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4 - Med > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Describe the general differences between inflam and non-inflam conditions?

A

Inflam: pain worse after rest/in morning, morning stiffness >30 min, systemic symptoms present, actue/sub-acute symptoms

non-inflam: pain after use/at end of day, morning stiffness <30 min, no systemic sx, chronic sx

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2
Q

name 2 acute inflammatory monoarthritic ?

A
  • gout
  • Septic arthritis
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3
Q

Name a chronic inflammatory polyarthritis ? (2)

A
  • Rheumatoid arthritis
  • Psoriatic (actually oligo most the time)
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4
Q

name a chronic inflammatory axial arthritis ?

A

ankylosing spondylitis

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5
Q

name a non-inflammatory acute monoarthritic ?

A

torn cruciate ligament

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6
Q

name a non-inflam chronic polyarthritis ?

A

osteoarthritis

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7
Q

name a chronic non-inflammatory axial arthritis ?

A

scoliosis

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8
Q

What is osteoarthritis ? pathophysiology

A

degenerative joint disorder (wear and tear): result of mechanical and biological events that damage joints (degeneration + synthesis of cartilage chondrocyts)
- imbalance between cartilage worn down + chondrocyte repair => structural issues => pain

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9
Q

OA RF ?

A
  • obesity (low grade inflam state)
  • increasing age
  • occupation
  • trauma to joint
  • female
  • FHx of OA
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10
Q

OA presentation ? common joints ?

A

joint pain + stiffness (morning stiffness <30min), worsened by activity, crepitus
- common affected joints: knees, hips, sacroiliac, DIP (if distal the not RA!), CMC, wrist, asymmetrical

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11
Q

name the OA signs in hands + OE (7)

A
  • herberden’s nodes (high => DIP)
  • bouchard’s nodes (below => PIP)
  • squaring at base of thumb (CMC joint)
  • weak grip
  • reduced range of motion
  • effusions around the joint
  • crepitus on movement
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12
Q

where might OA patients present with referred pain ?

A

consdier OA in the hip in patients presenting with lower bakc or knee pain

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13
Q

how is OA diagnosed ?

A

clinical diagnosis if the patient is over 45
(typical pain associated with activity and morning stiffness lasting less than 30 mins)

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14
Q

OA Mx ?

A
  • lifestyle changes: weight loss, physiotherapy, arthotics
  • analgesia: paracetamol + topical NSAID (diclofenac)
  • add oral NSAID (Ibuprofen) + PPI (lanzoprazole)
  • consider opiates: codeine, intra-articular joint infections
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15
Q

What is RA ?

A

autoimmune condition that causes chronic inflam of synovial lining of joints, tendon sheaths + bursa (synovitis)

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16
Q

what type of arthritis is RA ? distribution

A

inflammatory symmetrical polyarthritis

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17
Q

RA RF ?

A
  • female
  • > 50
  • smoking
  • fam history of RA
  • genetic association (HLA DR4)
    (smoking doubles risk, FHx doubles risk, both together is x20 risk)
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18
Q

what are the 2 antiobodies associated with RA ? present in how many ppl ?

A
  • rheumatoid factor (RF): present in 70% of ppl with RA
    anti-CCP antibodies: present in 80% of ppl with RA
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19
Q

what is RF ? what does it do/target?

A

RF is an autoantibody taht targets Fc region on IgG => activation of immune system against patients own IgG => systemic inflam + erosions

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20
Q

Why are RF and anti-CCP important to know in RA ?

A

they affect prognosis
- double positive means more likely to have persistent disease and will need lifelong meds
- double negative means could potentially come off treatment

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21
Q

RA presentation ? what joints affected ?

A

typically symmetrical distal polyarthropathy (pain, swelling, stiffness)
- wrist, ankle, MCP, PIP (almost never DIP)
- systemic symptoms: fatigue, weight loss, malaise

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22
Q

what are the RA signs in the hands ? (4)

A
  • Z shape deformity of the thumb
  • Ulnar deviation
  • swan neck deformity
  • boutonniere deformity
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23
Q

extra articular manifestations of RA ? (6)

A
  • pulmonary fibrosis
  • secondary Sjogren’s
  • CVD
  • Rheumatoid nodules
  • Lymphadenopathy
  • carpul tunnel
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24
Q

RA initial Ix ?

