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Conditions + definitions > Rheum > Flashcards

Rheum Flashcards

1
Q

What are the symptoms af arthritis?

A 
Pain
Stiffness
Swelling
Functional impairment
Systemic symptoms
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2
Q

What are the signs of arthrtiis?

A 
Tenderness
Swelling
Restriction of movement
Heat
Redness
Systemic features
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3
Q

What are the types of rheumatoid disease?

A 
RA
Sero-negative arthritis
Crystal arthritis
Connective tissue diseases
Systemic vasculitis
Bone disease
Osteoarthritis
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4
Q

What are the functions of the synovium?

A

Maintenance of intact tissue surface
Lubrication of cartilage
Control of synovial fluid volume + composition
Nutrition of chondrocytes within joints

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5
Q

How does rheumatoid affect a joint?

A

Cartilage thinned
Inflammed synovium across joint surface
Inflammed tendon
Erosion of corner of bone

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6
Q

What is rheumatoid arthritis?

A

Chronic symmetric polyarticular inflammatory joint disease
Characterised by inflammatory cell infiltration, synoviocyte proliferation and neoangiogenesis
Synovial fluid contains neutrophils
Synovial panus causes bone and cartilage destruction

Primarily affects small joints of hand and feet

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7
Q

What auto-antibodies are associated with rheumatoid arthritis?

A

Rheumatoid factors

Anti-citrullinated protein

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8
Q

In what type of rheumatoid arthritis are autoantibodies found?

A

Seropositive RA

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9
Q

What genes are associated with RA?

A

HLA-DRB1 - role in promoting autoimmunity
PTPN22
CTLA4

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10
Q

What environmental factors are associated with RA?

A

Smoking and bronchial stress
Infective agents
Repeated insults to joints

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11
Q

What infective agents are associated with RA?

A

Viruses
E. coli
Mycoplasma
Perodontal disease

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12
Q

What is the pathophysiology of synovitis in RA?

A

Villous hyperplasia
Infiltration of T cells, B cells, macrophages and plasma cells
Intimal cell proliferation causing thickening of membrane
Production of cytokenes
Cytokines along with local hypoxic conditiosn causes increase vascularity
Makes self worse

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13
Q

Whar are the main cytokines produced?

A

TNF-a

IL-6

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14
Q

What is the action of the inflammatory cytokines?

A

Induce expression of endothelial cell adhesion molecules
Promote angiogensis
Supress T-regs
Activate leukocytes
Promote autoAB production
Activates synovial fibroblasts, chondrocytes, osteoclasts

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15
Q

What is the action of IL-6?

A

Mediates systemic effects

Acute phase response
Anaemia
Cognitive dysfunction
Lipid metabolism dysregulation

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16
Q

What mediates cartilage and bone destruction in RA?

A

Bone mediated y osteoclasts that are activated under the influence of RANKL
Cartilage - metalloproteinases + aggrecanases

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17
Q

What are teh systemic consequences of uncrontrolled chronic RA?

A

Vasculitis
Nodules
Scleritis
Amylodosis

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18
Q

What are the systemic consequences of RA?

A

Cardiovascular disease - altered lipid metabolism
Secondary fibromyalgia (congnitive fuction decline as well)
Muscles - sarcopenia
Bone - osteoporosis
Secondary sjogrens syndrome
Liver - anaemia (IL-6)

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19
Q

Who is likely to get rheumatoid arthritis?

A

1% of population
3x more common in women
Often 4-5th decade - any age from 16

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20
Q

What is the aeitiology of rheumatoid?

A

Genetic ~ 50-60% contribution

Environmental - smoking, chornic infection

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21
Q

How do you investigate rhuematoid arthritis?

A

Immunology - rheumatoid factor (IgG, IgM)
Anti-cyclic citrullinated antibodies (anti-CCP, ACPA) - Better test, more specificity
Ultrasound

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22
Q

How do you diagnose RA?

A

Joint involvement (multiple more likely)
Serology
Acute phase reactants
Duration more than 6 weeks

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23
Q

What are the therapeutic categories for reheumatoid arthritis?

A

NSAIDS
Disease modifying anti rheumatic drugs
Biologics
Corticosteroids

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24
Q

What are the common disease modifying anti rheumatic drugs?

A

Methotrexate!

Sulfasalazine
Hydrochloroquine
Leflunomide

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25
Q

How do you approach rheumatoid treatment?

