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Year 2 > MSK: Part 3 > Flashcards

MSK: Part 3 Flashcards

1
Q

What is Scleroderma

A

Systemic Scloerosis: Multisystem disease with involvement of skin and Raynauds

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2
Q

How does Systemic Sclerosis distinguish itself from localised scleroderma such as morphed

A

Latter: Do not involve organ disease and no vasospasm (Raynauds)

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3
Q

What gender does Scleroderma effect

A

Females

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4
Q

Peak incidence of Scleroderma

A

Between 30 and 50

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5
Q

Is Scleroderma common in children

A

No

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6
Q

Risk factors for Scleroderma

A
  1. Exposure to vinyl chloride, silica dust, adulterated rapeseed oil and trichloroethylene
  2. Drugs such as bleomycin
  3. Genetic
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7
Q

Pathophysiology for Scleroderma

A
  1. Widespread vascular damage involving small arteries, arterioles and capillaries is an early feature
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8
Q

Initial stage of scleroderma

A
  1. Initial endothelial damage with release of cytokines (endothelia-1) = VASOCONSTRICTION
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9
Q

What does continued vascular damage and increased vascular permeability and activation of endothelial cells lead to

A
  1. Upregulation of adhesion molecules: E-selectin, VCAM and intracellular adhesion molecule 1 (ICAM-1)
  2. Cell Adhesion: T and B cells, monocytes and neutrophils
  3. Migration of cells through leaky endothelium and into extracellular space
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10
Q

What do these cell-cell and cell-matrix interactions stimulate

A

Production of cytokines and growth factors which mediate PROLIFERATION and ACTIVATION of vascular and connective tissue cells - particularly fibroblasts

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11
Q

What mediators activate fibroblasts

A

IL1, 4, 6, 8, TGF-B and PDGF

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12
Q

What do fibroblasts secrete in Scleroderma

A
  1. Increased quantities of COLLAGEN TYPE I + 2
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13
Q

Consequence of secreted COLLAGEN TYPE I + 2

A

Fibrosis in lower dermis of the skin and internal organs

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14
Q

What is the end-product of scleroderma

A
  1. Uncontrolled and irreversible proliferation of connective tissue and thickening of vascular walls with narrowing of the lumen
  2. Damage to small blood vessels produces widespread obliterative arterial lesions and chronic ischaemia
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15
Q

Clinical presentation of Scleroderma

A
  1. RAYNAUDS
  2. Limited cutaneous scleroderma (CREST SYNDROME)
  3. Diffuse cutaneous scleroderma (30% of cases)
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16
Q

What is limited cutaneous scleroderma

A
  1. Starts with Raynaud’s for many years BEFORE skin changes
  2. Skin involvement limited to hands, face, feet and forearms
  3. Skin is tight over fingers and causes flexion deformities
  4. Face and skin produce beak-like nose and small mouth (microstomia)
  5. Painful digital ulcers and telangiectasia (spider veins on the skin)
  6. Oesophageal dysmotility or strictures
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17
Q

Why was it previously called CREST syndrome

A
  1. Calcinosus (calcium deposits in subcutaneous tissue)
  2. Raynauds
  3. Oesophageal Dysmotility or strictures
  4. Sclerodactyly (tightness of skin)
  5. Telenagiectasia (spider veins)
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18
Q

Why is Diffuse cutaneous scloerderma different to limited cutaneous scleroderma

A

Skin changes more rapidly and more widespread

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19
Q

What organs are involved in diffuse cutaneous scleroderma

A
  1. GI
  2. Renal
  3. Lung
  4. Heart
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20
Q

GI involvement in diffuse scleroderma

A
  1. Oesophagus loses strength and dilates = heartburn and dysphagia
  2. Small intestines loses strength and dilates = bacterial overgrowth and malabsorption
  3. Colon has pseudo-obstruction
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21
Q

Renal involvement in diffuse scleroderma

A
  1. Acute and CKD

2. Acute hypertensive crisis is a complication of renal involvement

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22
Q

Lung disease in diffuse scleroderma

A
  1. Fibrosis
  2. Pulmonary vascular disease
  3. Pulmonary hypertension
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23
Q

Herat in diffuse scleroderma

A

Arrhythmias and conduction disturbances due to myocardial fibrosis

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24
Q

Diagnostics for Scleroderma

A
  1. FBC
  2. Urinalysis
  3. CXR
  4. Hand X-ray
  5. Barium swallow
  6. High res CT
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25
Q