A
  • RF
  • Anti-CCP
  • Inflam markers: CRP + ESR
  • X-rays of the hands and feet for bone changes
    (Dx based on clinical findings and blood results)
    (also FBC, U+E, LFT for baseline Ix)
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25
Q

What XR changes would be seen RA ?

A
  • joint destruction and deformity
  • periarticular osteopenia
  • boney erosions
  • soft tissue swelling
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26
Q

RA Mx ?

A

short course steroids initially + in flare ups, NSAIDs, PPI
- DMARDS: methotrexate
- biologics: adalimumab, infliximab, rituximab (these all cause immunosuppression)

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27
Q

What needs to be prescribed alongside methotrexate ?

A

folic acid
- methotrexate interferes with folate metabolism and suppresses the immune system. Folic acid is taken once a week (on a different day to the methotrexate)
(methotrexate uses folic acid transporter)

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28
Q

methotrexate SE ? what reduces the side effect risk

A
  • nausea/diarrhoea
  • mouth ulcers
  • liver toxicity
  • !bone marrow supression! and leukopenia
  • teratogenic
  • pneumonitis
    (taking folic acid reduces risk of all)
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29
Q

What are the symptoms of low folic acid ? (5)

A
  • fatigue
  • weakness
  • thinning hair
  • mouth ulcers
  • visual problems
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30
Q

What blood tests would you do for a patient on methotrexate ? (4) why ?

A
  • LFT: as it is metabolised in the liver
  • U+E: as reduced renal fun affects methotrexate metabolism and can cause levels to rise in the blood
  • FBC: check white cells and platelets (assess for bone marrow failure)
  • ESR/CRP: check disease progression/activity
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31
Q

What is Psoriatic arthritis ?

A

inflammatory seronegative spondyloarthropathy arthritis associated with psoriasis
(can vary in stiffness to join completely destroyed)

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32
Q

what % of ppl with psoriasis will develop psoriatic arthritis ?

A

10-20 %
(the arthritis can occur before the skin changes)

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33
Q

what is the complete joint destruction associated with psoriatic arthritis called ? what is it?

A

arthritis mutilans
-osteolysis of the bones around the joints leasing to progressive shortening of the digits (telescoping digit)

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34
Q

psoriatic arthritis presentation ? distribution ? signs

A

asymmetrical oligoarthritis
symmetrical polyarthritis
- DIP joint involvement
- Signs: plaques, nail pitting, onycholysis, dactylitis, enthesitis
(can affect any joint !)

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35
Q

How to check for enthesitis in a psoriatic arthritis patient ?

A

check for pain on foot flexion

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36
Q

what screening tool is used for psoriatic arthritis ?

A

Psoriasis Epidemiological screening tool (PEST)

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37
Q

what are the XR changes in psoriatic arthritis ? (4)

A
  • periostitis (inflam of the periosteum)
  • ankylosis
  • Osteolysis
  • Dactylysis
  • Penicl-in-cup (classic finding): assocaited with arthritis mutilans
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38
Q

Psoriatic arthrits Mx ?

A
  • NSAIDs:
  • Steroids
  • DMARDs (methotrexate)
  • Anti-TNF meds (etanercept, infliximab)
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39
Q

what is reactive arthritis ?

A

sero-negative spondyloarthropathy: it involves synovitis in one of more joints in reaction to recent infective trigger (the joints are sterile therfor not septic). Immune respone => inflam that affects joints
- typically cases acute monoarthritis

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40
Q

most common reactive arthritis trigger ?

A
  • gastroenteritis (salmonella, shigella)
  • STI (chlamydia)
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41
Q

what is the classic triad of symptoms in reactive arthritis ?

A
  • bilateral conjunctivits
  • urethritis
  • arthritis
    (cant pee, see or climb a tree)
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42
Q

Reactive arthritis Ix ?

A

assume septic arthritis until differential excluded: aspirate joints (gram staining + culture, crystal examinations)

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43
Q

reactive arthritis Mx ?

A
  • treatment of triggering infection (e.g. chlamydia)
  • NSAIDs
  • steroid infection into the affected joints
  • systemic steroids may be required
    (30-50 will develop some form of chronic ReA)
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44
Q

what are the seronegative arthritis ? (5) why are they called this ?

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Enteropathic arthritis
  • Undifferentiated spondyloarthritis
    (RF and anti-CCP are typically negative)
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45
Q

Which RA/rheum drugs are safe during pregnancy ? (3)

A
  • hydroxychloroquine
  • sulfasalazine
  • adalimumab
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46
Q

What is the first line bioligic in rheumatology ?