A

Early and aggressive intervention

Effective suppression of inflammation improves symptoms + prevents disaability

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26
Q

What are the downsides to biologics?

A

Toxciity - increased rate of infection
Expensive
Injection
Efficacy - increased when used with methotrexate

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27
Q

What are the advantages of biologics?

A

Work rapidly and well tollerated

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28
Q

What are the benefits of methotrexate?

A

Effective
Well tollerated
Cheap

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29
Q

What gene is seronegative arthritis associated with?

A

HLA-B27

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30
Q

What is seronegative arthritis?

A

Arthritis with negative rheumatoid factor
Usually asymmetric
Involves axial skeleton (spine)
Enthesitis (soft tissue irritability)
Extra-articular features - uveitis, inflammatory bowel disease

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31
Q

What are the different presentations of seronegative arthritis?

A

Ankylosing spondylitis
Psoriatic arthritis
Bowel related arthritis (chron’s, UC)
Reactive arthrits

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32
Q

What is ankylosing spondylitis?

A

Chronic inflammatory rheumatic disorder

Predilection for axial skeleton + Antheses

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33
Q

Who is most likelt to get ankylosing spondylitis?

A

Males more than females

Onsets 2nd-3rd decade

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34
Q

How is spinal mobility tested?

A

Modified shober test
Lateral spinal flexion
Occiput/tragus to wall
Cervical rotation

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35
Q

What is the modified shober test?

A

Patient stading erect
Line connected posterior superior iliac spine. Then line 10cm above
Patient bends and see difference between two lines

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36
Q

What is the lateral spinal flexion test?

A

Hand down against thigh without bending

Measure difference between normal hand + how far it can go

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37
Q

What is the cervical rotation test?

A

Sit in chair
Goniometer in line with nose
Record how far they can turn head

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38
Q

What are the clinical features of anylosing spondylitis?

A

Inflammatory back pain
Limitation of movements in antero-posterior + lateral planes at lumbar spine
Limitation of chest expansion
Bilateral sacroiliitis on x-rays

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39
Q

What is the grading for sacroiitis?

A

0 - normal
1 - suspicious changes
2 - minimal abnormality (no alteration to joint width)
3) unequivicol abnormality (moderate-advanced, erosions, sclerosis, widening, narrowing or partial ankylosis)
4 - severe, total ankyloitis

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40
Q

What are the other features of anyylosing spondylitis?

A 
Peripheral joint arthritis
Achilles tendonitis, dactylitis
Uveitis
Cardiac (aortic incompetence, heart block)
IBD
Osteoporosis /spinal fractures
Cauda equina syndrom
Secondary amyloidosis
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41
Q

How do you manage aknylosing spondylitis?

A 
Physio
NSAIDs
Disease modifying rheumatoid drugs - sulfasalazine
Anti-TNF
Anti-IL-17
Joint replacements
42
Q

What joints are commonly affected by psoriatic arthritis?

A 
Neck/shoulder
Elbows/knees
Toes + ankles
Hand + wrist
Base of spine
43
Q

What is the treatment for psoaritic arthritis?

A

DMARD - sulfasalazine
Methotrexate
Leflunomide

Cyclosporine
Anti-TNF
Anti-IL 17/23
Steroids
Physio/occupational therpay
44
Q

What isreactive arthritis?

A

Sterile synovitis after distant infection

45
Q

What infections often cause reactive arthritis?

A 
Salmonella
Shingella
Campyloobacter
Chlamydia (often recurrent attacks)
Trachomatis
Pneumonia
Borrelia
Neisseria
Streptococci

(throat, urogenital, GI)

46
Q

How does reactive arthritis present?

A

Mono or oligoarthritis
Dactylitis or enthesitis also seen
Skin/mucous membrane involvement

47
Q

What conditions are seen in skin/mucous membrane involvement?

A 
Keratoderma Blenorrhagica 
Circinate Balanitis 
Urethritis 
Conjunctivitis 
Iritis
48
Q

What is reiters syndrome?

A

Arhtritis
Urethritis
Conjunctivitis

49
Q

What indicates chronic reactive arthritis?

A

Hip/heel pain
High ESR
Family history + HLA-B27 positive

50
Q

How do you treat reactive arthritis?

A

NSAIDs
If acute - joint injection if no infection
Antibiotics in chlamudia

If chronic - DMARD

51
Q

What is enteropathic arthritis?

A

A chronic inflammatory arthritis developing in people with inflammatory bowel diseases
Rarely seenin infectious enteritis, whipples disease or coeliac disease however
Enthesopathy common

52
Q

How do you treat enteropathic arthritis?

