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Yr3 - General Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

ANA

A

Anti-Nuclear Antibodies

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2
Q

ANCA

A

Anti-Neutrophilic Cytoplasmic Antibodies

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3
Q

Anti-CCP

A

Anti-Cyclic Citrullinated Peptide

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4
Q

CTS

A

Carpal Tunnel Syndrome

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5
Q

DXA

A

Dual Energy X-Ray Absorptiometry

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6
Q

GPA

A

Granulomatosis with PolyAngiitis

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7
Q

PV

A

Plasma Viscosity

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8
Q

RF

A

Rheumatoid Factor

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9
Q

Causes of acute monoarthritis

A 
Septic arthritis until proven otherwise
- streptococcal most common
Crystal-induced
- gout - often men
- pseudogout - often elderly women with severe OA
Trauma
- haemarthrosis
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10
Q

Causes of chronic monoarthritis

A 
Infections
- TB
Inflammatory
- Psoriatic arthritis
- Reactive arthritis
- Foreign body
Non-inflammatory
- OA
- Traumatic - meniscal tear
- Osteonecrosis - a/w prednisolone use
- Neuropathic - Charcot's joint
Tumours - rare
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11
Q

Causes of acute polyarthritis

A 
Inflammatory arthritis
- RA
- PsA
- Reactive arthritis
Autoimmune arthritis
- SLE
- vaculitis
Viral infection
- HIV
- Chikungunya
- Parovirus
Crystal arthritis
- Uncontrolled gout
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12
Q

Caues of chronic polyarthritis

A 
Inflammatory arthritis
- RA
- PsA
- Reactive arthrits
Autoimmune arthritis
- SLE
- vasculitis
Crystal arthritis
- Uncontrolled gout
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13
Q

Causes of arthritis of DIPJs

A

PsA
- nail dystrophy on affected digit
OA - common
- Heberden’s nodes

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14
Q

Features to ask for rheumatology history

A 
Pain
- location, duration, pattern, relief/exacerbation
Stiffness
Joint swelling and deformity
Fatigue
Weakness
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15
Q

Features of inflammatory disease

A 
Morning stiffness - > 1 hour
Better on activity
Worse on resting
Significant fatigue
Systemic involvement
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16
Q

Features of mechanical disease

A 
Morning stiffness < 30 mins
Worse on activity
Better on rest
Minimal fatigue
Non systemic involvement
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17
Q

Features of GALS assessment

A

Gait, Arms, Legs, Spine

- quick screening assessment for MSK disorders

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18
Q

Stages of Arms of GALS assessment

A

Inspect hands - palmar and dorsal
Assess pincer-grip and power-grip
Squeezes across 2nd-5th MCPJs - tenderness
Assess active elbow flexion/extension and pronation/supination
Assess active shoulder external rotation

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19
Q

Stages of Legs of GALS assessment

A

Inspects the legs - deformities, leg length, inequality, swellings or muscle wasting
Knee joint effusion
Passive knee flexion and extension
Hip flexion and internal rotation
Inspects feet for deformities and callosites
MTPJ squeeze - tenderness

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20
Q

Stages of Spine of GALS assessment

A

Inspect spine from behind and sides
Palpates supraspinatus
Tests cervical spine lateral flexion
Tests hip and lumbar spine flexion

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21
Q

Features of antalgic gait

A

Pain causes patient to reduce time spent on the affected side

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22
Q

Features of Trendelenberg gait

A

Due to poor hip abduction (weak gluteus medialis)

- pelvis drops to opposite side when standing on affected leg

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23
Q

Features of sensory ataxia gait

A

Wide-based stamping

  • stamping attempt to compensate for lack of sensory input
  • worse when eyes shut
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24
Q

Features of cerebellar ataxia gait

A

Wide-based staggering

- arms often flung out to try to improve balance

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25
Q

Features of hemiplegic gait

A

Narrow-based

  • leg swung forwards
  • toes scrap ground
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26
Q

Features of festinant of projectile gait

A

Difficulty initiating walking

  • shuffling run
  • reduced arm swing
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27
Q

Features of waddling gait

A

Duck-like

- due to bilateral hip muscle weakness

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28
Q

Features of psychogenic gait

A

Variable

- worse under observation

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29
Q

Define varus

A

Bow-legged

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30
Q

Define valgus

A

Knock-kneed

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31
Q

Sensory nerve supply to hand of median nerve

A

Skin over thenar eminence
Lateral 2/3 palm of hand
Palmar aspect of lateral 3.5 fingers
Dorsal fingertips of lateral 3.5 fingers