A

adalimumab

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47
Q

What is poly myalgia rheumatic (PMR) ? strong association with what ?

A

It is an inflam condition causing pain and stiffness in shoulders, pelvic girdle and neck
- strong association with GCA (often occur together)

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48
Q

PMR epi ?

A

usually affects old adults (50+), women, caucasian

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49
Q

PMR presentaiton ? when are symptoms worse ? uni or bilateral ?

A

present for at least 2 weeks:
- bilateral shoulder pain (radiates to upper arm)
- bilateral pelvic girdle pain
- worse after inactivity, interferes with sleep, stiffness in morning (>45 mins)

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50
Q

what are addition symptoms of PMR ?

A
  • weight loss
  • fatigue
  • low grade ever
  • low modd
  • carpal tunnel syndrome
  • screen for GCA !
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51
Q

What are the typical GCA symptoms that you should screen for in suspected PMR patient ?

A
  • painful and tender scalp (over the temporal arteries)
  • Headaches (new temporal headache)
  • jaw claudication (pain in jaw after eating/chewing)
  • visual changes (blurring or loss of vision)
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52
Q

Describe the headache in GCA ?

A

severe unilateral headache around the temple
- plus scalp tenderness

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53
Q

what features would push you away from a GCA diagnosis ? (5)

A
  • vomiting
  • fever
  • menigitis
  • encephalitis
  • normal inflam markers
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54
Q

how is PMR diagnosed ?

A

clinical presentation and if responds well to management
- inflam markers are usually raised but absence doesn’t exclude diagnosis

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55
Q

PMR mx ? (with no GCA sx)

A

steroids
- 15mg oral prednisolone (the wean down over yrs)

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56
Q

what dose of steroids for PMR if visual GCA changes present

A

40-60 mg oral prednisolone
(60 if visual loss has started)

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57
Q

What are the different categories of rheumatological drugs available ? (5)

A
  • NSAIDs
  • Steroids
  • DMARDs
  • Biologic agents
  • JAK inhibitors
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58
Q

what are some side effects of steroids ? (5)

A
  • GI: indigestion, ulcers, GI bleed
  • Osteoporosis
  • diabetes/glucose intolerance
  • infection
  • skin thinning
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59
Q

explain why patients should never abruptly stop their steroids ?

A
  • exogenous steroids result in suppresion of ACTH
  • Adrenal suppression with an inability to respond to appropriate to stress
    => life-threatening fluid unresponsive hypotension
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60
Q

biological treatment SE ?

A

infection: can present in a more subtle fashion, and patients may become very unwell very quickly

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61
Q

When would you advise a patient to stop taking their boiling treatment ?

A
  • if they have infeciton
    0 if they are having an operation
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62
Q

how long men and women need to be off methotrexate to safely conceive pregnancy ?

A

3 months (?)
safe for men

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63
Q

what are the main connective tissue disorders ?

A
  • SLE
  • scleroderma
  • granulomatosis with polyangitis
  • EDS
  • Sjörgrens
  • raynauds
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64
Q

what are antinuclear antibodies ?

A

autoantibiotides that bind to contents of nucleus (instead of foreign proteins)
- when ANAs signal body to target itself => autoimmune => scarring + damage to Orans affected

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65
Q

What is systemic sclerosis ?

A

autoimmune inflam and fibrotic connective tissue disease
- causes hardening or scarring of skin and internal organs
(cause unknown)

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66
Q

what are the two main patterns of disease in systemic sclerosis ?

A
  • limited cutaneous systemic sclerosis
  • diffuse cutaneous systemic sclerosis
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67
Q

what are the features of limited cutaneous systemic sclerosis

A

aka CREST syndrome
- Calcinosis
- Raynaulds
- oEsophageal dysmotility
- Scleroderma
- Telangiectasia

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68
Q

what are the features of diffuse cutaneous systemic sclerosis

A

CREST symptoms plus:
- internal organs (CVD, lung, kidney problems)

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69
Q

what does scleroderma mean ?

A

refers to the hardening of the skin => shiny tight skin without normal skin folds

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70
Q

what is sclerodactyly ?

A

describe the skin changes in the hands in systemic sclerosis
- skin tightening around the joints restrict ROM and reduces function

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71
Q

What is calcinosis ? associated with what condition ?

A

systemic sclerosis
- calcium deposits under the skin, most commonly fond on the fingertips

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72
Q

What are some lung complications associated with SS ? what tests should you do to monitor ?

