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Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Monitoring of rheumatoid arthritis

A 
DAS28 (Disease activity Score)
Based on how many tender joints, how many swollen joints, and ESR/CRP results
Less than 2.6 = remission
2.6-3.8 = low disease activity
3.8-5.1 = moderate disease activity
Over 5.1 = high disease activity
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2
Q

X-ray findings in osteoarthritis

A 
LOSS
Loss of joints space
Osteophytes (Heberden/Bouchard nodes)
Subchondral sclerosis
Subchondral cysts
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3
Q

X-ray findings in rheumatoid arthritis

A 
LOSED
Loss of joint space
Osteopenia
Soft tissue swelling
Erosions
Deformities
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4
Q

Joints affected in rheumatoid arthritis

A

Symmetrical small joints

EXCUDING: DIPs, 1st MTP/MCP

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5
Q

Joints affected in osteoarthritis

A

Females: DIPs, PIPs, 1st CMC
Males: Hip

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6
Q

Side effects of MTX

A 
GI (stomatitis, n&v, diarrhoea)
Photosensitivity
Increased risk of infections - especially varicella
Miscarriage (make sure on contraception)
Bone marrow toxicity
Hepatitis/fibrosis
Intersitial lung disease
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7
Q

Side effects of plaquenil (hydrochloroquine)

A

Similar to MTX (GI symptoms, hair loss)

+ loss of peripheral vision due to fibrosis around macula

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8
Q

Side effects of biological DMARDs

A 
Infections
Malignancy
Neurological syndromes (MS, GBS etc)
Severe CHF
Autoimmune like syndromes
Pancytopaeia, aplastic anaemia
Raised transanimases
Eczema/psoriatic skin rashes

CANNOT GIVE LIVE VACCINATIONS

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9
Q

Monitoring while being treated with MTX/other DMARDs

A

CBE, renal function and LFT every 2-4 weeks for first 3 months of treatment
3 monthly thereafter

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10
Q

Baseline investigations before beginning MTX or other DMARDs in RA

A 
CBE
Renal function
LFT
CXR (in last year)
PFTs (in last year)
Hep B and C serology (if at high risk)
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11
Q

Extra-articular manifestations of RA

A

Neurological symptoms (if C-spine instability)
Nodules on extensor surfaces/pressure points
Eye symptoms (red, itchy, sore)
Constitutional symptoms: mild weight loss, low-grade fevers, fatigue, weakness)
Resp: ILD
Heart: CAD, pericarditis, myocarditis

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12
Q

Investigations in RA

A 
CBE: anaemia of chronic disease
ESR or CRP: raised
RF
Anti-CCP (very specific, only present in 50%)
Plain x-ray
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13
Q

Anti-Ro (SS-A) antibody association

A

Sjogren’s syndrome

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14
Q

Anti-La (SS-B) antibody association

A

Sjogren’s syndrome

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15
Q

Anti-smith antibody association

A

SLE

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16
Q

Anti-RNP antibody association

A

Mixed connective tissue disease

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17
Q

Anti- Scl70 antibody association

A

Scleroderma

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18
Q

Anti-Jo antibody association

A

Dermatomyositis

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19
Q

HLA-DR4 association

A

Polymyalgia rheumatica, temporal arteritis

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20
Q

HLA-B27 association

A

spondyloarthritides (Ankylosing spondylitis, IBD-associated, reactive arthritis, psoriatic arthritis etc.)

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21
Q

Anti-dsDNA antibody association

A

SLE

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22
Q

Classic SLE triad

A

fever, joint pain and rash in a woman of childbearing age

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23
Q

Erosive osteoarthritis

A

May resemble RA but limited to fingers (DIP, PIP, 1st CMC)
Characterised by CENTRAL erosions (as opposed to marginal erosions in RA) and pseudocysts at DIP and PIP joints

Central subchondral erosions lead to “gull wing” appearance

No soft-tissue swelling or osteopenia

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24
Q

Non-pharmacologic therapy of osteoarthritis

A 
Patient education and self-management
Exercise therapy
Weight loss
Topical application of cold or heat packs
Walking sticks to aid in ambulation
Braces
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25
Q

Pharmacologic therapy of osteoarthritis

A
  1. Paracetamol 1g QID PRN (or panadol osteo 600mg TDS)
  2. NSAID if insufficient pain relief
  3. Topical NSAID or capsaicin
  4. Intra-articular corticosteroid injection, intra-articular hyaluronan higher cost and slower onset