Test results in FBA for scleroderma

A
  1. Normochromic, normocytic anaemia
  2. Microangiographic haemolytic anaemia
  3. Urea and creatine rise in acute kidney injury
    4, Autoantibodies
  4. Rheumatoid factor positive in 30%
  5. ANA positive
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26
Q

What antibodies are found n Limited cutaneous scleroderma

A
  1. Speckled, nucleolar or ANTI-CENTROMERE ANTIBODIES (ACAs) - 70% cases
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27
Q

What antibodies are found in Diffuse cutaneous scleroderma

A
  1. Anti-topoisomerase-1 antibodies

2. Anti-RNA polymerase

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28
Q

What would urinalysis show in scleroderma

A

Albumin/creatinine ratio

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29
Q

What would CXR show in scleroderma

A

Exclude other pathologies (e.g. cardiomegaly)

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30
Q

What would hand x-ray show in scleroderma

A
  1. See deposits of calcium around fingers
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31
Q

What would Barium Swallow show in scleroderma

A
  1. Confirms impaired oesophageal motility
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32
Q

What does high res CT show in scleroderma

A

Confirm fibrotic lung involvement

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33
Q

How is scleroderma treated

A

NO CURE:
Raynauds: Hand warmers and ORAL VASODILATORS

Oesophagus: LANSOPRAZOLE

Nutrition supplement for malabsorption

ACE Inhibitor: RAMIPRIL

Early detection of pulmonary hypertension

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34
Q

What oral vasodilator is given for raynauds

A

Calcium channel blocker: ORAL NIFEDIPINE

Endothelia receptor antagonist: ORAL BOSENTAN

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35
Q

How is pulmonary fibrosis caused in scleroderma treated

A

IMMUNOSUPRESSION: IV CYCLOPHOSPHAMIDE

ORAL PREDNISOLONE

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36
Q

What is polymyositis

A

RARE muscle disorder of unknown aetiology in which there is inflammation and necrosis of skeletal muscle fibres

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37
Q

What is Polymyositis called when it effects the skin

A

DERMATOMYOSITIS

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38
Q

What organ can be effected in POLYMYOSITIS

A

Lungs = interstitial lung disease

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39
Q

What gender does polymyositis effect

A

Females

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40
Q

What viruses can cause POLYMYOSITIS

A

Coxsackie
Rubella
Influenza

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41
Q

Clinical presentation of POLYMYOSITIS

A
  1. Symmetrical progressive muscle weakness and wasting affecting muscles of shoulder and pelvic girdle
  2. Patients struggle squatting, going upstairs, rising from a chair and raising hands above their heads
  3. Pain and tenderness are uncommon
  4. Involvement of pharyngeal, laryngeal and respiratory muscles can lead to dysphagia and respiratory failure
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42
Q

Clinical presentation of DERMATOMYOSITIS

A
  1. Purple discolouration of eyelids and scaly erythematous plaques all over the knuckles (GOTTRON’s PAPULES)
  2. Arthralgia, dysphagia resulting from oesophageal muscle involvement and RAYNAUDS
  3. Increased incidence of malignancy
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43
Q

Diagnostics of MYOSITIS

A
  1. MUSCLE biopsy
  2. FBC
  3. Electromyography
  4. MRI
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44
Q

Role of Muscle biopsy

A

Shows fibre necrosis and inflammatory cell infiltrates - CONFIRMS

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45
Q

What would FBC show in MYOSITIS

A
  1. ESR NOT raised
  2. Serum antibodies:
    ANA positive
    Rheumatoid factor positive in 50%
    Myositis-specific antibodies
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46
Q

What does an EMG show in MYOSITIS

A

Typical muscle changes

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47
Q

What does an MRI show for myositis

A

Abnormally inflamed muscles

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48
Q

How is MYOSITIS treated

A
  1. Bed rest helpful with excersise
  2. ORAL PREDNISOLONE
  3. HYDROXYCHLOROQUINE helps with skin disease
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49
Q

What early intervention can be given for MYOSITIS

A
  1. ORAL AZATHIOPRINE
  2. ORAL METHOTREXATE
  3. ORAL CICLOSPORIN
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50
Q

When is ORAL PREDNISOLONE STOPPED in myositis

A

Continued until at least 1 month after myositis has become clinically and enzymatically inactive then tapered down SLOWLY