A
  • pulmonary fibrosis
  • ILD
  • Lung Function test (TLCO, FVC), Echo
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73
Q

What autoantibodies iare associated with systemic sclerosis ?

A
  • antinuclear antibodies (ANA)
  • anti-centromere
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74
Q

systemic sclerosis Mx ?

A

steroids + immunospressents
- non-medical: avoid smoking, gentle skin stretching, regular emoliatns, avoid cold triggers

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75
Q

What is raynauds phenomenon ? what are the two types?

A

episodes of vasospasm in the extremities (usually in fingers and toes) in response to cold or stress
- can be either primary or secondary

76
Q

explain primary raynauds phenomenon ? typical patient and presentaiton ?

A

raynaud’s disease (occurs without any associated underlying disease)
- young women
- symptoms less severe, typically ffects both hands and feet
- final risk of complications

77
Q

explain secondary Raynaud’s phenomenon ?

A

associated with other underlying medical condition (usually systemic sclerosis, lupus, RA, sjögren’s)
- older
- symptoms are more severe and prolonged and can present with digital ulcers

78
Q

describe the colour changes in raynauds phenomenon ? why ?

A
  • first white (due to vasoconstriction)
  • then blue (due to cyanosis)
  • then red (due to repercussion and hyperaemia)
79
Q

how can you investigate if raynauds is primary or secondary cause ? what would suggest secondary cause ? (3)

A

nail fold capillaroscopy (to examine the peripheral capillaries)
- SS: abnormal capillaries, avascular areas, micro-haemorrhages)
(if ulcers present on fingertip then is secondary cause)

80
Q

raynauld’s mx ? (2)

A
  • keep the hands warm
  • CCB (nifedipine)
81
Q

What is systemic Lupus Erythematosus ?

A

SLE: it is an inflam autoimmune connective tissue disease (with autoantibodies)
- systemic (affects multiple organs + systems)
- erythematosis (red molar rash)

82
Q

what is the leading cause of death in SLE ?

A

CVD (and infection)
- chronic inflam => shortened life expectancy

83
Q

SLE epi ?

A
  • women
  • asian, African, Caribbean and hispanic ethnicity
  • young to middle-aged adults
84
Q

SLE pathophysiology ?

A

anti-nuclear antibodies => immune system target these proteins => inflam response

85
Q

SLE presentation

A

relapsing-remitting + flares
- fatigue
- weight loss
- arthralgia (joint pain)
- non-erosive arthritis
- myalgia
- fever
- photosensitive molar rash
- sob
- pleuritic chest apin
- mouth ulcers
- hair loss
- raynauds phenomenon

86
Q

SLE investigations ?

A
  • ANA (85% patient +ve)
  • anti-dsDNA (highly specific) (anti-double stranded DNA)
  • FBC
  • ESR/CRP
  • urinalysis (sign of lupus nephritis)
87
Q

what condition can occur secondary to SLE in 40% of patients ?

A

antiphospholipid syndrome
=> increased risk of VTE

88
Q

SLE complications ?

A
  • CVD (chronic inflam in blood vessels => hypertension => fatty deposits => CAD)
  • Infection
  • anaemia
  • pericarditis
  • ILD
  • Lupus nephritis
89
Q

SLE Mx ?

A

First line: hydroxychloroquine, NSAIDs, Steroids, suncream (and sun avoidance)
Second: DMARDs, Biologics

90
Q

What is discoid lupus erythematosus ?

A

chronic scarring skin condition (different to lupus)
- sub-type of chronic cutaneous lupus erythematosus

91
Q

Discoid lupus evythmatosus presentation ?

A

initial dry red patches that form plaques with scale
- can progress to atrophic scarring and alopecia

92
Q

What is antiphospholipid syndrome ? with what other things is it associated ? (2)

A

it is a disorder associated with persistently elevated antiphosphlipid antibodies => blood become prone to clotting (hyper coagulable state) => throbus + miscarriages
- SLE (secondary to it), recurrent miscarriages

93
Q

what are the key antiphospholipid syndrome complications ? (3) (go into each one a bit)

A
  • VTE (DVT/PE)
  • Arterial thrombosis (stroke, MI, renal thrombosis)
  • Pregnancy-related complications (recurrent miscarriage, stillbirth, pre-eclampsia)
94
Q

what skin condition is associated with antiphospholipid syndrome ?