Glucosamine sulphate and chondroitin sulphate - symptomatic benefit

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26
Q

Definition of rheumatoid arthritis

A

A chronic systemic inflamamtory disease of unknown cause, leading to a chronic symmetrical polyarthritis of both small and large joints and a range of extra-articular manifestations

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27
Q

What is pannus

A

Hypertrophied synovium which causes erosion of contiguous cartilage and bone in RA

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28
Q

Management of rheumatoid arthritis

A

NSAIDs for pain relief
+/- intra-articular steroids
Systemic steroids have shown some disease modifying properties

Non biologic DMARDS:

  • start early (irreversible damage occurs within 1-2 years of diagnosis)
  • MTX + foilc acid
  • Leflunomide
  • Sulfasalazine
  • Hydroxychloroquine

Biologic DMARDs:

  • indicated if DAS28 greater than 3.2 + failed adequate therapy after at least 3-6 months treatment of 2 standard DMARDS of which MTX must have been one
  • TNF-a antagonists (etanercept, infliximab, adalimumab)
  • Others (abatacept, rituximab)
  • MTX must be given with to reduce tolerance

Non-pharmacological:

  • Physical therapy and physical activity
  • Occupational therapy: exercises, splinting, ergonomics
  • patient education and self-management
  • surgical (joint replacement, synovectomy etc)
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29
Q

Prognosis of rheumatoid arthritis

A
  • most likely to inc. in severity in first 2 years
  • Only 5% have rapid progression to total disability
  • Life expectancy 3-10 years less than average
  • 50% are disabled or unable to work within 10 years of diagnosis
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30
Q

What is Felty syndrome

A

Rheumatoid arthritis + splenomegaly + neutropenia

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31
Q

definition of podagra

A

Acute arthritis involving the first MTP joint

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32
Q

Definition of gout

A

A mono- or oligarthritis of metabolic origin caused by tissue deposition of monosodium urate crystals due to prolonged hyperuricaemia

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33
Q

Precipitants of gout episode

A 
Stress
Trauma
Infection
Surgery
Crash dieting
Initiation of urate-lowering drugs or drugs than can cause raised urate
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34
Q

Diagnosis of gout

A

Serum uric acid level

  • not always elevated in acute attack
  • chronic hyperuricaemia needs to be treated if over 3 episodes per year (test 2 weeks after resolution of attack)

Joint-fluid analysis:
Monosodium urate crystals:
- needle shaped
- strongly NEGATIVELY birefringent (yellow when parallel to axis of red compensator, blue when aligned across direction of polarisation)

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35
Q

Management of Gout

A

Acute episode:
- Oral NSAID OR colchicine OR prednisolone until symptoms abate (usually 3-5 days)

Life-style modifications:

  • low purine diet
  • limit alcohol
  • limit fructose-containing soft drink

Urate-lowering therapy:
- indicated if recurrent attacks despite lifestyle modifications (over 3 per year)
Allopurinol

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36
Q

Mechanism of allopurinol

A

inhibition of xanthine oxidase - reduced hypoxanthine/xanthine conversion (one of the steps in uric acid production - reduced uric acid prodcution

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37
Q

Definition of septic arthritis

A

Acute infectious inflammation of a joint space requiring urgent diagnosis to prevent rapid joint degeneration

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38
Q

Common pathogens in septic arthritis

A

Kids: kingella (often systemically well)
Young adults: gonorrhoea
Non-gonococcal: S aureus, S pyogenes, S agalictiae, S pneumoniae
Elderly, ISS or IVDU: G-ve (H influenzae, enterobacteriacaea, salmonella, pseudomonas)

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39
Q

Diagnosis of septic arthritis

A 
Raised WCC, ESR and CRP
Blood culture may indicate organism
Joint fluid analysis:
- yellow colour
- turbid, purulent
- PMNs predominantly
- Synovial fluid:serum glucose ratio less than 0.5
- culture!
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40
Q

Management of septic arthritis

A

Immediate joint aspiration
Antibiotic therapy for 3-4 weeks
Initially IV, should not be switched to oral until clinical improvement
Infected prosthetic joints require longer treatment

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41
Q

Definition of psoriatic arthritis

A

A seronegative chronic asymmetrical oligoarthritis of mainly large joints in patients with psoriasis