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32
Q

Motor supply of median nerve to hand

A 
All muscles of anterior compartment except
- flexor carpi ulnaris
- medical parts of flexor digitorum profundus
Intrinsic mucles of hand - LOAF
- lateral two lumbricals
- opponens pollicis
- abductor pollicis brevis
- flexor pollicis brevis
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33
Q

Features of median nerve palsy

A

Numbness of hand in median nerve distribution
- sparing of palm due to intact palmar cuaneous branch
Weakness of thumb opposition and abduction
Thenar eminance wasting

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34
Q

Sensory supply of ulnar nerve to hand

A 
Skin over hypothenar eminence 
Medial 1/3 palm of hand
Palmar aspect of lateral 1.5 fingers
Medial 1/3 dorsum of hand
Dorsal aspect of medial 1.5 fingers
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35
Q

Motor nerve supply of ulnar nerve to hand

A

Two muscles of forearm
- flexor carpi ulnaris
- flex ring and little fingers at DIPJs
Most intrinsic muscles of hand

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36
Q

Clinical features of ulnar nerve palsy

A

Numbness over hypothenar eminence and in ulnar nerve distribution of hand
Paralysis of flexor carpi ulnaris
- weak wrist flexion and adduction
Paralysis of medial two parts of flexor digitorum profundus
- weakness of flexion of ring and little finger DIPJs
Paralysis of most intrinsic mucles of hand
- weak MCPJ flexion and IPJ extension of ring and litter finger, loss of finger abduction and adduction, loss of opposition of little finger
Claw hand deformity
- fixed flexion of IPJs and hyperextension of MCPJs of ring and little fingers due to unopposed median nerve function

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37
Q

Interpreting blood tests in rheumatic disease

A 
Hb
- anaemia of chronic disease - RA
- NSAIDs
Platelets
- rise in inflammation or bleeding
- fall in SLE
Neutrophils
- rise in inflammation, sepsis and prednisolone usage
- fall in SLE or with DMARD toxicity
Lymphocytes
- fall in SLE or DMARD incuded
U&amp;E
- rise in NSAIDs, renal disease in lupus/vasculitis or gout
Uric acid
- elevated in gout
- falls in inflammation
LFTs
- hepatic rise due to DMARD toxicity
CK, ALT, LDH
- rise in myositis
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38
Q

What does ESR test reflect the presence of?

A

Fibrinogen

Immunoglobulins

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39
Q

Advantages of ESR test

A

Widely understood

Well established in diagnosis and monitoring of GCA

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40
Q

Disadvantages of ESR test

A

No technique for calibration to test for accuracy
Poor reproducibility
Test takes 1 hour
Must be carried out within 4 hours of blood sampling

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41
Q

What does PV test reflect the presence of

A

Fibrinogen

Immunoglobulins

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42
Q

Advantages of PV test

A

Automatable
Sensitive
No affected by haemocrit
Measurement can be made on stored blood samples

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43
Q

Disadvantages of PV test

A

Not widely used - lack of familiarity with interpretation

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44
Q

What does CRP test reflect the presence of

A

C-Reactive Protein

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45
Q

Advantages of CRP test

A

Automatable
Very sensitive
Not affected by haematocrit
Measurement can be made on stored blood samples

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46
Q

Disadvantages of CRP test

A

Short lived indicator

Good at monitoring sepsis as rises and falls quickly

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47
Q

Autoantibodies in RA

A

Rheumatoid factor (RF)
- antibody directed against Fc fragment in human immunoglobulin G
- seropositive patients tend to have more severe disease
Anti-cyclic citrullinated peptide antibody (ACPA)
- more specific for RA for RF
Neither rise in disease flares

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48
Q

Antinuclear antibodies (ANA) and their disease associations

A 
Anti-dsDNA = SLE
- rises with disease activity
Anti-RO and anti-LA = SLE, Sjogren's
Anti-centromere and anti-Scl70 = Systemic Sclerosis
Anti-Jo-1 = Polymyositis
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49
Q

What are anti-neutrophil cytoplasmic antibodies directed against?

