Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MUSCULOSKELETAL > ARTHRITIS > Flashcards

ARTHRITIS Flashcards

1
Q

Arthralgia vs arthritis?

A

Arthralgia is pain in a joint
Arthritis is a diagnosis that involves articular inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Inflammatory vs non-inflammatory arthritis?

A

E.g. osteoarthritis is non-inflamamtory and RA is inflammatory
There is a degree of inflammation in the joint in osteoarthritis but no clinical signs of inflammation, little early morning stuffiness, normal or mild biochemical markers of inflammation compared to RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

joint changes osteoarthritis vs rheumatoid arthritis

A

In OA - thinning of synovial membrane and friction between bones
In RA - synovial membrane is swollen, inflamed and there are bony erosions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is osteoarthritis?

A

A disorder of synovial joints which occurs when damage (i.e. from repeated excessive loading, injury or stress or a joint) triggers repair processes leading to structural changes within a joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Structural changes in the joint in osteoarthritis?

A

Localized loss of cartilage.
Remodelling of adjacent bone and the formation of osteophytes (new bone at joint margins).
Mild synovitis (inflammation of the synovial membrane that lines the joint capsule).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which joints are most commonly affected in osteoarthritis?

A

Weight bearing and axial skeleton
I.e. knees, hips, DIP joints in hands, CMC at base of thumb, lumbar spine and cervical spine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Epidemiology of osteoarthritis?

A

The most common joint disease worldwide
Affects 10% of men and 18% of women >60
Risk develops with age
Prevlance is higher in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Risk factors for osteoarthritis?

A

Genetic
Increasing age
Female sex
Obesity
High bone density
Joint injury and damage
Joint laxity and reduced muscle strength e.g. hypermobility
Joint malalignment e.g. PHx of DDH, valgus knee deformity
Exercise stresses
Occupational stresses e.g. repetitive squatting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why does obesity increase the risk of osteoarthritis?

A

It increases the load on weight bearing joints
This increases the risk of developing knee osteoarthritis more than 3 fold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complications of osteoarthritis?

A

Joint deformity
Functional impairment and disability
Psychosocial issues
Occupation impact
Falls
Chronic pain sundrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prognosis of osteoarthritis?

A

Quite often a progressive condition that leads to increased pain and functional impairment but not always! Hand involvement usually becomes asymptomatic after a few years
Hip involvement has poorest prognosis and a significant proportion of people require a hip replacement within 5 years of diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

General presentation of osteoarthritis?

A

Joint pain and stiffness that tends to worsen with activity and at the end of the day (if morning stiffness then it should not last >30 mins)
Bulky bony enlargements of the joint
Restricted range of motion
Weak grip
Crepitus on movement
Fluid around the joint
Muscle wasting
Joint instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Presentation of osteoarthritis of the hand?

A

Affects first Carpometacarpal joint at the base of the thumb, the DIP joint and PIP joint
Pain can radiate dismally towards thumb or proximally to wrist and distal forearm. Exacerbated by pinching or strong grip
Wasting of thenar muscles
CMC joint may develop a fixed flexion deformity
In advanced disease… Squaring of the joint caused by subluxation, formation of osteophytes and remodelling of bones, ulnar or radial deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Presentation of osteoarthritis of the hip?

A

Deep pain in anterior groin on walking/climbing stairs with possible referred pain to the lateral thigh and buttock anterior thigh, knee and ankle
Pain may occur at rest and distrurb sleep
Painful restriction of internal rotation with the hip flexed
Antalgic gait

In advanced disease - trendelenburg gait and a fixed flexion external rotation deformity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Presentation of osteoarthritis of the knee?

A

Presentation depends on where it affects…

Medial tibiofemoral involvement causes anteromedial pain, mainly on walking.
Lateral tibiofemoral involvement causes anterolateral pain, mainly on walking.
Patellofemoral involvement causes anterior knee pain worsened on inclines or stairs, particularly when going down; and progressive aching on prolonged sitting that is relieved by standing.

Others: giving way, locking, crepitus, tenderness, restricted flexion &extension
In advanced disease - bony swelling of femoral condyles, varus deformity and an antalgic gait

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diagnosing osteoarthritis according to NICE?

A

NICE suggest a diagnosis can be made without any investigations if the patient id >45, has typical pain associated with activity and has no morning stiffness (or lasts <30 mins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Typical radiological features of osteoarthritis?