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42
Q

Epidemiology and timing of psoriatic arthritis

A

1% of population
Classically 30-55y
Develops in up to 30% of patients with psoriasis
- often lags 20y after onset of skin disease
- may precede rash in up to 40% of children and 15% of adults
HLAB27 in 60%

43
Q

Clinical features of psoriatic arthritis

A 
Commonly affects hands
Morning stiffness
Pain, heat, joint tenderness
Nail lesions (in 90%)
- pitting
- ridging
- onycholysis
- subungal hyperkeratosis
Dactylitis
Hand or foot deformity
Painful, red eyes (uveitis)
Rash
Sacroilitis - back stiffness and pain
44
Q

X-ray findings in psoriatic arthritis

A 
Loss of joint space
Pencil in cup deformities
Bone proliferation (fuzzy bone around affected joint)
Subluxation
Marginal erosions
45
Q

Severe form of psoriatic arthritis

A

Arthritis mutilans
Bony resorption - collapse of soft tissue - telescoping fingers (only in very severe cases)
“Opera glass hands”

46
Q

Management of psoriatic arthritis

A 
No cure, symptom control
Non-pharmacological:
- physical therapy
- lifestyle changes
- phototherapy (for rash)

Pharmacological:

  • NSAIDs
  • intra-articular corticosteroids
  • DMARDs (MTX, leflunomide)
  • TNFa inhibitors (etanercept)

Surgical

47
Q

Which is the most common spondyloarthropathy

A

Ankylosing spondylitis

48
Q

Definition of ankylosing spondylitis

A

The most common of the spondyloarthropathies, a chronic systemic inflammatory disease primarily affecting the joints of the spine

49
Q

Symptoms of ankylosing spondylitis

A

Lower back pain
- begins unilaterally and intermittently
- inc. persistence as progresses
- becomes bilateral
- morning stiffness over 30min
- nocturnal back pain (second half of night)
Symptoms worse in morning or with inactivity
Symptoms improve with exercise/physical activity
Fatigue
Responds to NSAIDs

50
Q

Clinical signs of ankylosing spondylitis

A

Reduced ROM of lumbar spine (reduced Schober test)
Stooped forward-flexed posture
Tenderness of joints
Increased Thoracic kyphosis
Enthesitis at insertion of Achilles
Uveitis (painful red eye, photophobia, increased tearing, blurred vision)

51
Q

Xray findings in ankylosing spondylitis

A

SI joint:

  • symmetrical bilateral sacroilitis
  • joints intially widen - then narrow as progress
  • subchondral erosions, sclerosis and proliferation of iliac side of SI joint
  • at end stage, SI joint may be a thin line or not visible

SPINE:

  • small erosions at corners of vertebral bodies (Romanus lesions of the spine - shiny corner sign)
  • vertebral body squaring
  • Bamboo spine (fusion of vertebral bodies
  • dagger spine (ossification of supraspinous and interspinous ligaments - single central radiodense line)
  • calcification of spinal ligaments
52
Q

What are romanus lesions

A

Small erosions at corners of vertebral bodies

53
Q

Management of ankylosing spondylitis

A

NSAIDS:
- suppositories in evening will reduce morning pain (indomethacin)

DMARDs:
- sulfasalazine only helps peripheral symptoms

TNF inhibitors:

  • for patients with severe AS not responsive to NSAIDs
  • Infliximab (IV at 0,2,6w then 6 weekly)
  • etanercept (SC 2x/week)
  • adalimumab (SC fortnightly)

Non-pharmacologic:

  • exercise therapy
  • daily stretching
  • hydrotherapy or swimming
54
Q

Definition of reactive arthritis

A

AKA Reiter’s syndrome: an uncommon autoimmune condition that develops in response to an infection with a classic triad (in 30%) of non-infectious urethritis, arthritis and conjunctivitis

55
Q

Infections which trigger reactive arthritis

A

Genitourinary:
- Chlamydia

Gastrointestinal:

  • Shigella
  • salmonella
  • yersinia
  • campylobacter
  • clostridium difficile
56
Q

Clinical features of reactive arthritis

A

Transient ASYMMETRIC arthritis of 1 or 2 large joints, distal lower limb most affected

  • MTP most common, followed by calcaneus, ankle, knee
  • settles within 6 months
Fever, malaise, anorexia etc. 
Dysuria, UTI symptoms
Mucopurulent vaginal/penile discharge
- uveitis/conjunctivitis
- mouth ulcers
- nail changes
- new murmur
- dactylitis
57
Q