A

Directed against enzymes present in neutrophils

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50
Q

Anti-neutrophil cytoplasmic antibodies and their disease associations

A

C ANCA = GPA, infection, neoplasia
- antibody to proteinase-3
P ANAC = microscopic polyangiitis, infection, neoplasia
- antibody to myelopreoxidase

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51
Q

Features of Human Leukocyte Antigen B27 (HLA-B27)

A 
Class 1 surface antigen
- found in 10% of white people
- present in 90% of white people with AS
Strongly associated with
- ankylosing spondylitis
- iritis
- juvenile arthritis
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52
Q

Features of synovial fluid analysis

A

Gram stain and culture - septic arthritis
Polarized light microscopy
- negatively birefringent needle shaped crystals = gout
- positively birefringenet rhomboid shaped crystals = pseudogout

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53
Q

Uses of biopsies in rheumatoid diseases

A

Temporal artery - vasculitis in GCA
Muscle - polymyositis or dermatomyositis
Skin - vasculitis, dermatomyositis and SLE
Lip/salivary gland - Sjogren’s
Lymph node - rule out lymphoma or TB in SLE
Synovial - rare tumours or infection
Sural nerve - vasculitis with monoeuritis multiplex / peripheral neuropathy
Renal - vasculitis, SLE

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54
Q

Use of NSAIDs

A

Initial therapy

Provide symptomatic relief

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55
Q

Side effects of NSAIDs

A

GI problems
Renal impairment
Caution in patients with cardiovascular risk and asthma

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56
Q

Uses of corticosteroids

A

For inflammatory arthritis - used initially for a few weeks till DMARDs kick in
PO, IV, IM or directly into joint or soft tissue
Mainstay of treatment for PMR and GCA

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57
Q

Uses of non-biological DMARDs

A

RA, PsA, SLE and vasculitis
Started asap
Life-long

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58
Q

Most common non-biological DMARDs for inflammatory arthritis

A

Methotrexate
Hydroxychoroquine
Sulfasalazine

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59
Q

Effects of non-biological DMARDs

A

Sustained reductions in pain, stiffness and fatigue and improvements in physical function
Make take up to 3 months

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60
Q

Uses of biological DMARDs

A

RA, PsA and AS

Psoriasis and IBD

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61
Q

Biological DMARDs used in RA

A

Rituximab - CD-20 inhibitor
Tocilizumab - IL-6 inhibitor
Adalimumab (Humira) - TNF-alpha inhibitors
JAK inhibitors

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62
Q

Biological DMARDs used in AS and PsA

A

IL-17 antagonists

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63
Q

Biological DMARDs used in Crohn’s disease and its enteropathic arthritis

A

IL-12/23 blocker

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64
Q

Long term effects of DMARDs

A

Increased infection risk - immunosuppressive
Malignancy
Ractivation of hepatitis B and TB
Regular flu and pneumococcal vaccination - no live vaccinations

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65
Q

Drug treatment for osteoporosis

A

Calcium and vitamin D

Oral bisphosphonates

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66
Q

How to take oral bisphosphonates

A

Taken on empty stomach
Avoid food, water or other drugs for 30 mins post - maximise gut absorption
Swallow whole with water and avoid bending for 30 mins - reduce chance of ingestion

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67
Q

Drugs for acute attacks for crystal arthritis

A

NSAIDs
Colchicine
- avoid in renal failure
Intra-articular steroid injections

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68
Q

Drugs for prophylaxis for crystal arthritis

A

Allopurinol - urate-lowering
- flares common in first 6th months so cover with NSAIDs, colchicine or prednisolone
- avoid in renal failure
Feboxostat - used if allopurinol not tolerated

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69
Q

Side effects of Methotrexate

A 
Nausea
Oral ulcers
Hair thinning
Hepatitis, cirrhosis
Pneumonitis
Bone marrow suppression
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70
Q

Side effects of Hydroxycholorquine

A

GI disturbance
Retinal pigmentation and loss of vision - annual eye tests
No blood tests needed

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71
Q

Side effects of Sulfasalazine

A

GI upset
Rash
Hepatitis
Bone marrow suppression

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72
Q

Side effects of Azathioprine

A

GI upset

Bone marrow suppression

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73
Q

Side effects of Cyclophosphamide

A

Bone marrow suppression
Infertility
Increased cancer risk

74
Q

Side effects of Ciclosporin

A

Renal impairment

Hypertension

75
Q

Side effects of Leflunomide

A

GI upset
Hypertension
Bone marrow suppression
Hepatitis

76
Q

What is dermatomyositis and polymyositis

A

Rare idiopathic muscle diseases

Characterised by inflammation of striated muscles

77
Q

Epidemiology of dermatomyositis and polymyositis

A

M:F = 1:1

Peak onset 40-50 years

78
Q

Symptoms and signs of dermatomyositis and polymyositis

A

Insidious onset of muscle proximal weakness - often painless
SOB
Rash
Raynaud’s syndrome common