A 
Sulfasalazine
Methotrexate
Steroids
Anti-TNF
Bowel resection may alleviate peripheral disease
53
Q

What is a crystal depositation disease?

A

Where mineralised material is deposited in joints and periarticular tissue

54
Q

What are the common crystal deposition diseases?

A

gout - Monosodium urate

pseudogout - Calcium pyrophosphate dihydrate (CPPD)

calcific perarthritis/tendonitis - Basic calcium phosphate hydroxy-apatite (BCP)

55
Q

What is a tophi?

A

A massive accumulation of uric acid

56
Q

What are the methods by which hyperuricaemia can occur?

A

Overproduction

Underexcretion

57
Q

What can cause overproduction of uric acid?

A 
Malignancy
Severe exfoliative psoriasis
Drugs (ethanol, cytotoxic drugs)
Hereditary erros of metabolism
HGPRT deficiency
58
Q

What can cause under excretion of uric acid?

A 
Renal impairment
Hypertension
Hypothyroidism
Drugs (alohol, low dose, aspirin, diuretics, cyclosporin)
Exercise, starvation, dehydration
Lead poisoning
59
Q

What is Lesch Nyan syndrome?

A 
Deficiency of HGPRT
X-linked recessive disease
Intellectual disability
People have aggressive + impulsive behaviour
Self mutilate
Have gout + renal disease
60
Q

Who is likely to get gout?

A

Men more common in all ages

After menopause gout rate increases in women

61
Q

How is an acute flare up of gout treated?

A

NSAIDs
Colchine
Steroids

62
Q

When is hyperuricaemia treated?

A

1st attack not treated unless - single attack of polyarticular gout
Tophaceous gout
Urate calculi
Renal insufficiency

Do not treat asymptomatic hyperuricaemia

63
Q

What drugs are used to lower uric acid?

A

Xanthine oxidase inhibitor (allopurinol)
Febuxostat
Uricosuric agents (sulphinpyrazone)
Canakinumab

64
Q

What are the rules regarding lowering uric acid levels?

A

Wait until any acute attack has settled before treatment
Prohylatic NSAIDs/low dose cholchinie/steroids until urate acid normal
Adjust allopurinol dose occording to renal function

65
Q

What is the main treatment for gout?

A

Adjust lifestyle factors

66
Q

What is pseudogout?

A

Common in knee

Erratic flares, often triggered by trauma or intercurrent illness

67
Q

Who gets pseudogout?

A

Elderly females

68
Q

How do you manage pseudogout?

A

NSAIDs

Steroids

69
Q

What is polymyalgia theumatica?

A

Inflammatory arthritic condition of the elderly

Associated with giant cell arteritis & high ESR

70
Q

Who is likely to get polymyalgia pheumatica?

A

Women 2x than men

Rare in under 50s, usually over 70

71
Q

What are the clinical features of polymyalgia rheumatica?

A 
Sudden onset of shoulder +/- pelvic girdle stiffness
ESR > 45, often over 100
Anaemia
Malaise
Weight loss
Fever
depression
Arthralgia /synovitis occasionally
72
Q

How do you diagnose polymyalgia rheumatica?

A 
50+
ESR 50+
Dramatic steroid response
Compatible hisotry
No specific diagnostic test
73
Q

How do you treat polymyalgia rheumatica?

A

Prednisolone 15mg/day for 18-24 months

Bone prophylaxis

74
Q

What are the differentials of polymyalgia rheumatic?

A 
Myalgic onset inflammatory joint disease
Underlying malignancy
Inflammatory muscle disease
Hypo/hyper thyroidism
Bilateral shoulder capsulitis
Fibromyalgia
75
Q

What is juvenile idiopathic arthtis?

A

A group of systemic inflammatory disorders affecting children younger than 16
Important cause of disability and blindness

76
Q

What is the most common juvenile idiopathic arthritis?

A

Rheumatic disease

77
Q

What type of disease is JIA?

A

autoimmune disease

78
Q

What are the diagnostic criteria for juvenile idiopathic arthritis?

A 
Younger than 16
Symptoms for more than 6 weeks
Joint swelling or 2 of following
Painful/limited joint motion
Tenderness
Warmth
79
Q

What are the three main subtypes of juvenile idiopathic arthritis?

A

Pauciarticular (most common - 55%)
Polyarticular
Systemic onset

80
Q

What is pauciarticular juvenile idiopathic arthritis?