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51
Q

What is RAYNAUDS PHENOMENON

A
  1. Intermittent spasms in the arteries supplying fingers and toes
52
Q

What precipitates RAYNAUDS

A

COLD

53
Q

What relives RAYNAUDS

A

Heat

54
Q

No underlying cause vs underlying cause in Raynauds nomenclature

A

No underlying - RAYNDAUD’S DISEASE

Underlying - RAYNAUDS PHENOMENON

55
Q

What gender does Raynauds effect

A

FEMALES

56
Q

Pathophysiology of RAYNAUDS

A

Bilateral and effects fingers more than toes

57
Q

Clinical presentation of RAYNAUDS

A
  1. Ischaemia causes PALLOR and CYANOSIS due to sluggish blood flow then redness due to hyperaemia (white -> blue -> red)
  2. Numbness, a burning sensation
  3. Severe pains as fingers warm
  4. Infarction and digital loss
  5. Smoking can aggravate symptoms
58
Q

How is Raynauds diagnosed

A
  1. Primary causes needs to be distinguished from secondary causes
59
Q

What conditions can cause Raynauds

A
  1. SLE
  2. Systemic Sclerosis
  3. RA
  4. DERMATOMYOSITIS
60
Q

Occupation cause of raynauds

A

Vibrational tools

61
Q

What drugs can cause RAYNAUDS

A

Beta-blockers

Smoking

62
Q

How is RAYNAUDS treated

A
  1. Wear gloves and warm clothes
    2, Stop smoking
  2. beat blockers
  3. ORAL NIFEDIPINE (vasodilator)
63
Q

Why is NIFEDIPINE unsuitable sometimes

A

Cerebral vasodilatation causes headaches

64
Q

What do Seronegative spondyloarthropathies and SPONDYLOARTHRITIS

A
  1. Axial Inflammation (spine and sacroiliac joints)
  2. Asymmetrical peripheral arthritis
  3. Absence of RA (seronegative)
  4. Strong association with HLA B27
65
Q

What type of antigen is HLA-B27

A

Class I surface antigen

66
Q

What is a class I surface antigen

A

Present on all cells except RBC s

67
Q

What encodes a HLA B27 gene

A

MHC on chromosome 6

68
Q

What cells express HLA B27

A

APCs

69
Q

Role of HLA B27

A

Immunity and self-recognition

70
Q

What is the molecular mimicry theory of spondyloarthritis

A
  1. Infection triggers an immune response and infectious agent has peptides similar to HLA-B27 molecules = auto-immune response triggered against HLA-B27
71
Q

Clinical presentation of spondyarthropathies

A

SPINEACHE:

  1. Sausage digits
  2. Psoriasis
  3. Inflammatory back pain
  4. NSAID good response
  5. Enthesitis in heel
  6. Arthritis
  7. Crohn’s/Colitis/elevated CRP (can be normal in AS)
  8. HLA-B27
  9. Eye (Uveitis)
72
Q

What is Ankylosing Spondylitis

A

Chronic inflammatory disorder of spine, rides and sacroiliac joints

73
Q

Define ankylosis

A

Abnormal stiffening and immobility of joint due to new bone formation

74
Q

What gender does AS effect

A

Males

75
Q

What age does AS effect

A

16 years - young adult

76
Q

What ethnicity are most commonly effected by AS

A

NA

77
Q

Risk factors for AS

A
  1. HLA-B27 positive

2. Klebsiella, Salmonella, Shigella

78
Q

Pathophysiology of AS

A
  1. Lymphocyte and plasma infiltration occurs with local erosion of bone at the attachments of the intervertebral and other ligaments which heals with new bone formation (SYNDESMOPHYTE)
79
Q

What is enthesitis

A

Inflammation where tendons and ligaments insert into bone

80
Q

What is a syndesmophyte

A

New bone formation and vertical growth from anterior vertebral corners

81
Q

Clinical presentation of AS

A
  1. Men less than 30 yrs
  2. Gradual onset of back pain, worst at night
  3. Spinal morning stiffness that is relieved by exercise
  4. Pain radiates from sacroiliac joints to hips/buttocks which improves towards end of the day
  5. Progressive loss of spinal movement = reduced thoracic expansion )
  6. Asymmetrical joint pain unlike RA
82
Q

What kind of joint pain is usually seen in AS

A

Oligoarthritis (1 or two joints)