A

lived reticularis
- purple lace-like rash that gives a mottle appearance to the skin

95
Q

antiphospholipid syndrome Dx + Mx ? in pregnancy Mx ?

A
  • clinical Dx + persistent antiphospholipid antibodies
  • long-term warfarin (INR 2-3)
  • LMWH and aspirin used in pregnancy (warfarin contraindicated in pregnancy)
96
Q

What are spondyloarthropathies ?

A

range of rheumatic autoimmune inflammatory arthritis which can predominantly affect the spine (axial spondyloarthritis) or peripheral joints (peripheral spondyloarthritis)

97
Q

What are zero negative spondyloarthopathies ? name them (4) ?

A

group of conditions associated with HLA-B27 antigen
- psoriatic arthritis
- enteropathic arthritis
- reactive arthritis
- ankylosing arhtirits

98
Q

What similarities do serotonin-negative spondyloarthopathies share ?

A

similar clinical, radiographic and lab features (spinal inflam, HLA-B27 antigen)
- joint pain + inflam in absence of RF

99
Q

which cells express the HLA-B27 antigen ?

A

all cells except RBC

100
Q

zero negative spondyloarthopaties pathophysiology ?

A

molecular mimicry: get infection => immune response => infection agent has antigens similar to HLA-B27 => body presents antibody defence => autoimmune

101
Q

What is ankylosing spondylitis (AS) ?

A
  • zero negative spondyloarthropathy (related to HLA B27 gene)
    chronic progressive inflammatory condition affecting the axial skeleton causing fusion of the joints
102
Q

what are the key joints affected in AS ?

A
  • sacroiliac joints
  • joints of vertebral column
103
Q

AS pathophysiology ?

A

inflam => erosive damage repair => lay down of fate => fusion of joints (bamboo spine)

104
Q

AS presentation ?

A

young adult male in their 20s, slow onset >3 months
- pain and stiffness (in the lower back)
- sacroiliac pain (in the buttock region)
- can affect other systems: systemic sx, chest pain (costoverterbal joints, dacyltit, anaemia, aortitis, IBD, enthesitis)

105
Q

when AS symptoms worse ?

A
  • pain and stiffness worse with rest and improve with movement
  • pain worse at night and in the morning (may wake from sleep)
    mornings tiffness last >30 min
  • symptoms improve with activity and worsen with rest
106
Q

what test can be used in AS to assess spinal mobility ? explain it

A

schobers test
- measure 10cm above and 5cm below L5 vertebrae
- ask patient to bend over
-> 20cm = normal. less than this indicates a restriction in lumbar movement and helps support AS dx

107
Q

AS Ix ? (4)

A
  • Inflam markers (CRP/ESR)
  • HLA B27 genetic testing (present in 90% of patients)
  • XR of the spine and sacrum
  • MRI of the spine can show bone marrow oedema
108
Q

AS XR changes ?

A
  • bamboo spin (typical finding)
  • squaring of vertebral bodies
  • subchondral sclerosis and erosions
  • fusion of the sacroiliac and costovertebral joints
109
Q

AS Mx ? (4)

A

rheum MDT
-NSAIDs are first line
- anti-TNF meds (adalimumab): stops pain and boy formations
- intra-articular steroid injections for specific joints
- additional: physiotherapy, avoid smoking, bisphosphonates (osteoporosis)

110
Q

What is sjögren’s syndrome ?

A

autoimmune condition that affects the exocrine glands => symptoms of dry mucus membranes (often lacrimal and salivary glands)

111
Q

what are the two distributions of Sjögren’s syndrome ?

A
  • primary: where condition occurs in isolation
  • secondary: where is occurs due to other disease such as SLE and RA
112
Q

what are the antibodies associated with sjögren’s ?

A
  • anti-Ro
  • anti-La
113
Q

sjögren’s epi ?

A

usually starts in ppl aged 40-60 and more common in women
- F:M 9:1
- 60% of the disease secondary to RA, SLE

114
Q

sjögren’s presentaiton ?

A
  • dry eyes + mouth
  • arthritis
  • rash
  • neurological features
  • vasculitis
115
Q

what test is useful in assessing sjögren’s presentation ? describe

A

schemer test
-insert folded filter paper under the lower eyelid with the end handing out
- wait 5 min for moisture to travel along
- should be >15mm (<10mm is significant)

116
Q

sjögren’s Mx ?