A

4 joints or less affected

Split into three types

81
Q

who is affected by type 1 pauciarticular juvenile idiopathic arthritis?

A 
Mainly girls (8:1)
Before 5 yrs, most commoon 1-3
82
Q

How does type 1 pauciarticular juvenile idiopathic arthritis present?

A 
Limp rather than pain
No constitutional manifestations
Mainly lower limb affected
With knee being most common (ankle, then hand or elbow)
\+ve ANA in 40-75%
Chronic uveitis in 20%
Asymptomatic in 50%
Irregular iris due to posterior synechiae
83
Q

Who is affected by type 2 pauciarticular juvenile idiopathic arthritis?

A

Boys more often than girls (7:1)

After 8-9 yrs old

84
Q

What is the presentation of type 2 pauciarticular juvenile idiopathic arthritis?

A

Constiutional features rare
Limp due to LL affection (knee, ankle mostly)
Hip can be affected with rapid damange (needs total hip replacement early in life)
Enthesitis
Sacroilliac joints affected
Acute iridocyclitis in 10-20%

85
Q

Who is characterised to have juvenile ankylosing spondylitis?

A

HLA-B27 positive people with back involvement

86
Q

Who presents with type 3 pauciarticular juvenile idiopathic arthritis?

A

Girls (4:1) more than boys

Any age during childhood

87
Q

How does pauciarticular juvenile idiopathic arthritis present?

A 
Asymmetric UL/LL arthritis (destructive)
Dactylitis
Family history of psoriasis 
Nail pitting
Chronic iridocyclitis (10-20%)
88
Q

What is polyarticular juvenile idiopathic arthritis?

A

5+ joints involved

89
Q

What are the subtypes of polyarticular juvenile idiopathic arthritis?

A

Rhuematoid factor positive

Rhuematoid factor negative

90
Q

Who gets RF negative polyarticular juvenile idiopathic arthritis?

A

Girls (9:1) more than boys

Any age, but often early

91
Q

What is the presentation of RF negative polyarticular juvenile idiopathic arthritis?

A

Constitutional manifestations (low grade fever, malaise)
Hepato-splenomegaly
Mild anaemia
Growth abnormalities
Symmetric large and small joints affection: knees, wrists, ankles, MCPs, PIPs, neck

Iridocyclitis rare.

92
Q

What is the presentation of RF positive polyarticular juvenile idiopathic arthritis?

A

Constitutional manifestations (low grade fever, malaise, weight loss)
Anaemia
Nodules.
Can be complicated by sjogren’s, Felty or vasculitis, AR, pulmonary fibrosis, AAS, CTS.
Similar to adult RA but in a child
Erosions in x ray occur early
Iridocyclitis rare.

93
Q

What is likely to get RF positive polyarticular juvenile idiopathic arthritis?

A

Girls (7:1) more than boys

Late childhood - teens (12-16)

94
Q

What defines systemic onset JIA (still’s disease)?

A

Extra-articular features

Start eraly and dissappear after 2-5 years

95
Q

Who gets systemic onset juvenile idiopathic arthritis?

A

Throughout childhood, bu ages 4-6 most common

Roughly equal across gender girls (3:2) to boys

96
Q

How does systemic onset juvenile idiopathic arthritis present?

A

Fever rising to 39.5 for at least weeks
Rash
Lymph nodes non-tendor generalise lymphadenopathy
Abdominal pain (hepatosplenmegaly in 50-75%)
Serositis
Arthritis (within 3-12 months of fever)

97
Q

Describe the fever in systemic onset juvenile idiopathic arthritis present.

A

Evening/late afternoon, then returns to normal in morning

Whilst feverish looks toxic with chills, normal otherwise

98
Q

Describe the rashin systemic onset juvenile idiopathic arthritis present.

A

Evanescent salmon red erruption on trunk/thighs
Accompanies fever
Brought on by scratching

99
Q

How do you treat Juevenile idiopathic arthritis?

A 
Simple pain killers
NSAIDs
If no response steroid injections
Then disease modifying drugs/biologics
Local steroids
RARELY systemic steroids
100
Q

When are systemic steroids used in JIA?

A

In systemic JIA to control pain/fever
In the case of serious disease complications
Bridge between DMARDs
If child undergoing surgery

101
Q

What are the surgical treatments for JIA?

A

Synovectomy

Reconstructive/joint replacement

Conditions + definitions (68 decks)

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