A

L – Loss or narrowing of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Heberden’s nodes vs Bouchard’s nodes?

A

Heberdens nodes are bony bumps on DIPs
Bouchards are on the PIPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management of osteoarthritis?

A

Weight loss if overweight
Muscle strengthening and supervised therapeutic exercise and aerobic fitness training
Offer psychosocial support
Simple analgesia for symptom relied
Topical NSAIDs for knee osteoarthritis

If this doesn’t help…
Intra-articular injections for short-term benefits for knee and possibly hip
Consider referral to PT or local MSK clinic
Consider referral to OT
Consider referral to podiatry
Consider referral to orthopaedic surgeons for joint replacements in severe cases
Consider referral to pain clinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the Oxford Hip Score?

A

A self-assessment tool designed to assess function and pain in patients undergoing hip replacement surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Complications of total hip replacement secondary to osteoarthritis ?

A

Perioperative - VTE, intraoperative fracture, nerve injury, surgical site infection
Leg length discrepancy
Posterior dislocation on extremes of hip flexion
Aseptic loosening - failure of joint prosthesis without infection
Prosthetic joint infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How long can intra-articular steroid injections work for in osteoarthritis?

A

2-10 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Post-op recovery from hip replacements?

A

patients receive both physiotherapy and a course of home-exercises
walking sticks or crutches are usually used for up to 6 weeks after hip or knee replacement surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What basic advice should patients recieve to minimise the risk of dislocation following a hip replacement?

A

avoiding flexing the hip > 90 degrees
avoid low chairs
do not cross your legs
sleep on your back for the first 6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Epidemiology of RA?

A

1% prevalence in the UK - most common inflammatory arthritis
Occurs at any age but most commonly 30-50
2-4 times more common in women than men
Approximately 1/3rd stop work within 2 years of its onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complications of RA?

A

Amyloidosis
Anaemia
Ketatoconjunctivitis sicca, corneal ulceration, episcleritis, scleritis, keratitis
Feltys syndrome
Fatigue
Increased mortality
Interstitial lung disease, pleural effusion, fibrosis alveolitis
Neuropathy
Orthopaedic e.g. carpal tunnel, tendon ruptures, osteoporosis etc
Vasculitis, ulcers, rheumatoid nodules
Weight loss

Severe - depression, CVD, lymphomas, serious infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is feltys syndrome?

A

Rare extra-articulated manifestation of RA

Causes presentation remembered as SANTA:
Splenomegaly
Anaemia
Neutropenia
Thrombocytopenia
Arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Presentation of RA?

A

Presentation insidiously develops over a few months
Symmetrical synovitis of the small joints of the hands and feet - pain, swelling, early morning stiffness lasting over 1 hour
Rheumatoid nodules
Positive squeeze test across metacarpal or metatarsal joints
Swan neck and boutonnière deformities in late disease
Extra-articular features
Systemic features - malaise, fatigue, fever, sweats, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is palindromic rheumatism?

A

Self-limiting relapsing/remitting episodes of monoarthritis of different large joints with joints appearing normal between episodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Risk factors for RA?

A

Female - due to oestrogen
Smoking
FHx - HLA DR4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which gene is most commonly associated with RA?

A

HLA DR4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Most commonly affected joints in RA?

A

MCP
PIP
Wrist
MTP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hand signs in RA?

A

Z-shaped deformity to the thumb
Swan neck deformity (hyperextended PIP and flexed DIP)
Boutonniere deformity (hyperextended DIP and flexed PIP)
Ulnar deviation of the fingers at the MCP joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What causes Boutonnière deformity in RA?

A

caused by a tear in the central slip of the extensor components at the PIP joint.
The central slip connects to the middle phalanx at the PIP, and the lateral bands go around the PIP and connect to the distal phalanx.
When the patient tries to straighten their finger, the lateral bands pull on the distal phalanx, causing the DIP joint to hyperextend and the PIP joint to flex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is atlantoaxial subluxation?

A

A potential complication of RA where synovitis and ligament damage around the odontoid peg of the axis (C2) allows it to shift within the atlas (C1)
This can cause spinal cord compression and is an emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How common are ocular manifestations of RA? What are the common types?