A

clinical dx
- symptomatic: artificial tears, artificial saliva, vaginal lubricants
- hydroxychloroquine (may be considered in patients with associated joint pain)

117
Q

What is vasculitis ? and what are the different categories ?

A

it is inflammation of the blood vessels
- categories: small, medium-sized or large vessels

118
Q

how does vasculitis cause damage ? (generally)

A
  • vessel wall destruction => perforation + haemorrhage into tissues
  • endothelial damage => thrombosis + ischaemia/infarction of dependant tissues
119
Q

name some small vessel vasculitis ? (4)

A
  • Honoch-schonlein Purpura
  • granulomatosis with polyangitis
  • microscopic polyangitis
  • eosinophilic granulomatosis with polyangitis
120
Q

name some medium vessel vasculitis ? (2)

A
  • Kawasaki disease
  • polyarteritis nodosa
121
Q

name some large vessel vasculitis ? (2)

A
  • giant cell arteritis
  • takayasu’s arteritis
122
Q

general vasculitis presentation ? (6)

A
  • joint and muscle pain
  • peripheral neuropathy
  • renal impairment
  • purpura
  • GI symptoms
  • systemic symptoms
123
Q

what are the ANCA associated vasculitis ? (3)

A
  • GPA
  • EGPA
  • Microscopic polyangitis
124
Q

what is granulomatosis with polyangitis (GPA) ?

A

small vessel (ANCA associated) vasculitis mainly affecting the resp tract and kidney (glomerulonephritis)

125
Q

what 3 areas does GPA generally affect ?

A

1) URT/LRT
2) systemic vasculitis
3) Kidney involvement

126
Q

GPA pathophys ?

A

granuloma formation => partial/total occlusion of blood vessels

127
Q

GPA typical presentaiton ?

A

think GPA when:
- nose bleeds, crusty nasal secretions, kidney failure
- cough with wheeze + haemoptysis

128
Q

GPA Ix ? what specific blood test ?

A
  • CXR may show consolidation
  • C-ANCA (+ve)
  • CT chest (lung nodules if lung involvement)
129
Q

GPA Mx ?

A
  • high dose red + methotrexate
    (wean off steroids)
130
Q

what are polymyositis and dermatomyositis ?

A

they are autoimmune disorders where there in inflam in the muscles (myositis)
- polymyositis is condition of chronic inflam of muscles
- dermatomyositis is connective tissue disorder where there is chronic inflam of skin + muscle

131
Q

polymyositis and dermatomyositis presentation ?

A

gradual onset, symmetrical, proximal muscle weakness (difficult standing form chair)
- +/- myalgia
- potential skin changes: heliotrope rash, cotton lesions, periorbital oedema, photosensitive erythematous rash

132
Q

what is important blood test for polymyositis and dermatomyositis ? (2) describe

A

creatine kinase
- it is an enzyme found inside muscle cells that is released from muscles when there is inflam

antibodies: anti-Jo-1 antibodies

133
Q

causes of raised creatine kinase ? (5)

A
  • rhabdomyolysis
  • AKI
  • MI
  • statins
  • strenuous exercise
134
Q

polymyositis and dermatomyositis Mx ?

A

corticosteroids
- if inadequate then methotrexate

135
Q

important dermatomyositis hand sign ?

A

gottron papules

136
Q

What is Ehlers-Danlos Syndrome ? (EDS)

A

group of genetic conditions involving defects in collagen => hyper mobility in the joints and abnormalities in the connective tissues (of skin, bones, blood vessels + organs)

137
Q

what are the different types of EDS ? which most common ? which most severe ? explain each a bit

A
  • hypermobile EDS (most common): hyper mobility + soft/stretchy skin
  • Classical EDS: smooth/velvetty skin, joint pain/hypermobility, abnormal wound healing
  • Vascular EDS (most severe): blood vessels prone to rupture (FHx of sudden death)
138
Q

EDS presentation ?

A

joint pain, hyper mobility, joint dislocations
- association with POTS

139
Q

what score is useful in EDS Dx ?

A

Leighton score (assesses hyper mobility)

140
Q

EDS Mx ?

A

no cure
- physio
- hyper mobility => additional wear + tear => premature OA

141
Q

What is Behcets disease ? main feature ?

A

complex inflam condition affecting blood vessels + tissues
- Main feature: recurrent oral and genital ulcers (can affect eyes, skin, GIT, lungs, blood vessels, MSK, CNS)

142
Q

Behcets disease features ?