Investigations in diagnosis of reactive arthritis

A

Serology for chlamydia antibodies
Urine PCR for chlamydia
Urine, discharge or stool culture

X-ray: similar to psoriatic

  • ill-defined erosions
  • bone proliferation
  • asymmetric sacroilitis
58
Q

Management of reactive arthritis

A

NSAIDs
Oral prednisolone for more severe articular and extra-articular disease (daily until symptoms improve, followed by slow dose tapering)

59
Q

Definition of systemic lupus erythematous

A

A chronic autoimmune connective tissue disease that can affect almost any organ system and follows a relapsing and remitting course

60
Q

Epidemiology of SLE

A

90% are women
Onset in child-bearing age
Higher incidence in blacks and asian
Family history

61
Q

Arthritis presentation in SLE

A

Symmetrical (may be asymmetrical)
Polyarticular
Small joints of hands, wrists and knees

62
Q

Dermatologic manifestations specific to SLE

A

Malar rash
Photosensitivity
Discoid lupus

63
Q

Diagnosis of SLE

A

CBE: red. WCC and PLT, anaemia of chronic disease
Raised ESR, CRP
ANA- homogenous, speckled or peripheral rim pattern
Anti-dsDNA - more specific for lupus
Anti-smith (highly specific, not sensitive)
Antiphospholipid antibody - 30%

64
Q

Management of SLE

A

Non-pharm:

  • avoid fatigue
  • adequate sleep
  • broad spectrum sunscreen + slip, slop, slap

Pharm;
- NSAIDs
- Hydroxychloroquine
Topical glucocorticoids for skin lesions
Systemic glucocorticoids (if conservative therapy fails)
Immunosuppressive therapy - cyclophosphamide, AZA, mycophenolate mofetil (for life-threatening manifestations - GN, CNS involvement, thrombocytopenia, haemolytic aneamias)
MTX + folic acid for persistent arthritis (steroid-sparing)

65
Q

Clinical features of disseminated gonococcal infection

A

May not have symptoms of urethritis/cervicitis by time these symptoms appear

Fever
Joint or tendon pain
- migratory polyarthralgia
- Knees, elbows and more distal joints
- single joint in 25%
Skin rash (25%)
- torso, limbs, palms, soles
- painful before visible
- paculopapular or pustular
66
Q

Diagnosis of disseminated gonorrhoea

A

Raised WCC and ESR

Blood and synovial fluid MCS

67
Q

Management of disseminated gonorrhoea

A 
Ceftriaxone 1g IV daily
OR
cefotaxime 1g IV 8-hourly
Continue for 48 hours after abatement of fever, then change to oral regimens based on culture and sensitivity results
Total duration of therapy at least 7d
68
Q

Clinical features of sarcoidosis

A

50% present with chronic respiratory symptoms only

General:

  • fatigue, fever, weight loss
  • lymphadenopathy

Pulmonary:

  • cough
  • SOB, wheeze
  • chest pain on exertion

Skin rash

Ocular:

  • gritty or dry eyes
  • misty/blurry vision
  • pain, redness
  • uveitis
  • yellow cnjunctival nodules

Cardiac:

  • arrhythmias, palpitations
  • syncope or pre-sycnope
  • pitting oedema

Rheumatological system

  • acute symmetrical oligoarthritis
  • large joints of lower limb
69
Q

Which joints are affected in sarcoidosis

A

Large joints of lower limb

acute symmetrical oligoarthritis

70
Q

Management of sarcoidosis

A

Prednisolone +/- steroid sparing agent (e.g. MTX)

71
Q

Definition of mixed connective tissue disease

A

An autoimmune connective tissue disease with overlapping features of 2 or more connective tissue disease such as SLE, scleroderma, Sjogren syndrome, rheumatoid arthritis and polymyositis

72
Q

Common features of mixed connective tissue disease

A

Wide range of symptoms, no typical presentation

  • nonspecific (fever, arthritis)
  • Raynaud phenomenon
  • Swollen hands/fingers
  • Digital ulcers
  • Carpal tunnel syndrome
  • Skin involvement (photosensitivity, discoid plaques, malar rash)
Muscle weakness
Synovitis
Telangiectasia
Livedo reticularis
Pericarditis or pleuritic features
73
Q

diagnostic investigations in mixed connective tissue disease

A

ANA: high-titre, speckled pattern

Anti-RNP antibodies

74
Q

Management of mixed connective tissue disease

A

MTX and hydroxychloroquine

75
Q

Definition of polymyalgia rheumatica

A

Chronic inflammatory condition on unknown aetiology that affects elderly individuals, characterised by proximal myalgia of the hip and shoulder girdles with accompanying morning stiffness for more than 1h and full response to corticosteroid therapy