83
Q

Tow characteristics of spinal abnormalities in AS

A
  1. Loss of lumbar lordosis (normal inward curve of spine) and increased kyphosis
  2. Limitation of lumbar spine motility in saggital and frontal pain
84
Q

How is reduced spinal flexion in AS demonstrated clinically

A

SCHOBER TEST

85
Q

What is the SCHOBER test

A

make made at 5th lumbar spinous process and 10 cm above, with patient in erect position -> on bending forward, distance should increase to more than 15 cm in normal individuals

86
Q

What enthesitis is seen in SA

A
  1. Achilles tendinitis
  2. Plantar fasciitis
    Tenderness around pelvis and chest wall
87
Q

What are non-articular features of SA

A
  1. Anterior uveitis (inflammation of middle eye)

2. Osteoporosis

88
Q

How is SA diagnosed

A
  1. FBC
  2. X-ray
  3. MRI
89
Q

What would FBC show for SA

A
  1. ESR and CRP raised (CRP can be normal)
  2. Normocytic anaemia
  3. HLA-B27 positive (NOT DIAGNOSTIC)
90
Q

What would an X-ray show for SA

A
  1. Erosion of sclerosis of margins of sacroiliac joints which proceed to ankylosis
  2. Blurring of upper and lower vertebral rims at the thoracolumbar junction caused by enthesitis at insertion of intervertebral ligaments
  3. Heals with new bone formation resulting in bony spurs (SYNDESMOPHWYTES) - progressive calcification of these can lead to bamboo spine (fusion of spinous process)
  4. Fusion of sacroiliac joints
91
Q

What would MRI show for SA

A

Gadolinium shows sacrolitis before seen on X-ray

92
Q

How is SA treated

A
  1. Treated quickly to prevent irreversible syndesmophyte formation and progressive calcification
  2. Morning excersise to maintain posture and spinal motility
  3. NSAIDs (IBUPROFEN) at night
  4. METHOTREXATE for peripheral arthritis
  5. TNF-alpha blocker:
    infliximab, Etanercept or ADAlimumab
  6. Local steroid injection for pain relief
  7. Surgery (hip replacement)
93
Q

Why re TNF-alphas given for SA

A

Improves spinal and peripheral joint inflammation, the earlier you start the less syndesmophwytes form

94
Q

Does psoriasis have to occur with Psoriatic arthritis

A

No

95
Q

Risk factors for Psoriatic arthritis

A
  1. Family history of psoriasis
96
Q

Clinical presentation for psoriatic arthritis

A
  1. Asymmetrical oligoarthritis
  2. Symmetrical seronegative polyarthritis (RA)
  3. Spondylitis
  4. Distal interphalangeal arthritis
  5. Arthritis Mutilans
97
Q

Characteristics of spondylitis in psoriatic arthritis

A
  1. Unilateral or bilateral sacrolitis and early cervical spine involvement (only 50% are HLA-B27 positive)
98
Q

Characteristics of distal interphalangeal arthritis in psoriatic arthritis

A
  1. DIPs involved only
  2. Adjacent nail dystrophy and enthesitis extending into nail root
  3. Dactylics (sausage fingers) in which an entire finger or toes is swollen, with joint and tendon sheath involvement
99
Q

How common is arthritis mutilans in psoriatic arthritis

A

5% preverlance

100
Q

What is arthritis mutilans

A
  1. Destruction of small bones in hands and feet
  2. Pencil in cup X-ray changes
  3. Bone respiration (periarticular osteolysis) and bone shortening
101
Q

Where are hidden sites for psoriasis

A
  1. Behind and inside ears
  2. Scalp
  3. Pitting in nails and onokylisis (where nail lifts off nail bed and looks brittle and flaky)
  4. Umbilicus, natal cleft and penile psoriasis
102
Q

Diagnostics for psoriasis

A
  1. FBC

2. X-ray

103
Q

FBC results for psoriasis

A
  1. Bloods normal

2. CRP and ESR normal

104
Q

What would an X-ray show in psoriasis

A
  1. Psoriatic arthritis is erosive but the erosions are central in the joint, not juxta-articular
  2. May be a ‘pencil in cup’ deformity in the IPJs - bone erosions create a pointed appearance and the articulating bone is concave
  3. Skin and nail disease can be mild and may develop AFTER arthritis
105
Q

Treatment of psoriasis

A
  1. NSAIDs or analgesics (can worsen skin lesions tho)
  2. Intra-articular corticosteroid injections for local synovitis
  3. DMARDs - METHOTREXATE, SULFASALAZINE and LEFLUNOMIDE (mild)

METHOTREXATE and CYCLOSPORIN (severe)

Anti-TNF alpha agents: ETANERCEPT and GOLIMUMAB when METHOTREXATE fails

106
Q

What is sidrah so fit?