79
Q

Diagnostic criteria of dermatomyositis and polymyositis

A

Symmetricial proximal muscle weakness
Raised serum muscle enzyme levels
Typical electromyographic changes
Biopsy evidence of myositis

PM if >3
DM if rash and >2

80
Q

Investigations of dermatomyositis and polymyositis

A

Raised inflammatory markers
Raised ALT (from muscle) with liver enzymes normal
80% antinuclear antibody positive
- specific auto-antibodies include anti-Jo-1 and anti-Mi2
Myositis on MRI

81
Q

Treatment for dermatomyositis and polymyositis

A

High dose corticosteriods - mainstay for first few weeks
Inflammatory markers and CK used to monitor disease
EMG studies/MRI
Long term control
- MTX or AZA
- IV immunoglobulin
- Rituximab
In DM sun-protection and HCQ may reduce rash

82
Q

Complications of dermatomyositis and polymyositis

A

Aspiration pneumonia - upper oesophagus is striated muscle
Respiratory failure - diaphragmatic involvement
Inflammatory lung disease
Increased malignancy risk (DM)

83
Q

Features of dermatomyositis rash

A

Photosensitive
Post inflammatory hyper or hypo pigmentation
Appears in light exposed areas such as scalp, face and neck
Linear plaques on dorsal aspects of hands - Gottron’s papules
Dilated nail-fold capillaries, dry cracked palms and fingers
Periorbital oedema
Violet rash to eyelids

84
Q

What is fibromyalgia

A

Central pain processing characterised by chronic widespread pain in all 4 quadrants of the body
Allodynia is heightened and painful response to innocuous stimuli

85
Q

Pathogenesis of fibromyalgia

A

Can be induced by deliberate sleep deprivation
Sleep disturbance likely trigger in most patients
- EEG studies show reduced REM sleep and delta sleep wave
Causes hyper-activation in response to noxious stimulation, and neural activation in brain regions associated with pain perception in response to non-painful stimuli

86
Q

Symptoms and signs of fibromyalgia

A 
Pain
Joint/muscle stiffness
Profound fatigue
Unrefreshed sleep
Numbness
Headaches
Irritable bowel/bladder syndrome
Depression and anxiety
Poor concentration and memory "fibrofog"
87
Q

Risk factors for fibromyalgia

A

Affects 5% of population
F:M = 9:1
Peak age onset 40-50
Onset may have an obvious trigger - emotional or physical

88
Q

Treatment for fibromyalgia

A 
Education
CBT
Physical
- sleep improvement
Drugs
- pregabalin
- amitriptyline
89
Q

What is Giant Cell Arteritis

A

Chronic vasculitis of large and medium sized vessels that occurs among individuals over 50 years of age
Most commonly causes inflammation of arteries originating from the arch of the aorta

90
Q

Risk factors for giant cell arteritis

A

Age is greates risk
Increased prevalence in individuals in northern latitude
2-4 times for common than women
Strong association with polymyalgia rheumatica
Genetic predisposition: HLA-DR4

91
Q

Symptoms of giant cell arteritis

A 
Headache
- localised, unilateral, boring or lancinating in quality over the temple
Tongue or jaw claudication upon mastication
Constitutional symptoms
Visual findings - weeks to months
- amaruosis fugax
- blindness
- diplopia
- blurring
Scalp tenderness
92
Q

How is diagnosis made of giant cell arteritis

A

Presence of two or more of the following in patients over 50

  • raised ESR, CRP or PV
  • new onset of localised headache
  • tenderness or decreased pulsation of temporal artery
  • new visual symptoms
  • biopsy revealing necrotising arteritis
93
Q

Treatment of giant cell arteritis

A

Prednisolone 60-100mg PO per day for at least 2 weeks before tapering down slowly
For acute onset visual symptoms consider
- 1g methylprednisolone IV pulse therapy 1-3 days
Low dose aspirin therapy to reduce thrombotic risks

94
Q

What is gout?