A

25% have ocular manifestations - keratoconjunctivits sicca is most common.
Others are episcleritis, scleritis, corneal ulceration and keratitis.
Iatrogenic - steroid-induced cataracts and chloroquine retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some examples of extra-articular manifestations of RA?

A

Ocular manifestations
Pulmonary fibrosis, bronchiolitis obliterans
Feltys syndrome
Sjögren’s syndrome
Anaemia
CVD
Rheumatoid nodules - elbows and fingers
Lymphadenopathy
Carpal tunnel syndrome
Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do we diagnose RA?

A

If its suspected clinically investigations are not necessary

You may consider doing:
- rheumatoid factor blood test
- measure anti-CCP
- x-ray of hands and feet

You may also consider the following tests to acts as a baseline measure prior to Tx:
- FBC, U&Es, LFTs
- CRP or ESR
- US or MRI of joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Discuss the sensitivity and specificity of rheumatoid factors for RA?

A

RF is positive in up to 80% of pt with RA and high levels are associated with severe progressive disease

RF can be positive in feltys syndrome, Sjögren’s syndrome, infective endocarditis, SLE, systemic sclerosis
It can also be seen in 5% of general population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What tests can be done to detect rheumatoid factor for diagnosing RA?

A

Rose-Waaler test: sheep red cell agglutination
Latex agglutination test (less specific)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Discuss the sensitivity and specificity of anti-CCP for RA?

A

May be detectable up to 10 years before the development of RA
Present in 70% of pt with RA
Specificity is 90-95%

(Because the specificity is much higher… if pt are suspected RA but get a negative RF test they should then be tested for anti-CCp)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

X-ray changes you may see in RA?

A

loss of joint space
juxta-articular osteoporosis
soft-tissue swelling
periarticular erosions
subluxation and disclocation e.g. ulnar deviation at MCPJs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Scoring systems for RA?

A

Health Assessment Questionnaire (HAQ) - measures functional ability which should be done at baseline to assess response to treatment
Disease Activity Score 28 joints (DAS28) - used to monitor disease activity and response to treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Management of RA?

A

DMARD monotherapy +/- a short-course of bridging prednisolone
E.g. methotrexate, leflunomide, sulfasalazine
Hydroxychloroquine for palindromic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How should you monitor response to treatment in RA?

A

CRP and disease activity e.g. using a score like DAS28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How do you manage flares of RA?

A

Oral, IM or intraarticular glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How should you manage RA if there is inadequate response to at least 2 DMARS, 1 of which being methotrexate?

A

TNF inhibitors can be tried e.g. etanercept, infliximab or adalimumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Biological therapies that can be tried for RA?

A

Tumour necrosis factor (TNF) inhibitors (e.g., adalimumab, infliximab, etanercept, golimumab and certolizumab)
Anti-CD20 on B cells (e.g., rituximab)
Anti-interleukin-6 inhibitors (e.g., sarilumab and tocilizumab)
JAK inhibitors (e.g., upadacitinib, tofacitinib and baricitinib)
T-cell co-stimulation inhibitors (e.g., abatacept)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What must be monitored whilst on methotrexate?

A

FBC, U&Es and LFTS every 1-2 weeks until therapy is stabilised and then 2-3 months after that - risk of myelosuppression and liver cirrhosis
Advise pt to report all symptoms suggesting infection, particularly sore throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Side effects of methotrexate?

A

Mouth ulcers and Mucositis
N&v&d
Liver toxicity
Bone marrow suppression and leukopenia
Pneumonitis
Teratogenic and needs to be avoided 3-6 months before conception in both women and men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

RA sympotms in pregnancy?

A

Tend to improve in pregnancy but likely to have a flare following delivery and post-breastfeeding!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Management of RA in pregnancy?

A

Sulfasalazine and hydroxychloroquine are three safest drugs
NSAIDs can be used until 32/40 - risk of early closure of ductus arteriosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Side effects of hydroxychloroquine?

A

Bull’s eye retinopathy which may result in severe and permenant visual loss
Blue-grey skin pigmentation
Hair bleaching

54
Q

Main risk of anti-TNF medications?

A

Reactivation of TB

55
Q

How does hydroxychloroquine work?

A

It suppresses the immune system by interfering with Toll-like receptors, disrupting antigen presentation and increasing the pH in the lysosomes of immune cells

56
Q

How does sulfasalazine work?