A

she just is. jealousy is a disease bitch

107
Q

What is reactive Arthritis

A

Sterile inflammation of the synovial membrane (synovitis), tendons and fascia triggered by an infection at a distant site, usually GI or genital

108
Q

What part of the body does reactive arthritis effect

A

Lower-limb

109
Q

What people does reactive arthritis effect

A

Males in HLA-B27 positive have a 50 fold risk

110
Q

Main causes of reactive arthritis

A
  1. GI Infections:
    Salmonella
    Shigella
    Yersinia Enterocolitica
  2. Sexually acquired:
    Urethritis from chlamydia trachomatis
    Ureaplasma Urealyticum
111
Q

Clinical presentation of Reactive Arthritis

A
  1. acute, ASYMMETRICAL, lower-limb arthritis
  2. Acute Anterior uveitis
  3. Circinate balantis: Painless ulceration of the penis
  4. Enthesitis: Common
  5. Sterile conjunctivitis in 30%
112
Q

What does enthesitis of the heal do

A
  1. Causes plantar fasciitis and Achilles tendon enthesitis
113
Q

What clinical features can be found in patients with reactive arthritis who are HLA-B27 positive

A

Sacroilitis and Spondylitis

114
Q

What skin lesions resemble psoriasis

A
  1. Circinate Balanitis: In the uncircumcised male causes painless superficial ulceration of the glans
  2. In circumcised males, the lesion is raised, red and scaly

Both heal without scarring

Keratoderma Blennorrhagica:
Involves skin of the feet and hands, which develop painless, red and often confluent raised plaques and pustules that are histologically similar to pustular psoriasis

Nail dystrophy occurs

115
Q

Diagnosis of reactive arthritis

A
  1. ESR and CRP raised in acute phase
  2. Culture stool if diarrhoea
  3. Sexual health review
  4. Aspirated synovial fluid is sterile with high neutrophil count:

If joint is hot and swollen can exclude crystal arthritis infection using aspiration
5. X-ray may show enthesitis

116
Q

Treatment of reactive arthritis

A
  1. NSAIDs and corticosteroid injections for joint inflammation
  2. Treat persisting infection with antibiotics
  3. Screen sexual partners
  4. Majority of individuals with reactive arthritis have a single attack that settles but a few develop disabling relapsing and remitting arthritis
117
Q

How are relapsing remitting cases of reactive arthritis treated

A

METHOTREXATE

SULFASALZINE

118
Q

If METHOTREXATE and SULFASALAZINE are ineffective then what can we sue

A

TNF-alpha blockers: ETANERCEPT and GOLIMUMAB

119
Q

Define Systemic Vasculitis

A
  1. Inflammation of vessel wall
  2. Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow resulting in:
    - Vessel wall destruction: aneurysm, rupture and stenosis resulting in perforation and haemorrhage into tissues
  • Endothelial injury:
    resulting in thrombosis + ischaemia/infarction of dependent tissues
120
Q

What diseases can systemic vasculitis be seen in

A
  1. RA
  2. SLE
  3. Polymyositis
  4. Allergic drug reactions
121
Q

How is systemic vasculitis treated

A
  1. By size of blood vessels involved and presence or absence of anti-neutrophil cytoplasmic antibodies
122
Q

What does large-vessel vasculitis refer to

A

Aorta and major tributaries

123
Q

Give examples of large-vessel vasculitis

A
  1. Giant cell arteritis/ polymyalgia rheumatic

2. Takayasu’s arteritis

124
Q

What does medium-vessel vasculitis refer to

A
  1. Medium and small-sized arteries and arterioles
125
Q

Examples of medium-vessel vasculitis

A
  1. Classical polyarteritis nodes

2. Kawasaki’s disease

126
Q

What does small-vessel vasculitis refer to

A

Small arteries, arterioles, VENUES and capillaries

127
Q

Examples of small-vessel vasculitis

A
  1. ANCA-associated:
    - Microscopic polyangitis
    - Granulomatosis with polyangitis
  2. ANCA- negative:
    - essential cryoglobulinaemia
    - cutaneous lecuocytoclastic vasculitis

Year 2 (155 decks)

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