A

ulcers > 3 times per year
- painful, sharply circumscribed erosion with a red halo in oral mucosa

143
Q

What is crystal arthropathy ? what causes it ? 2 types ?

A

crystal deposition in joints results in local inflammation and tissue damage
- gout
- pseudogout

144
Q

What is gout ? associated with high levels of what in blood ? what crystals ?

A

gout is a crystal arthropathy associated with chronically high uric acid
- urate crystals

145
Q

what are gouty tophi ? where are they located ?

A

gouty tophi are SC deposits of uric acid under the skin (rather than in joint)

146
Q

What is uric acid produced from ? where is it excreted ?

A
  • produced from nucleic acids (xanthine oxidase (inhibited in treatments))
  • excreted by intestine + kidneys (underexcretion can be caused by alcohol)
147
Q

Gout RF ? (6)

A
  • Male
  • Obesity
  • High purine diet (meat + seafood)
  • Alcohol
  • Diuretics
  • CKD
148
Q

Gout presentation ? and natural disease course ?

A
  • single acute, hot, swollen + painful joint (excruciating)
  • typical joints: base of big toe, writs, base of thumb (carpometacarpal joint)
  • will naturally resolve in around 3 weeks but is excruciating (so analgesia)
149
Q

gout Ix ? and results ?

A
  • aspirate fluid from joint (no bacterial growth, needle shaped crystals, negatively birefringent of polarised light, monosodium nitrate)
  • x-ray: lytic lesions, punched out erosions
150
Q

Gout Mx ? (3) which groups would you avoid what in ?

A

NSAIDs, or colchicine or steroids
- but high dose colchicine => diarrhoea (so start with lower dose in elderly)
- NSAIDs not good for kidney (which could be causing gout)
- steroids not good in elderly (osteoporotic)

151
Q

Gout prevention ?

A
  • allopurinol, febuxistat (xanthine oxidase inhibitor)
  • lifestyle changes: lose weight, good hydration, reduce alcohol + red meat
  • losartan (anti-HTN but also increases renal uric acid clearance)
152
Q

What is pseudogout ? What crystals ? triggered by ?

A

it is a crystal arthropathy caused by calcium pyrophosphate crystals
- triggered by direct trauma, surgery, blood transfusion of spontaneous (most common)

153
Q

pseudogout presentation ?

A

older adult with hot, swollen, stiff, painful knee (monoarthiritis) or asymtpomatic

154
Q

psuedogout Ix ? and results

A

calcium pyrophosphate crystals
- rhomboid crystals that are positively birefringent in polarised light
- x-ray: chondrocalcinosis (diagnostic)

155
Q

pseudogout Mx ?

A

symptoms usually resolve spontaneously over weeks
- NSAODs, colchicine, aspirate fluid

156
Q

What is fibromyalgia ?

A

chronic condition characterised by widespread pain + pressure hypersensitivity
- unknown aetiology but thought stress and sleep play important role

157
Q

fibromyalgia RF ?

A
  • female 35-45
  • poor sleep
  • smoking
  • obesity
  • sedentary lifestyle
158
Q

fibromyalgia signs and symptoms ?

A
  • chronic widespread pain
  • increase pain to pressure (allodynia)
  • fatigue
  • sleep disturbance
  • anxiety
  • parasthesia
  • dysmennorhoea
    (linke with IBS, chronic fatigue)
159
Q

fibromyalgia investigations ?

A

diagnosis of exclusion so other test unremarkable, often come back normal, clinical dx
- widespread pain index (0-19 points) + symptom severity score (0-12)
- symptoms present for >3 months + no other differential

160
Q

fibromyalgia treatment ?

A

no cure, symptom management
- non-pharma: exercise, reduce stress, avoid caffeine, sleep hygiene
- SNRI (duloxetine), amitriptyline

161
Q

What is osteoporosis ?

A

skeletal disease characterised by reduced bone density, microarchetectual defects => increased bone fragility => increased bone fracture susceptibility
- osteopenia isa less severe reduction intone density

162
Q

osteoporosis RF ?

A
  • increase age
  • female (PM)
  • reduced mobility
  • low BMI
  • RA
  • alcohol
  • Smoking
  • Long term steroids
  • SSRI
  • PPI
163
Q

explain osteoporosis and Post menopausal women ? pathophys

A

oestrogen is protective against osteoporosis
- osteoblasts severed OPG which inhibit RANKL (RANKL => osteoclast action)
- PM women with ostergoen deficiency have over expression of RANKL with overrides OPG)

164
Q

What is FRAX tool for ? takes what into account ?

