium + Vitamin D
  • Surgery
  • Monitoring-> symptoms + ALP
194
Q

What are the serious complications of Paget’s disease of the bone?

A
  • Osteosarcoma

- Spinal stenosis (canal narrowing due to deformity)

Medicine (13 decks)

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