A

Inflammatory arthritis related to a hyperuricemia
Acute gout can affect > 1 joint - commonly 1st metatarsalphalangeal joint
Associated with high risk of CVD

95
Q

What causes gout?

A

Deposition of monosodium urate (MSU) crystals that accumulate in joints and soft tissues

  • acute and chronic arthritis
  • tophi - soft tissue masses
  • urate nephropathy
  • uric acid nephrolithiasis
96
Q

Risk factors for gout

A 
Non-modifiable
- age > 40
- male
Modifiable
- increased purine intake - meats and seafood
- alcohol intake
- high fructose intake
- obesity
- CCF
- coronary artery disease
- dyslipidemia
- renal disease
- organ transplant
- hypertension
- smoking
- DM
97
Q

Conservative management of gout

A 
Maintain optimal weight
Regular exercise
Diet modification 
Reduce alcohol consumption
Smoking cessation
Maintain fluid intake and avoid dehydration
98
Q

Medical management of gout

A

Acute
- NSAIDs
- oral/IM steriods
- colchicine
Chronic - urate lowering therapy
- allopurinol and febuxostat - xanthine oxidase inhibitors and reduce urate formation
- benzbromarone and sulfinpyrazone - increase renal excretion of uric acid

99
Q

Features of urate crystals

A

Negatively birefringent needles

100
Q

Cause of pseudogout

A

Calcium pyrophosphate crystals

101
Q

What is hypermobility

A

Pain syndrome in people with joints that move beyond normal limits

  • due to laxity of ligaments, capsules and tendons
  • thought that pain originates from microtrauma
  • may affect any number of joints
102
Q

Epidemiology of hypermobility

A

10% of population - only few symptomatic
Often familial
More common in women and asian people
Usually presents in childhood or young adulthood
May feature recurrent subluxations or disclocations

103
Q

Symptoms and signs of hypermobility

A 
Pain
- around joints
- worse after activity
Fatigue
Soft tissue rheumatism 
- epicondylitis
Abnormal ski
- papyraceous scars
- hyperextensible
- thin striae
Marfanoid habitus
Arachnodactyly
Drooping eyelids
Hernias and uterine/rectal prolapse
104
Q

Treatment aims for hypermobility

A

Improve pain and reduce disability

105
Q

Treatment for hypermobility

A 
Strengthening exercises to reduce joint subluxation
Work on posture and balance
Splinting and surgical interventions
Advice on pacing and goal setting
Specialist pain management
Paracetamol mainstay of pain relief
106
Q

Features of hypermobility scoring

A

One point for each feature (left and right)

  • put hands flat on floor with knees straight
  • bend elbows backwards
  • bend knee backwards
  • bend thumbs back to front of forearm
  • bend little finger at 90° to back of hand
107
Q

Heritable connective tissue disorders

A

HSD
Marfan syndrome
Ehlers Danlos syndrome

108
Q

What is osteoarthritis

A

Degenerative joint disorder

- progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis

109
Q

Aetiology of osteoarthritis

A

Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of cartilage due to defective stiffened subchondral bone passing more load to it

110
Q

Key features of osteoarthritis

A

Loss of elasticity with a reduced tensile strength

Cellularity and proteoglycan content are reduced

111
Q

Risk factors for osteoarthritis

A

Increasing age
Female
Obesity
Trauma and joint malalignment through trauma or muscle weakness

112
Q

Symptoms and signs of OA

A

Hip, knee and spine most commonly affecgted
Pain provoked by movement and weight bearing
- intermittent at first by later constant
Inactivity gelling and feeling of joint giving way

113
Q

X-ray signs of OA

A

Joint space narrowing
Subarticular sclerosis
Bone cyts
Osteophytes

114
Q

Treatment aims for OA

A

Improve pain and reduce disability

115
Q

Treatment for OA

A 
Non-drug
- strengthening and ROM exercises
- weight loss
- laterally wedged insoles (medial compartment OA) or walking stick
Pharmacological
- paracetamol
- NSAIDs short term
- topical NSAIDs and rubefacients and capsaicin
- intra-articular corticosteriods
Surgery
- joint replacement
116
Q

Features of nodal OA

A 
More common in women
Affects PIPJs (Bouchard's nodes) and DIPJs (Herberden's nodes) and thumb CMCJ
117
Q

What is polymalgia rheumatica (PMR)