A

predication of the risk of a fragility fracture over the next 10 yrs
- Age, BMI, comorbidities, smoking + alcohol, FHx

165
Q

what is a DEXA scan ? what are the different relevant ranges ?

A

checks bone mineral density
- more than -1 => normal
- -1 to -2.5 => osteopenia
- less than -2.5 => osteoporosis

166
Q

osteoporosis mangement ?

A
  • activity + exercise, maintain healthy weight, ensure enough calcium + vit D, avoid falling, stop smoking, reduce alcohol
  • calcium + vit D suppléments
  • bisphsphonates (interfere with osteoclasts)
167
Q

how should a patient take a bisphosphonate ?

A

need to take on empty stomach and sitting up (prevent reflux)

168
Q

What is pages disease of bone ? pathophys ? increased risk of what ?

A

it is a disease of bone turnover, excessive bone turnover (formation + reabsorption)
- due to excessive osteoblast + class activity
- not coordinated => patchy areas of high density (sclerosis) + low density (lysis) => enlarge + misshapen bones with structural problems => increase risk of fracture

169
Q

pagets disease of bone presentations

A
  • bone pain
  • bone deformity
  • fractures
  • hearing loss
170
Q

pagets disease of bone Ix ?

A
  • XR (enlarged + deformed, osteoporosis, cotton wool appearance of skull, va shaped defects)
  • raised Alkaline phsphatase, normal Ca + phosphate
171
Q

pagets disease of bone Mx ?

A
  • bisphsphonates, NSAIDs, calcium + vit D supplementation
172
Q

What is osteomyelitis ? most common aetiology ?

A

It is inflam in a bone + bone marrow, usually caused by bacterial infection
- mainly staphylococcus aureus

173
Q
A
174
Q

osteomyelitis presentation ?

A
  • fever, pain + tenderness, erythema, swelling (usually single bone)
175
Q

osteomyelitis Ix and Mx ?

A
  • XR (often doesn’t show changes in early disease)
  • MRI (best imaging)
  • blood tests (raised WBC, ESR, CRP), blood cultures (before Abx)
    Mx: surgical debridement of infected bone + tissue, Abx (6 weeks flucloxacillin)
176
Q

What is septic arthritis ?

A

its occurs where there is infection within a joint (emergency - 10% mortality)
- common complication of joint replacement

177
Q

septic arthritis presentation ?

A

mono arthritis (90%), often knee, rapid onset of red, hot, swollen, painful joint + stiffness and reduced ROM
- systemic symptoms (fever, lethargy, signs of sepsis)

178
Q

septic arthritis aetiology ?

A
  • s-aureus
  • neisseria gonorrhoea (sexual transmission
  • strep pyogneis
179
Q

septic arthritis mx ?

A

(always suspect septic arhtirits in red hot swollen joint)
- aspirate the (prior to abx), send sample for gram string + crystal microscopy + culture + abx sensitivity
- antibiotics (2 weeks IV, 4 weeks oral), analgesia, aspirate joint to dryness

180
Q

What is osteomalacia ?

A

it is where defective bone mineralisation causes soft bones, as a result of low vit D (aka rickets in children)

181
Q

explain vit D synthesis - what is the precursor ? where is it activated ?

A

Vit D is created from cholesterol by the skin in response to UV radiation, also obtained from food as fat soluble vitamin
- activated in the kidney

182
Q

what medical conditions would be a risk factor for low vit D ? other RF ?

A
  • IBD (due to malabsorption)
  • CKD (kidneys convert vit D to active form)
  • Darker skin (require more UV to synthesis vit D)
  • spending time indoors
183
Q

what metabolism is vit D important in ? how does low vit D affect this

A
  • calcium and phosphate absorption in intestines
  • calcium and phosphate reabsorption in kidneys
  • low vit D => low serum Ca + Phos => reduce bone mineralisation (osteomalacia)
184
Q

osteomalacia presentation ?

A
  • fatigue
  • bone pain
  • muscle weakness and aches
  • pathological fracture
185
Q

osteomalacia Ix ?

A
  • serum 25-hydroxy vitmin-D
  • XR osteopenia
  • DEXA: reused bone mineral density
  • low serum Ca + Phos, high PTH (secondary hyperparathyroidism)
186
Q

osteomalacia Mx ?

A

cholecalciferol (vit D3)

4 - Med (12 decks)

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