A

a prodrug for 5-ASA which works through decreasing neutrophil chemotaxis alongside suppressing proliferation of lymphocytes and pro-inflammatory cytokines.

57
Q

Cautions for starting sulfasalazine?

A

G6PD deficiency
allergy to aspirin or sulphonamides (cross-sensitivity)

58
Q

Possible adverse effects of sulfasalazine?

A

oligospermia = male infertility
Stevens-Johnson syndrome
pneumonitis / lung fibrosis
myelosuppression, Heinz body anaemia, megaloblastic anaemia
may colour tears → stained contact lenses
Rashes
May cause orange urine

59
Q

Leflunomide SE?

A

Liver impairment
Interstitial lung disease
Hypertension

60
Q

Poor prognostic factors for RA?

A

RF positive
anti-CCP antibodies
poor functional status at presentation
X-ray: early erosions (e.g. after < 2 years)
extra articular features e.g. nodules
HLA DR4
insidious onset

61
Q

what are seronegative spondyloarthropathies?

A

A family of rheumatological disorders which are RF and anti-CCP antibody are negative and have an association with the HLA B27 antigen

Types:
- psoriatic arthritis
- ankylosis spondylitis
- reactive arthritis
- enteropathic arthritis - associated with IBD

62
Q

What % of patients with psoriasis develop psoriatic arthritis?

A

10-20%

63
Q

Patterns of psoriatic arthritis?

A

Symmetrical polyarthritis like RA - most commonly (40%)
asymmetrical oligoarthritis where it usually affect 1-4 joints on 1 side of the body - 30%
Sacroiliitis - axial skeleton
DIP-predominant joint disease - 10%
Arthritis mutilans

64
Q

What is arthritis mutilans?

A

severe deformity fingers/hand, ‘telescoping fingers’

65
Q

How can you distinguish between psoriatic arthritis and RA just based on joint affected?

A

Psoriatic arthritis tends to affect the DIP joints and axial skeleton
RA tends to affect MCP, PIP abd wrist

66
Q

Symptoms of psoriatic arthritis?

A

Arthritis most commonly symmetrical but can have other patterns
Psoriatic skin lesions
Periarticular disease e.g. tenosynovitis, dactylitis or enthesitis
Nail changes - pitting or oncholysis

67
Q

What is enthesitis?

A

Inflammation of the entheses which are the points of insertion of tendons into bone
E.g. Achilles tendinitis and plantar fasciitis

68
Q

What is dactylitis?

A

Inflammation of an entire finger

69
Q

What screening tool can be used for psoriatic arthritis for pt with psoriasis?

A

Psoriasis epidemiological screening tool - PEST
It involves questions about joint pain, swelling, history of arthritis and nail pitting. A high score leads to a rheumatology referral

70
Q

Classic x-ray changes in psoriatic arthritis?

A

Periostitis - thickened, irregular outline of the bone
Ankylosis
Osteolysis
Dactylitis
Pencil-in-cup appearance in digits - central erosion of the bones on one side of the joint - this is associated with arthritis mutilans

71
Q

Management of psoriatic arthritis?

A

Mild disease may be treated with just NSAID
Mod-severe disease - methotrexate

Other treatments that can be tried - monoclonal antibodies and apremilast

72
Q

Prognosis of psoriatic arthritis vs RA?

A

Psoriatic arthritis has a better prognosis than RA

73
Q

What % of pt with psoriatic arthropathy have nail changes?

A

80-90%

74
Q

Nail changes seen in psoriasis and psoriatic arthropathy?

A

pitting
onycholysis (separation of the nail from the nail bed)
subungual hyperkeratosis
loss of the nail

75
Q

What is gout?

A

A type of arthritis caused by monosodium urate crystals forming inside and around joints causing sudden flares of severe pain, heat and swelling

76
Q

Which joints are most commonly affected in gout?

A

Most commonly MTP, CMC at base of thumb and wrist
But can also affect larger joints e.g. knee and ankle

77
Q

4 clinical phases of gout?

A

Asymptomatic hyperuricaemia — the risk of developing gout increases with the degree of hyperuricemia.
Acute gout — in almost all initial episodes a single peripheral joint is affected, most commonly the metatarsophalangeal joint.
Intercritical gout — after resolution of the first attack the second attack may occur within one year and chronic symptoms develop within 10 years.
Chronic tophaceous gout — large crystal deposits (tophi) produce irregular firm nodules and chronic joint damage.