A

Clinical syndrome characterised by pain and stiffness of shoulders, hip girdles and neck
Primarily impacts the elderly
Associated with morning stiffness and elevated inflammatory markers

118
Q

Epidemiology of PMR

A

Increasing incidence with age
- average onset 70 years
Associated with GCA

119
Q

Symptoms of PMR

A

New sudden onset proximal limb pain and stiffness
Difficulty rising from chair of combing hair - proximal muscle involvement
Night time pain
Systemic symptoms

120
Q

Signs of PMR

A

Decreased ROM of shoulders, neck and hips
Muscle strength normal
Muscle tenderness

121
Q

Treatment for PMR

A

Prednisolone
- 15mg then taper down
Methotrexate
- steriod-sparing in relapsing patients

122
Q

What is Raynaud’s phenomenon

A

Due to vasospasm of the digits
Painful
Characterised by typical sequence of colour changes in response to cold stimuli
Often precipitated by stress

123
Q

Colour change in Raynaud’s phenomenon

A

White - inadequate blood flow
Blue - venous stasis
Red - re-warming hyperaemia

124
Q

What is Raynaud’s syndrome

A

Idiopathic Raynaud’s phenomenon

125
Q

Treatment of Raynaud’s syndrome

A

Measures to keep warm

Avoid smoking

126
Q

Diseases associated with Raynaud’s phenomenon

A 
Scleroderma
SLE
Dermatomyositis and polymyositis
Sjogren's syndrome
Use of heavy vibrating tools
Cervial rib
Drug induced - beta blockers
127
Q

Treament for Raynaud’s phenomenon

A

Keep warm and avoid smoking
CCB
Phosphodiesterase-5 inhibitors and prostacyclins

128
Q

Complications of Raynaud’s phenomenon

A

Digital ulcers
Severe digital ischaemia
Infection
Gangrene

129
Q

What is rehumatoid arthritis

A

Autoimmune disease associated with antibodies to Fc portion of IgG (rheumatoid factor) and anti citrullinated cycle peptide (anti-CCP)

130
Q

Pathogenesis of RA

A

Citrullination of self-antigens which are recognised by T & B cells which can then produce antiboides (RF and anti-CCP)
Stimulated macrophages and fibroblasts release TNFalpha
Inflammatory cascade leads proliferation of synoviocytes -> grow over cartilage and restrict nutrients and cartilage damaged
Activated macrophages stimulate osteoclast differentiation -> bone damage

131
Q

Epidemiology of RA

A

Female - 3:1

30-50 years old

132
Q

Signs of RA

A

Usually MCPs/PIPs/MTPs - spares DIPs
Pain > 6 week history
Morning stiffness > 30 mins
Commonly fatigue and malaise

133
Q

Symptoms of RA

A

Soft tissue swelling and tenderness first
Ulnar deviation/palmar subluxation of MCPs
Swan-neck and Boutonniere deformity
Rheumatoid nodules - elbow
Check median nerve - carpal tunnel association

134
Q

Investigation for RA

A

RF and anti-CCP
FBC - normocytic anaemia
WCC - rule out sepsis
X-ray changes in establised disease - USS/MRI more sensitive in early disease

135
Q

Treatment for RA

A 
DMARD monotherapy
- methotrexate
Combintation DMARDs
- lefluomide, hydroxychloroquine, sulfasalazine
Steriods - acutely
Symptom control with NSAIDs + PPI cover
Biologics 
Supportive - OT, PT, podiatry, psychological
136
Q

Extra-articular manifestations of RA

A 
3Cs
- carpal tunnel syndrome
- elevated cardiac risk (CVD)
- cord compression - atlanto-axial subluxation
3As
- anaemia
- amyloidosis -> CKD and nephrotic syndrome
- arteritis
3Ps
- pericarditis
- pleural disease
- pulmonary disease
3Ss
- Sjogren's
- scleritis
- splenic enlargement
137
Q

X-ray features of RA

A

Loss of joint space
Erosions
Soft tissue swelling
Subluxation

138
Q

What is Sjogren’s syndrome

A

Chronic autoimmune inflammatory disorder

- characterised by diminished lacrimal and slaivary gland secretion

139
Q

Symptoms of Sjogren’s syndrome

A 
Myalgia
Arthralgia
Dry mouth
Fatigue
Raynaud's phenomenon
Enlarged parotids
Dry eyes
140
Q

Investigations for Sjogren’s syndrome

A

Anti-Ro and anti-La antibodies
RF and anti ds-DNA antibodies
Schirmer’s test - measures tear volume
Salivary gland biopsy

141
Q

Treatment for Sjogren’s syndrome

A

Symptomatic

  • avoid dry or smoky atmospheres
  • dry eyes = artificial tears
  • dry mouth = artificial saliva, sugar free gum
  • skin emolliens
  • vaginal lubricants
142
Q

Diseases associated with Sjogren’s syndrome

A 
RA
SLE
Coeliac disease
PBC
Auto-immune thyroid disease
143
Q

What are spondyloarthropathies?