76
Q

Epidemiology of polymyalgia rheumatica

A 
0.5% prevalence
Median age 72
Rare below 55y
15% will develop GCA
50% of patients with GCA have associated PMR
HLA-DR4 haplotype
77
Q

Clinical feautres of polymyalgia rheumatica

A

Abrupt onset (50%)
Symmetrical aching and stiffness of shoulders, neck and hip girdle
- difficulty combing hair, getting up from chair etc
Stiffness after inactivity, especially at night (inability to turn in bed, difficulty arising), improves with activity or hot shower

May begin unilateral but will become bilateral within a few weeks

78
Q

Diagnostic investigations in polymyalgia rheumatica

A

ESR (higher than 40)
ALP mildly increased
CK= NORMAL
RF, ANA, Anti-CCP normal

79
Q

Core inclusion criteria required for the diagnosis of polymyalgia rheumatica

A

Bilateral shoulder and/or pelvic girdle aching
Morning stiffness for over 45 min
Age over 50
Duration over 2w
Evidence of acute phase response (ESR/CRP)

80
Q

Management of polymyalgia rheumatica

A

If no features of GCA: low-dose daily prednisolone
(if fails to respond promptly, reconsider diagnosis)

If features of GCA without visual complications: high dose oral prednisolone + aspirin

If GCA with visual symptoms: IV methylprednisolone for 3 days, then prednisolone as above + aspirin

81
Q

Typical features of giant cell arteritis

A

New headache, new visual symptoms, jaw claudication

Superficial temporal artery inflammation on palpation (tender, thickened, erythematous)
Scalp tenderness!

82
Q

Criteria for diagnosis of giant cell arteritis

A

Temporal artery biopsy findings:

  • Intimal proliferation with luminal stenosis
  • disruption of internal elastic lamina by a mononuclear cell infiltrate
  • invasion and necrosis of media progressing to involvement of entire vessel wall
  • giant cell formation with granulomata within mononuclear cell infiltrate
  • intravascular thrombosis
83
Q

Definition of Sjogren’s syndrome

A

An autoimmune disease characterised by the immune-mediated destruction of exocrine glands, particularly salivary and lacrimal (may affect pancreatic function, respiratory secretions - dry cough, and vaginal dryness)

84
Q

Epidemiology of Sjogren’s syndrome

A

Prevalence 0.5-2% of women
Increase with age
occurs in 10-25% of patients with SLE
30-50% of patients with RA

85
Q

Clinical features of Sjogren’s syndrome

A 
Constitutional: fatigue, low-grade fever
Xerophthalmia (dry eyes)
- itchy
- gritty feeling
- increased sensitivity to irritants e.g. smoke
- eyelid symptoms

Xerostomia (dry mouth)

  • difficulty swallowing
  • recurrent and unique dental infections
  • pain eating salty or spicy foods
  • difficult talking
  • oral erythematous thrusu

URT and LRT symptoms

  • dry cough
  • tracheobronchitis

Painless enlargement of salivary glands

  • begins unilaterally
  • generally absent unless RA

Neurological: peripheral and cranial neuropathies (MS ‘Look-alike’)

Skin:

  • palpable or non-palpable purpura
  • papules
  • urticarial lesions
  • annular lesions
  • xerosis
  • Raynaud’s phenomenon
86
Q

Diagnostic investigations in Sjogren’s syndrome

A

Schirmer test (measuring wetting of standardised tear strips applied between eyeball and lateral inferior lid)
ANA: homogenous or speckled patterns
Anti-Ro (60-75%) - SS-A
Anti-La (40%) - SS-B

87
Q

Management of Sjogren syndrome

A

Symptomatic relief only
For dry eyes;
- sodium eye drops
- polyvinol alcohol + povidone eye drops

For dry mouth:

  • chewing gum or lozenges can stimulate saliva production
  • artificial saliva
  • mouthwash and toothpaste
  • mouth gel

For vaginal dryness:

  • lubricant jellies
  • post-menopausal women: intravaginal oestradiol pessary or cream
88
Q

Definition of Raynaud’s disease

A

The primary idiopathic form of Raynaud phenomenon, a vasospastic disorder characterised by episodic ischaemia and triphasic colour change of the digits of the hands and feet when exposed to cold or emotional distress.