78
Q

What is urate?

A

A metabolite of purines
The ionised form of uric acid

79
Q

How is urate excreted?

A

70% by kidneys and 30% by GIT

80
Q

Risk factors for gout?

A

Hyperuricaemia

Risk factors for hyperuricaemia:
CKD, hypertension, DM, hyperlipidaemia, osteoarthritis, myeloproliferative disorders (high cell turnover), severe exfoliative psoriasis
High purine diet - excess alcohol, sugary drinks, meat, seafood
Obesity
FHx
Genetics e.g. glycogen storage disease
Males
Post-Menopausal women
Older age
Some meds e.g. diuretics, low-dose aspirin, Ciclosporin

81
Q

Pathophysiology behind gout?

A

Hyperuricaemia is caused in 90% of cases by under-excretion of urate
10% is caused by over-producers of urate

82
Q

Epidemiology of gout?

A

More common in men >30 and women post-menopause
Prevalence increases with age - rare in under 40s
Higher prevalence in Oceania, North America, indignious populations

83
Q

Complications of gout?

A

Chronic arthritis
Joint damage
Reduced QOL
Renal stones
Tophi which may create their own problems e.g. infection

Hyperuricaemia is associated with an increased risk of:
CVD
CKD

84
Q

Prognosis of gout?

A

Acute attacks are self-limited and will resolve spontaneously over 5-15 days
If not taking urate-lowering therapies, risk of recurrence is 62% in the first year, 78% in second year and 84% in third year following

85
Q

What are tophi?

A

Subcutaneous uric acid deposits - typically seen on hands, elbows, ears
They are firm, white nodules under translucent skin. They are usually pain-free but can become inflamed or infected

They typically affect 50% of people after 10 years

86
Q

Presentation of gout?

A

Rapid onset (often overnight) severe pain with redness and swelling - most commonly in MTP

87
Q

How do we diagnose gout?

A

Measure serum urate level - 360 or more confirms diagnosis
If serum urate level is <360 but high suspicion of gout, repeat serum urate measurement in 2-4 weeks after flare has settled

If diagnostic uncertainty:
Joint aspiration and microscopy of synovial fluid - Synovial fluid analysis will show needle-shaped negatively birefringent monosodium urate crystals under polarised light
X-ray may also be done

88
Q

X-ray findings of a joint affected by gout?

A

joint effusion
well-defined ‘punched-out’ erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
relative preservation of joint space until late disease
Para-articular erosions i.e. slightly away from the joint margins unlike in RA or OA
no periarticular osteopenia (in contrast to rheumatoid arthritis)
soft tissue tophi may be seen

89
Q

What can cause increased production of uric acid?

A

Severe psoriasis
High protein turn over e.g. Myeloproliferative or lymphoproliferative disorders
Cytotoxic drugs
Purine rich diet

90
Q

Management of acute gout?

A

NSAIDs or colchicine (if both contraindicated: short course of oral corticosteroid)

If not effective then intra-articular or IM corticosteroid injection can be done

91
Q

How does colchicine work?

A

It inhibits microtubular polymerization by binding to tubulin, interfering with mitosis
It also inhibits neutrophil motility and activity

92
Q

Caution for colchicine use for treating gout?

A

In renal impairment
Reduce dose if eGFR is 10-50
Avoid if eGFR is <10

93
Q

Main SE of colchicine?

A

Diarrhoea

94
Q

Indications for urate-lowering therapy after first attack of gout?

A

It is now recommended for everyone!

Particularly important it >=2 attacks in 12 months, there are tophi, renal disease, uric acid renal stones or if on cytotoxics/diuretics

95
Q

When should urate-lowering therapy be started after a first attack of gout?

A

2 weeks after the attack

96
Q

What therapies do we offer for urate-lowering in gout?

A

Allopurinol
Second line - febuxostat

In refractory cases: uricase or pegloticase

97
Q

How does allopurinol work? What should be used alongside it?

A

It’s a xanthine oxidase inhibitor. Xanthine oxidase is the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid
Recommended to use NSAIDS or colchicine alongside for the first 6 months as starting urate lowering therapy can trigger attacks!

98
Q

Lifestyle modifications for gout?