A

Group of conditions that affect the spine and peripheral joints and associated with presence of HLA-B27

144
Q

Conditions of spondyloarthopathies

A

Ankylosing spondylitis
Enteropathic arthritis
Psoriatic arthritis
Reactive arthritis

145
Q

Common clinical features of spondyloarthropathies

A

Sacroiliac/axial disease - back/buttock pain
Inflammatory arthropathy of peripheral joints
Enthesitis - inflammation of tendon insertions
Extra-articular features - skin, gut, eye

146
Q

Features of ankylosing spondylitis

A

Long term inflammation of joints of the spine

Usually young men (teens-mid-thirties)

147
Q

Complications of AS

A 
Osteoporosis
Spinal fractures
CVS
Pneumonia
Kidney disease
148
Q

Signs and symptoms of AS

A

Bilateral buttock pain, chest wall and thoracic pain
Exam often normal early
Later - loss of lumbar lordosis, exaggerate thoracic kyphosis, reduced chest expansion
Raised CRP
MRI spine and SI joints - inflammation

149
Q

Treatment for AS

A

NSAIDs
Physio
TNF inhibitors
IL-17 inhibitors

150
Q

Epidemiology of psoriatic arthritis

A

10% of patients with psoriasis

M=F

151
Q

Features of psoriatic arthritis

A

Oligo-arthritis
Dactylitis or “sausage” digit
Can be symmertrical or monoarthritis

152
Q

Investigations for psoriatic arthritis

A

CRP often raised
Central joint erosions seen early on USS or MRI
- pencil in cup x-ray appearance

153
Q

Treatment of psoriatic arthritis

A 
NSAIDs
DMARDs
- TNF inhibitors
- IL-17 inhibitors
- IL12/23 inhibitors
154
Q

What is reactive arthritis

A

Sterile synovitis developing after a distant infection

  • post dysentery - Salmonella, Shigella, Campylobacter
  • urethritis/cervicitis - Chlamydia trachomatis
155
Q

Presentation of reactive arthritis

A 
Few days - 2 weeks post infection
Acute asymmetrical lower limb arthritis develops
Other features incluce
- circinate balanits
- keratoderma blennorrhagica
- conjunctivitis
- uveitis
- enthesitis
156
Q

Investigations for reactive arthritis

A

Serology/microbiology
Inflammatory markers raised
Joint aspirate to rule out septic/crystal arthritis

157
Q

Treatment for reactive arthritis

A

Treat infection
NSAIDs and joint injections
Most resolve within 2 years - if not may need DMARDs

158
Q

What is enteropathic arthrits

A

Inflammatory condition affecting the spine and other joints

- associated with IBD

159
Q

Types of peripheral disease of IBD

A 
Type 1
- oligoarticular
- asymmetric
- correlation with IBD flares
Type 2
- polyarticular
- symmetrical
- less correlation with IBD flares
160
Q

Treatment of enteropathic arthritis

A

DMARDs
- TNF inhibitors treat both bowel and arthritis
NSAIDs can flare IBD

161
Q

Extra-articular manifestations of ankylosing spondylitis

A 
Anterior uveitis
Aortic incompetence
AV block
Apical lung fibrosis
Amyloidosis
162
Q

Features of inflammatory back pain

A 
Insidious onset
Pain at night - improvement with getting up
Age onset < 40
Improvement with exercise
No improvement with rest
163
Q

What is systemic lupus erythmatosus (SLE)?