89
Q

Epidemiology of Raynaud’s DISEASE

A

More common than secondary Raynaud phenomenon
F:M 4:1
More common in the young (under 40y)
5-15% though to have primary Raynaud disease will subsequently develop a secondary cause (frequently a connective tissue disorder)

90
Q

Clinical features of Raynaud’s disease

A

usually more mild than secondary Raynaud’s

Well demarcated triphasic digit discolouration associated with cold exposure (white - blue - red - normal)
+/- sensations of cold, numbness in pallor/cyanosis phases
Throbbing, painful sensation may accompany hyperaemic phase
Fingers more often affected than toes, thumbs rarely affected
Sclerodactyly develops in 10%
Normal nail-fold capillary pattern
No pitting scars, ulceration or gangrene of fingers or toes

91
Q

Management of Raynaud’s disease

A

Lifestyle:

  • stress reduction
  • avoid cold exposure
  • warm clothing
  • techniques to terminate an attack (hands in warm water, rotating arms like windmill etc.)
  • avoid smoking and sympathomimetic drugs

Pharm:

  • not generally necessary for primary Raynaud as mild disease
  • Nifedipine
  • Prazosin (sympatolytic)
  • topical nitroglycerin
92
Q

Definition of polyarteritis nodosa

A

Polyarteritis nodosa (PAN) is a relatively rare systemic vasculitis characterised by necrotising inflammatory lesions that affect medium-sized and small muscular arteries, preferentially at vessel bifurcations

93
Q

Risk factors for polyarteritis nodosa

A 
Male gender
40-60y
Hep B or C infection
IVDU
Hairy cell leukaemia
94
Q

Clinical features of polyarteritis nodosa

A 
Constitutional symptoms
Cutaneous symptoms
- most commonly on legs
- can be painful
- rash
- purpura
- gangrene
- nodules
- cutaneous infarcts
- livedo reticularis
- Raynaud phenomenon

GI:

  • abdo pain (sometimes post-prandial)
  • Nausea/vomiting
  • GI bleeding

Renal (60%)
- flank pain

CNS
- amaurosis fugax

PNS: (60%) - various peripheral neuropathies

GU:

  • pain over testicular or ovarian area
  • testicular infarction

Cardiac (35%)
- Chest pain, SOB, palpitations, MI, CHF

95
Q

What is livedo reticularis

A

Mottled reticulated vascular pattern appears as a lace-like purplish discolouration of the skin (caused by swelling of venules causing obstruction of capillaries by thrombi)

96
Q

Diagnosis of polyarteritis nodosa

A

Conventional angiograpy

Aneurysms and/or stenosis of medium sized vessels (most commonly in kidney, liver and mesenteric arteries)

97
Q

Diagnostic criteria for systemic sclerosis

A

A. MAJOR CRITERION: Proximal scleroderma: symmetrical thickening, tightening and induration of the skin of the fingers and the skin proximal to the MCP or MTP joints
B. MINOR CRITERIA:
1. Sclerodactyly (loss of skin creases, joint contractures and sparse hair limited to the fingers)
2. Digital pitting scars or loss of substance from the finger pad
3. Bibasilar pulmonary fibrosis

Presence of major criterion or 2+ minor criteria

98
Q

Definition of scleroderma

A

A group of conditions linked by the presence of thickened, sclerotic skin lesions - either systemic or localised.

99
Q

Classifications of systemic sclerosis

A

Limited cutaneous scleroderma (CREST syndrome)
Diffuse cutaneous scleroderma
etc.

100
Q

CREST syndrome components

A 
Calcinosis cutis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia
101
Q

What is calcinosis cutis

A

The deposition of calcium in the skin.
Appear as firm whitish/yellowish papules, plaques or nodules on the surface of the skin. Most likely to be multiple lesions. May become tender and ulcerated, discharging chalk-like creamy material of mainly calcium phosphate with a small amount of calcium carbonate.

102
Q

Anti-centromere antibody association

A

CREST syndrome 95% specificity

103
Q

Auto-antibody associated with CREST syndrome

A

Anti-centromere antibody

Medicine (12 decks)

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