A

reduce alcohol intake and avoid during an acute attack
lose weight if obese
avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
Increasing vitamin C intake may also decrease serum uric acid levels

99
Q

What is pseudogout?

A

A crystal arthropathy caused by calcium pyrophosphate crystals collecting in joints causing synovitis
It is also known as acute calcium pyrophosphate crystal deposition disease

100
Q

Who does pseudogout occur in?

A

Strongly associated with increasing age

Pt who develop pseudogout <60 usually have an underlying risk factors e.g. haemachromatosis, hyperparathyroidism, low magnesium, low phosphate, acromegaly or Wilson’s disease

101
Q

Presentation of pseudogout?

A

Knee, wrist and shoulders are the most commonly affected
Many pt are asymptomatic
Others present with chronic pain and stiffness in multiple joints. Can be hot and swollen

102
Q

Diagnosing pseudogout?

A

Exclude septic arthritis and gout - usually symptoms are much milder
Pseudogout more likely to affect proximal joints more than gout e..g knee and wrist

Joint aspiration to confirm the disease - will show calcium pyrophoshate crystals which are rhomboid-shaped and weakly-positively birefringent of polarised light

XR - will show chondrocalcinosis which are calcium deposits which show up in a thin white line in the middle of the joint space. Can also show same XR changes as osteoarthritis “LOSS”

103
Q

Management of pseudogout?

A

Note this is not fully treatable but you can manage symptoms. Symptoms will usually resolve spontaneously over several weeks but symptomatic management options include:
NSAIDs is first line
Or intra-articulate, IM or oral steroids

104
Q

Septic arthritis mortality rate?

A

10%

105
Q

Cause of septic arthritis?

A

Most commonly staph aureus
Young adults who are sexually active - neisseria gonorrhoea is the most common

The most common cause is haematogenous spread e.g. from distance bacterial infections
Be aware 1% of all joint replacements end in infection

106
Q

Presentation of septic arthritis?

A

Affects a single joint usually (commonly the knee)

Rapid onset of:
Hot, red, swollen, painful joint
Stiffness and reduced range of movement
Systemic symptms - fever, lethargy, sepsis

107
Q

Investigations for septic arthritis?

A

FBC, ESR, CRP
Synovial fluid sampling before antibiotics - gram staining, crystal microscopy, culture
Blood cultures as commonly hameatogenous spread
Joint imaging may be done

108
Q

Management of septic arthritis?

A

IV antibiotics which cover gram-positive cocci - flucloxacillin (or clindamycin if penicillin allergic) for 4-6 weeks ( usually switched to oral antibiotics after 2 weeks)
(Ceftriaxone is used for gonococcal infection)
Needle aspiration to decompress the joint
Arthroscopic lavage may be required

109
Q

What is reactive arthritis?

A

A seronegative spondyloarthropathies associated with HLA-B27
Formerly called Reiter’s syndrome
Classic triad - urethritis, conjunctivitis and arthritis

Defined as an arthritis that develops following an infection where the organism cannot be recovered from the joint

110
Q

Organisms most commonly associated with reactive arthritis?

A

Chlamydia trachomatis - particularly in men
Shigella, salmonella, yersinia, campylobacter

111
Q

Presentation of reactive arthritis?

A

Within 4 weeks of initial infection…
Bilateral conjunctivitis (non-infective) or anterior uveitis
Urethritis (non-gonococcal)
Circinate balanitis (dermatitis of the head of the penis)
Arthritis - asymmetrical oligoarthritis of lower limbs
Dactylitis

“Can’t see, can’t pee, can’t climb a tree”

112
Q

Management of reactive arthritis?

A

Septic arthritis most likely will need to be ruled out first using joint aspiration!

symptomatic: treat triggering infection, NSAIDS, intra-articular steroid injections or systemic steroids
sulfasalazine and methotrexate are sometimes used for persistent disease

113
Q

Prognosis of reactive arthritis?

A

Most cases rarely last >12 months

114
Q

What is ankylosing spondylitis?

A

A HLA-B27 associated seronegative spondyloarthropathy affecting the axial skeletal causing progressive stiffness and pain
Aka axial spondyloarthritis

115
Q

Who does ankylosing spondylitis typically affect?

A

Men 20-30 years old
Men:women 3:1 and men are more likely to get severe disease

116
Q

Presentation of ankylosing spondylitis?