A

Autoimmune disease
- inadequate T cell suppressor activity with increased B cell activity
- antibodies to certain cell nucleus components
Complex multisystem disease charactersied by remissions and flares

164
Q

Common signs and symptoms of SLE

A 
Serositis - pleurisy, pericarditis
Oral ulcers - painless
Arthritis - small joints, non-erosive
Photosensitivity - malar/discoid rash
Blood disorders - low WCC, lymphopenia, thrombocytopenia, haemolytic anaemia
Renal involvement - glomerulonephritis
Autoantibodies - ANA positive in 90%
Immunologic tests - low complements
Neurologic disorder - seizures or psychosis
165
Q

Investigations for SLE

A 
Raised ESR or plasma viscosity
- normal CRP
Anaemia and leukopenia common
95% antinuclear antibody positive 
- anti-Ro and anti-La common
- anti-dsDNA rises with disease activity
- anti-phospholipid antibodies
C3 and C4 fall with disease activity
Urinarlysis for renal disease
Skin or renal biopsy can be diagnostic
166
Q

Treatment for SLE

A

Sun protection
Advice on healthy lifestyle in view of CVS risk
Hydroxychloroquine for rash and arthralgia
Mycophenolate mofetil, azathioprine and rituximab common used
Short course prednisolone for flares

167
Q

Epidemiology of SLE

A

9x more common in women

Peak onset in early adulthood

168
Q

What is systemic sclerosis

A

Multisystem autoimmune disease
Increased fibroblast activity resulting in abnormal growth of connective tissue
-> vascular damage and fibrosis

169
Q

Types of systemic sclerosis (SSc)

A

Limited

Diffuse

170
Q

Features of limited SSc

A

Calcinosis cutis - calcium deposits in skin
Raynaud’s phenomenon
Oesophageal dysmotility
Sclerodactyly - thickening + tightness of skin of fingers/toes -> ulcers
Telangiectasia - widened venules -> threadlike red lines on skin

171
Q

Features of diffuse SSc

A

Less common but higher mortality risk

Sudden onset skin involvement - proximal to elbows/knees

172
Q

Investigations for SSc

A

Inflammatory markers normal
X-ray hands - calcinosis
CXR, HRCT, PFT - pulmonary disease
ECG + ECHO - PA hypertension, CCF, myocraditis and arrhythmias

173
Q

Antibodies is SSc

A 
Positive ANA in 90% patients
Limitied SSc
- anti-centromere
Diffuse SSc
- Scl-70 (topisomerase)
- anti RNA polymerase III
174
Q

Treatment for SSc

A

No cure
Psychological support
Calcium antagoinst / sildenafil / iloprost for Raynaud’s
Methotrexate and mycophenolae mofetil reduce skin thickening
ACEi prevent hypertensive crisis and reduce mortality from renal failure
Short course prednisolone for flares
PPI for GI symptomrs

175
Q

What is vasculitis

A

Inflammatory blood vessel disorder

176
Q

Features of vasculitis

A

Constitutional symptoms
Raynaud’s
MSK - arthralgia, myalgia, proximal muscle weakness
CNS/PNS - headaches, visual loss, tinnitus, stroke, seizure, encephalopathy
Nose bleeds
Heart/lung - pericarditis, cough, chest pain, haemoptysis, dyspneoa
Abdominal pain
Haematuria
Neuropahty, digital ulcers/ischaemia

177
Q

Signs of vasculitis

A

Hypertension
Palpable purpura, livedo reticularis, nodules, digital ulcers, gangrene, nail bed capillary changes
Scleritis, uveitis, episcleritis
Crackles, pleural rub, murmurs, arrhythmias
Abdominal tenderness and organomegaly

178
Q

Types of vasculitis

A 
Small-vessel
- microscopic polyangiitis (MPA)
- granulomatosis with polyangiitis (GPA)
- eosinophilc granulomatosis with polyangiitis (EGPA)
- IgA vasculitis
Medium-vessel
- polyarteritis nodosa (PAN)
- Kawasaki disease (KD)
Large-vessel
- Takayasu arteritis (TAK)
- giant cell arteritis (GCA)
179
Q

Causes of vasculitis

A 
Primary
Secondary
- infections
- drugs
- malignancy
- connective tissue diseases
180
Q

Diagnostic tests for vasculitis

A 
ANA, ANCA and RF antibodies
Complement levels C3 and C4
Hep screen for B and C and HIV
Cryoglobulins
Serum and urine protein
181
Q

Treatment of vasculitis

A

Rule out infection and stop offending drugs
Corticosteriods
DMARDs - cyclophosphamide, methotrexate, azathioprine, leflunomide, mycophenolate mofetil, rituximab

Yr3 - General Medicine (9 decks)

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