A

Gradual development over at least 3 months of pain and stiffness in the lower back and sacroiliac pain
Pain and stiffness is worse with rest and improves with movement. Stiffness takes at least 30 minutes to improve in the am
May have night pain

Other features may include chest pain, enthesitis (e.g. Achilles tendinitis or plantar fasciitis), dactylitis, vertebra fractures and SOB

117
Q

Clinical examination findings of ankylosing spondylitis?

A

Reduced lateral flexion
Reduced forward flexion - Schober’s test
Reduced chest expansion

118
Q

What are the associated conditions of ankylosing spondylitis?

A

Remembers the As

Anterior uveitis
Aortic regurgitation
AV block
Apical lung fibrosis
Anaemia of chronic disease
Achilles tendinitis
Amyloidosis
And caudal equina syndrome

119
Q

What is schobers test?

A

a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible
This is reduced in ankylosing spondylitis

120
Q

Investigations for ankylosing spondylitis?

A

ESR and CRP are raised
HLA-B27 is of little use
Plain XR of sacroiliac joints - If XR is negative for sacroiliac joint involvement but suspicion remains high then obtain MRI which may show early inflammation signs e.g. bone marrow oedema
Spirometers may show a restrictive defect due to combination of pulmonary fibrosis, kyphosis and ankylosis of costovertbral joints

121
Q

XR findings of sacroiliac joints in ankylosing spondylitis?

A

Sacroiliitis - subchondral erosions and sclerosis
Squaring of lumbar vertebrae
Syndesmophytes due to ossification of outer fibers of annulus fibrosus
Bamboo spine - late &uncommon sign

122
Q

Management of ankylosing spondylitis?

A

Encourage regular exercise e.g. swimming
First line - NSAIDs + PT
Second line - If very resistant to treatment then anti-TNF therapy can be tried

DMARDs are only used if peripheral joint involvement
Intra-articular steroid injections may be considered for specific joints

123
Q

Oligoarthritis vs polyarthritis?

A

Oligoarthritis means less than 5 joints affected
Polyarthritis is >5 joints

124
Q

What is chondrocalcinposis?

A

Presence of calcium deposits in the cartilage of a joint
Seen in calcium pyrophosphate deposition disease aka pseudogout
This can also be present in up to 1/3rd of healthy 65-75 year olds

125
Q

Pathophysiology of rheumatoid arthritis?

A

Trigger -> macrophages release TNF alpha, IL1 and IL6 -> Synovial membrane is inflamed + fibroblast-like synoviocytes are stimulated, activated and proliferate -> activation of osteoclasts = bone erosion
Proteases are also released which causes cartilage degradation
T cells secrete IL17 which promotes macrophage activity and stimulates fibroblast-like synoviocytes and help stimulate osteoclasts
Plasma cells assist in inflammation through cytokines and antibodies

In the synovial fluid we find neutrophils which produce proteases and ROS = bone and cartilage degradation
Immune complexes are also found in this synovial fluid

The fibroblast-like synoviocytes can migrate from joint to joint = this is why we get symmetrical arthritis

126
Q

Pathophysiology of osteoarthritis?

A

Chondrocytes in articular cartilage and inflammatory cells in surrounding tissues break down collagen and proteoglycans, destroying articular cartilage. The exposure of the underlying subchondral bone results in sclerosis, followed by reactive remodelling which leads to the formation of ostephytes and subchondral bone cysts
The joint space is progressively lost over time

127
Q

What % of patients with axial spondyloarthritis have HLA-B27?

A

90%

128
Q

How long do joint replacements typically last?

A

15-20 years

129
Q

What is enteropathic arthritis?

A

a type of arthritis that occurs with inflammatory bowel disease

130
Q

Complications of ankylosing spondylitis?

A

Ankylosis or spinal fusion
Apical fibrosis and other lung involvement - this is due to costovertebral involvement decreasing vital capacity
Joint damage - hips and knees due to change of gait to accommodate stiffness
Anterior uveitis
Osteoporosis and spinal fractures
CVD
Decreased QOL and work productivity
Risk of cauda equina

131
Q

Prognosis of gout and why?

A

It will continue to return and worsen
This is because as we age our renal function worsens

132
Q

What skin conditions are likely with reactive arthritis?

A

circinate balanitis (painless vesicles on the coronal margin of the prepuce)
keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)

MUSCULOSKELETAL (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions