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Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Back pain red flags

A

<20 or >55, acute onset in elderly, constant/progressive pain, nocturnal pain, worse pain on being supine, fever/night sweats/ weight loss, malignancy, abdo mass, thoracic back pain, morning stiffness, bilateral/alternating leg pain, neurological disturbance, sphincter disturbance, current or recent infection, immunosuppression, leg claudication or exercise-related leg weakness/numbness

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2
Q

Causes of back pain based on age
15-30
30-50
>50

A

15-30: prolapsed disc, trauma, fractuer, ank spon, spondylolisthesis, pregnancy
30-50: degenerative spinal disease, prolapsed disc, malignancy (primary, or secondary from lung/ breast/ prostate/ thyroid/ kidney
>50: degenerative, osteoporotic vertebral collapse, pagets, malignancy, myeloma, spinal stenosis

Other (rare) causes: cauda equina, psoas abscess, spinal infection (TB, Staph, E coli)

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3
Q

Investigations for back pain

A

FBC, ESR and CRP (myeloma, infection, tumour), U+E, ALP (pagets), serum/urine electrophroesis (myeloma), PSA
X-Ray
MRI IS THE IMAGE OF CHOICE

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4
Q

L2 Nerve root lesion

  • where the pain is
  • where the weakness is
  • reflex affected
A

Pain across upper thigh
Weakness in hip flexion and adduction
No reflex affected

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5
Q

L3 Nerve root lesion

  • where the pain is
  • where the weakness is
  • reflex affected
A

Pain across lower thigh
Weakness in hip adduction and knee extension
Knee jerk affected

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6
Q

L4 Nerve root lesion

  • where the pain is
  • where the weakness is
  • reflex affected
A

Pain across knee to medial malleolus
Weakness in knee extension, foot inversion and dorsiflexion
Knee jerk affected

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7
Q

L5 Nerve root lesion

  • where the pain is
  • where the weakness is
  • reflex affected
A

Pain across lateral shin to dorsum of foot and great toe
Weakness in hip extension and abduction, knee flexion, foot and great toe dorsiflexion
Great toe jerk affected

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8
Q

S1 Nerve root lesion

  • where the pain is
  • where the weakness is
  • reflex affected
A

Pain across posterior calf to lateral foot and little toe
Weakness in knee flexion, foot and toe plantar flexion and foot eversion
Ankle jerk affected

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9
Q

What causes osteoarthritis?

A

Mechanical (wear and tear): localised loss of cartilage, remodelling of adjacent bone, associated inflammation

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10
Q

What joints are affected in OA?

A

Large weight bearing joints (hip, knee), carpometacarpal joint, DIP, PIP joints

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11
Q

Signs and symptoms of OA

A

Pain and crepitus with movement, improves with rest, joints may feel unstable, unilateral symptoms, no systemic upset
Signs: joint tenderness, derangement and bony swelling (Heberdens at DIP and Bouchards at PIP), reduced range of movement, crepitus on movement, mild synovitis

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12
Q

Investigations for OA

A

X-Rays: (LOSS) loss of joint space, osteophytes at joint margin, subchondral sclerosis, subchondral cysts

CRP may be raised

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13
Q

Management of OA

A

Exercise, weight loss

Analgesia: regular paracetamol (+ topical NSAIDs if knee or hand) are first line.
Second line: codeine, short-term oral NSAID (+ PPI), intra-articular steroids, topical capsicain

Heat or cold packs at the site of pain, walking aids, stretching/manipulation, TENS

Surgery: joint replacement

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14
Q

NSAID risks

A

GI bleed (ulcers, perforation) - prescribe with PPI if >45 and those with increased risk of GI bleeding. Avoid concomitant prescribing of anticoags, antiplatelets, SSRIs, spironolactone, steroids and bisphosphonates -> increased risk of bleeding

Cardiovascular (MI, stroke) - diclofenac is CI if history of MI/PVD/stroke/HF, naproxen has lowest cardiovascular risk

Renal injury - higher if already on diuretics, ACEI/ARB. Risk also higher if elderly/HTN/DM

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15
Q

Septic arthritis causative organisms and most common joint affected

A

Most common is Staphylococcus aureus
Young sexually active adults - Neisseria gonorrhoeae should be considered

Most common location in adult = knee

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16
Q

Kocher criteria for septic arthritis diagnosis

A

fever >38.5
non-weight bearing
Raised ESR
Raised WCC

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17
Q

Management of septic arthritis

A

IV abx which cover gram pos cocci (flucloxacillin, clindamycin if pen allergic)
Abx for 6-12 weeks
Needle aspirate to decompress joint
May require arthroscopic lavage

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18
Q

Investigations for septic arthritis

A

Bloods: ESR (raised), FBC (raised WCC), blood culture
Urgent joint aspiration for synovial fluid microscopy and culture
X-ray

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19
Q

Aetiology of rheumatoid arthritis

Which gender is most affected

A

Autoimmune

most commonly seen in females

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20
Q

Which joints are typically affected in RA

A

MCP, PIP

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21
Q

Typical signs and symptoms of RA

A 
Morning stiffness (>30m), improves with use, bilateral symptoms
Systemic upset (fatigue, fever, weight loss)
Extra-articular manifestations
Signs: bilateral symmetrical swollen painful and stiff small joints, ulnar deviation and subluxation of the wrist and fingers
Boutonnière and swan neck deformities of the fingers, z-deformity of the thumbs, hand extensor tendons may rupture
Positive squeeze test - pain on squeezing across metacarpal or metatarsal joints
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22
Q

Extra-articular manifestations of RA

A

Nodules: elbows, lungs, cardiac, CNS, lymphadenopathy, vasculitis

Lungs: pleural disease, interstitial fibrosis, bronchiolitis obliterans, oragnizing pneumonia

Cardiac: IHD, pericarditis, pericardial effusion
Eyes: episcleritis, scleritis, keratoconjunctivitis sicca

Peripheral neuropathy, splenomegaly, carpal tunnel syndrome

Felty’s syndrome: RA + Splenomegaly + Neutropenia

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23
Q

X-ray findings for RA

A

Loss of joint space, juxta-articular osteoporosis, periarticular erosions, subluxation

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24
Q

Antibodies involved in RA

A

Anti-cyclic citrullinated peptide antibody (Anti-CCP) - may be detected up to 10 years before development of RA, has a high specificity compared to RhF

Rheumatoid factor (IgM circulating ab) - seen in 70-80% of patients. High levels are associated with severe progressive disease, but not a marker of disease activity

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25
Q

Conditions which cause positive RhF

A

Sjögrens (around 100%), Felty’s (around 100%), RA, infective endocarditis, SLE, systemic sclerosis, general population

TB, HBV, EBV, leprosy

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26
Q

RA investigations

A

Anti-CCP (anti-cyclic citrullinated peptide antibody)
RhF
FBC (anaemia of chronic disease, raised platelets)
Raised ESR
Raised CRP
X-rays
USS and MRI can identify synovitis

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27
Q

RA drug side effects:

methotrexate

A 
mucositis
myelosuppression
pneumonitis
pulmonary fibrosis
liver fibrosis
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28
Q

RA drug side effects: sulfasalazine

A

rashes, oligospermia, Heinz body anaemia, interstitial lung disease, myelosuppresion, lung fibrosis

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29
Q

RA drug side effects: hydroxychloroquine

A

Retinopathy, corneal deposits

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30
Q

RA drug side effects: leflunomide

A

Liver impairment, interstitial lung disease, HTN

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31
Q

RA drug side effects: prednisolone

A

Cushingoid features, osteoporosis, DM, HTN, cataracts

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32
Q

Management of RA

A
  1. Initial therapy: DMARD monotherapy +/- short-course of bridging prednisolone
  2. Combination DMARDs if monotherapy is ineffective
  3. TNF inhibitors if unresponsive to at least two DMARDs

Manage RA flares with oral or IM corticosteroids

Other important treatment options: analgesia, physiotherapy, surgery

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33
Q

Types of DMARDs

A

Methotrexate (most common, monitor FBC and LFTs)
Sulfasalazine
Leflunomide
Hydroxychloroquine

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34
Q

TNF-inhibitors

  • indications in RA
  • Examples
A

Used in RA if inadequate response to 2+ DMARDs

Etanercept (can cause demyelination and reactivation of TB)

Infliximab (monoclonal ab, can cause reactivation of TB)

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35
Q

2010 American College of Rheumatology diagnostic criteria for RA

A

Used for patients who: Have at least one joint with definite clinical synovitie, and with the synovitis not better explained by another disease

Add score of categories A-D -> a score of 6/10 is a definite diagnosis of RA

A. Joint involvement: 1 large joint (0), 2-10 large joints (1), 1-3 small joints (2), 4-10 small joints with or without large joint involvement (3), 10 joints with at least 1 small (5)

B. Serology: RhF-ve ACPA -ve (0), low positive RF or low positive ACPA (2), high positive RF or high positive ACPA (3)

C. Acute phase reactants: normal CRP and normal ESR (0), abnormal CRP or abnormal ESR (1)

D. Duration: <6w (0), >6w (1)

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36
Q

Gout features

  • symptoms during flares
  • which joints are affected
A

Inflammatory arthritis
Typically presents with an acute monoarthropathy with severe joint inflammation.
Flares: significant pain, swelling, erythema
Majority of patient’s first presentation affects the 1st metatarsophalangeal joint (big toe)
Other commonly affected joints = ankle, wrist, knee

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37
Q

Radiological features of gout

A
  • Joint effusion is an early sign
  • Well-defined punched out erosions with sclerotic margin in a juxta-articular distribution, often with overhanging edges
  • Relative preservation of joint space until late disease
  • Eccentric erosions
  • No periarticular osteopenia (in contrast to RA)
  • Soft tissue tophi
38
Q

Causes and predisposing factors to gout

A

Caused by deposition of monosodium urate crystals in the synovium
Caused by chronic hyperuricaemia

Decreased excretion or uric acid: drugs (diuretics), CKD, lead toxicity

Increased production of uric acid: myeloproliferative/ lymphoproliferative disorder, cytotoxic drugs, severe psoriasis

Lesch-Nyhan syndrome: X-linked recessive syndrome causing gout, renal failure, neuro deficits and learning difficulties

39
Q

Acute management of gout

A

First line: NSAID or colchicine
Continue max dose NSAID until 1-2 days after symptoms have settled
PPI may be indicated
Colchicine has slower onset of action than NSAID
Colchicine SE = diarrhoea
Consider oral steroids if NSAIDs and colchicine are contraindicated
If the person is already taking allopurinol it should be continued

40
Q

Indications for urate-lowering therapy

A

Offered to all patients after their first attack of gout

Urate lowering therapy is particularly recommended if:

  • > =2 attacks in 12m
  • tophi
  • renal disease
  • uric acid renal stones
  • prophylaxis if on cytotoxics or diuretics
41
Q

Urate lowering therapy

A

Allopurinol is first line
Delay starting urate-lowering therapy until after acute attack
Consider starting colchicine when starting allopurinol

42
Q

Lifestyle modifications for gout

A 
Reduce alcohol intake
Avoid alcohol during acute attack
Lose weight if obese
Avoid food high in purines (liver, kidney, sea food, oily fish, yeast products)
Stop precipitating drugs
Increase vit C
43
Q

Differential diagnoses for monoarthritis

A 
Septic arthritis
Trauma
Reactive arthritis (reiters)
Haemarthrosis
Psoriatic arthritis
Gout
Calcium pyrophosphate deposition (pseudogout)
44
Q

Investigations for gout

A

Joint aspirate
Polarised light microscopy of synovial fluid shows negatively birefringent urate crystals
Serum urate is usually raised
X-rays

45
Q

Pseudogout

  • Cause
  • Joints
  • Risk factors
  • Ix
  • Mx
A
  • Cause: Calcium pyrophosphate dihydrate crystal deposition in the synovium
  • Joints: Usually occurs in larger joints compared to gout (eg. knee, wrist, shoulders)
  • Risk factors: haemochromatosis, hyperparathyroidism, acromegaly, low magnesium, low phosphate, wilsons disease

-Ix: Joint aspiration shows weakly positive birefringent rhomboid-shaped crystals
X-ray shows chrondrocalcinosis

-management: joint fluid aspiration to exclude septic arthritis, NSAIDs or intra-articular/IM/PO steroids

46
Q

Features of spondylarthropathies

A
  1. Seronegative (RhF ive)
  2. HLA B27
  3. Axial arthritis (pathology in spine and sacroiliac joints)
  4. Asymmetric large joint oligoarthritis (<5 joints) or monoarthritis
  5. Enthesitis (inflam of tendon/ligament insertion)
  6. Dactylitis (inflam of entire digit)
  7. Extra-articular: iritis, psoriaform rashes, oral ulcers, aortic valve incompetence, IBD
47
Q

Types of spondylarthropathies

A

Ankylosing spondylitis
Psoriatic arthritis
Reiters syndrome
Enteropathic arthritis

48
Q

Ankylosing spondylitis features

  • typical presentation
  • clinical examination
  • the A’s
A

HLA-B27
More common in males, aged 20-30
‘young man who presents with lower back pain and stiffness of gradual onset, stiffness usually worse in the morning and improves with exercise, patient experiences pain at night which improves on getting up’

Clinical examination: reduced lateral flexion, reduced forward flexion (schober’s test), reduced chest expansion

The A’s: apical fibrosis, anterior uveitis, aortic regurgitation, achilles tendonitis, AV node block, amyloidosis, and cauda equina syndrome (peripheral arthritis, more common if female)

49
Q

Schober’s test

A

A line is drawn 10cm above and 5cm below the back dimples, the distance between the two lines should increase by more than 5cm when the patient bends forward as far as possible

Ankylosing spondylitis = reduced forward flexion

50
Q

Ankylosing spondylitis investigations

A

Inflam markers (ESR, CRP) typically raised

HLA-B27 is of little use in making diagnosis

Plain X-ray of sacroiliac joints is the most useful Ix for diagnosis

If the X-ray is negative but suspicion remains high -> MRI

Spirometry may show restrictive defect due to pulm fibrosis, kyphosis and ankylosis of costovertebral joints

51
Q

Radiological features of ankylosing spondylitis

A

Plain radiograph of the sacroiliac joints

  • sacroilitis: subchondral erosions and sclerosis
  • Squaring of lumbar vertebrae
  • bamboo spine
  • syndesmophytes (ossification of outer fibres of annulus fibrosus)

Apical fibrosis on CXR

MRI may show bone marrow oedema as an early sign

52
Q

Management of ankylosing spondylitis

A

Encourage regular exercise (swimming)
NSAIDs are first line
Physiotherapy
Anti-TNF for patients with persistently high disease activity despite conventional treatment
DMARDs if there is peripheral joint involvement

53
Q

Enteric arthropathy

  • associated diseases
  • treatment
A

HLA-B27

Associated with IBD, GI bypass, coeliacs and whipples disease
Arthropathy usually improved with treatment of IBD
Beware of NSAIDs
Use DMARD if resistant

54
Q

Psoriatic arthritis

  • different types
  • management
A

HLA-B27

Types: rheumatoid–like polyarthritis (most common), asymmetrical oligoarthritis (typically affects hands and feet), sacroillitis, DIP joint disease, arthritis mutilans)

Management: treat as RA (DMARDs), better prognosis than RA

55
Q

Reactive arthritis

  • what is it
  • cause
  • features
  • management
  • prognosis
A

-HLA-B27
-Arthritis that develops following an infection where the organism cannot be recovered from the joint
-Often develops post-STI or post-dysentry
-Chlamydia trachomatis
-Shigella, Slamonella, Campylobacter
-Features: typically develops within 4 weeks of infection, and usually lasts 4-6m. Asymmetrical oligoarthritis of lower limbs, dactylitis, urethritis, conjunctivitis, anterior uveitis, keratoderma blenorrhagica (raised brown plaques on soles and palms).
Reiter’s syndrome: can’t see, can’t wee, can’t climb a tree (conjunctivitis, urethritis, arthritis)
-Mx: analgesia, NSAIDs, intra-articular steroids
Sulfasalazine and methotrexate if persistent
-Symptoms rarely last beyond 12m

56
Q

Systemic sclerosis

  • gender
  • what is it
  • 3 types
  • antibodies involved
  • management
A
  • Hardened, sclerotic skin and connective tissue, more common in females
  • Limited cutaneous systemic sclerosis (face and distal limbs. Raynauds phenomenon, CREST syndrome)
  • Diffuse cutaneous systemic sclerosis (trunk and proximal limbs. ILD, pulm HTN, renal disease)
  • Scleroderma (tight fibrotic skin, plaques)

-Antibodies -
ANA in 90%, RhF in 30%, anti-scl07 (diffuse), anti-centromere antibodies (limited)

-manage with immunosuppressive therapy (cyclophosphamide)

57
Q

Dermatomyositis features

A

Inflam disorder -> symmetrical proximal muscle weakness and skin lesions

Skin features:

  • photosensitive
  • macular rash over back/ shoulders
  • heliotrope rash in periorbital region
  • Gottron’s papules (rough red papules over extensor surfaces of fingers)
  • dry scaly hands
  • nail fold capillary dilatation

Other features:

  • proximal muscle weakness +/- tenderness
  • Raynauds
  • Resp muscle weakness
  • ILD
  • Dysphagia/dysphonia
58
Q

Investigations for dermatomyositis

A
  • Muscle enzymes: ALT, AST, LDH, CK all raised in plasma
  • EMG shows characteristic fibrillation potentials
  • muscle biopsy confirms diagnosis and excludes differentials
  • ANA positive (80%)
  • Anti-synthetase antibodies (anti-Jo-1, anti-SRP, anti-Mi-2)
59
Q

Management of dermatomyositis

A

Prednisolone
Immunosuppressives and cytotoxics
Hydroxychloroquine/topical tacrolimus for skin disease

60
Q

Systemic Lupus Erythematosus at risk group

A

Females, afro-caribbeans/asian population, onset usually 20-40

61
Q

Pathophysiology of SLE

A

Autoimmune, type 3 hypersensitivity reaction
Associated with HLA B8, DR2, DR3
Immune system dysregulation -> immune complex formation and deposition throughout organs

62
Q

Features of SLE

A

General: fatigue, fever, mouth ulcers, lymphadenopathy

Skin: malar rash, discoid rash, photosensitivity, Raynauds, livedo reticularis, non-scarring alopecia

MSK: arthralgia, non-erosive arthritis

CVS: pericarditis, myocarditis

Resp: pleurisy, fibrosing alveolitis

Renal: proteinuria, glomerulonephritis

Neuro: anxiety, depression, psychosis, seizures

63
Q

Antibodies in SLE

A

90% ANA positive
20% RhF positive
Anti-dsDNA highly specific but less sensitive (70%)
Anti-Smith most specific but very low sensitivity (30%)
Anti-Ro, Anti-La

64
Q

diagnosis and monitoring for SLE

A
  1. Antibodies (Anti-dsDNA titre)
  2. Complement (low C3, low C4)
  3. ESR raised

Also: BP, urine for casts/protein, FBC, U+E, LFT, CRP (normal)

Skin or renal biopsies may be diagnostic

65
Q

Management of SLE

A
  • -Screen for comorbidities
  • High factor SPF
  • NSAIDs and hydroxychloroquine often used as maintenance
  • Steroids are usually used for flares
  • Azathioprine, methotrexate and MMF as steroid-sparing agents
  • Monoclonal ab (belimumab) as an add on therapy for autoantibody positive disease
  • mild flares (no organ involvement): hydroxychloroquine or low dose steroids
  • moderate flares (orgna involvement): DMARDs or mycophenolate
  • Severe flares (life/organ threatening): urgent high dose steroids, mycophenolate, rituximab, cyclophosphamide
66
Q

Polyarteritis nodosa

  • what is it
  • what gender
  • what age
  • what infection is it associated with
A

Medium-sized necrotising vasculitis leading to aneurysm formation
More common in middle-aged men
Associated with hep B

67
Q

Polyarteritis nodosa features

A 
Fever, malaise, arthralgia
weight loss
HTN
Mononeuritis multiplex, sensorimotor polyneuropathy
Testicular pain
Livedo reticularis
Haematuria, renal failure
p-ANCA (20%)
Hep B positive (30%)
68
Q

Takayasu’s arteritis

  • what is it
  • gender
  • features
A

Inflammatory, obliterative arteritis affecting aorta and its branches
Affects females > males
Upper limb claudication, diminished/absent pulses
ESR affected during acute phase

69
Q

Polymyalgia rheumatica

  • pathophysiology
  • features
  • investigations
  • treatment
A
  • overlaps with temporal arteritis (giant cell vasculitis)
  • typically >60yrs old
  • Rapid onset (<1m)
  • Aching, morning stiffness in proximal limb muscles, no weakness
  • Polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
  • Investigations: ESR >40, CK and EMG normal
  • Management: prednisolone
70
Q

Fibromyalgia features and diagnosis

A

Chronic pain at multiple sites, lethargy, cognitive impairment (fibro fog), sleep disturbance, headache, dizziness

Clinical diagnosis (all results normal)

71
Q

Fibromyalgia management

A

MDT
Aerobic/strength based exercise
CBT
Meds: pregabalin, duloxetine, amitriptyline

Steroids and NSAIDs not recommended as there is no inflammation

72
Q

Sjögren’s syndrome features

A 
dry eyes (keratoconjunctivitis sicca)
dry mouth
Vaginal dryness
Arthralgia
Raynauds
Myalgia
Sensory polyneuropathy
Recurrent episodes of parotitis
Renal tubular acidosis
73
Q

Investigations for Sjögren’s syndrome

A 
RhF in nearly 100%
ANA in 70%
Anti-Ro
Anti-La
Schirmer's test: filter paper near conjunctival sac to measure tear formation
Histology: focal lymphocytic infiltration
Hypergammaglobulinaemia
Low C4
74
Q

Management of Sjögren’s syndrome

A

Artificial saliva and tears

Pilocarpine may stimulate saliva production

75
Q

Paget’s disease of the bone pathophysiology

A

Increased but uncontrolled bone turnover
Thought to be primarily a disorder of osteoclasts, with excessive osteoclast resorption followed by increased osteoblast activity

76
Q

Features of Pagets disease of the bone

A

Stereotypical presentation: older male with bone pain and an isolated raised ALP
Bone pain (Pelvis, lumbar spine, femur)
Classical, untreated features: bowing of tibia, bossing of skull
Raised ALP (calcium and phosphate normal)
Skull X-ray: thickened vault, osteoporosis circumscripta

Ill defined sclerotic and lucent areas throughout X-ray

77
Q

Treatment and complications of pagets disease of the bone

A

Treatment with bisphosphonates or calcitonin indicated if bone pain, skull/long bone deformity, fracture or periarticular pagets

Complications: deafness (cranial nerve entrapment), bone sarcoma, fracture, skull thickening, high output cardiac failure

78
Q

Osteoporosis risk factors

A

Age, female, caucasian/asian

Important risk factors:
History of glucocorticoid use
RA
Alcohol excess
Hx of parental hip fracture
Low BMI
Current smoking
Other risk factors:
Sedentary lifestyle
Premature menopause
Hyperthyroidism
Hypogonadism/GH deficiency
Hyperparathyroidism
DM
Multiple myeloma/ Lymphoma
IBD
Liver disease
CKD
Osteogenesis imperfecta
79
Q

Drugs which may worsen osteoporosis

A 
Glucocorticoids
SSRIs
Antiepileptics
PPIs
Glitazones
Long term heparin therapy
Aromatase inhibitors
80
Q

What is a FRAX tool

A

Used in osteoporosis to assess the 10 year risk of patient developing a fragility fracture

81
Q

treatment of osteoporosis and indication for treatment

A

Indication for treatment is a DEXA scan T score of < -2.5

First line treatment is an oral bisphosphonate

82
Q

DEXA scan scores

A

T score: based on bone mass of young reference population

T score > -1.0 = normal
-1 to -2.5 = osteopenia
>-2.5 = osteoporosis

83
Q

Management of patients at risk of corticosteroid-induced ostoporosis

A

Risk of osteoporosis rises significantly one a patient is taking the equivalent of prednisolone 7.5mg OD for 3+ months. Start bone protection if this is likely.

Management of patients at risk of corticosteroid induced osteoporosis:

  1. Patients >65 or those who’ve previously had a fragility fracture should be offered bone protection
  2. Patients <65 should be offered a bone density scan, if T score < -1.5 then bone protection should be offered

First line treatment is bisphosphonate (alendronate) and calcium and vitamin D.

84
Q

Marfans syndrome features

A 
Tall stature
High arched palate
Arachnodactyly
Pectus excavatum
Pes planus
Scoliosis
Heart: aortic aneurysm, aortic dissection, aortic regurgitation, mitral valve prolapse
Lungs: repeated pneumothoraces
Eyes: upwards lens dislocation
85
Q

Cause of Marfans syndrome

A

Autosomal dominant connective tissue disorder

FBN1 gene on chromosome 15 -> defect in protein fibrillin-1

86
Q

Causes of hip pain in adults

A 
Osteoarthritis 
Inflammatory arthritis
Referred lumbar spine pain
Trochanteric bursitis
Meralgia paraesthetica
Avascular necrosis
Pubic symphysis dysfunction
Transient idiopathic osteoporosis
87
Q

Ehlers-Danlos syndrome cause

A

Autosomal dominant connective tissue disorder affecting type 3 collagen -> tissue more elastic than normal -> hypermobility and increased skin elasticity

88
Q

Features and complications of ehlers danlos

A 
Elastic, fragile skin
Joint hypermobility (recurrent joint dislocation)
Easy bruising
Aortic regurgitation
Mitral valve prolapse
Aortic dissection
SAH
Angioid retinal streaks
89
Q

Features of Behcet’s syndrome

A

Classic triad of oral ulcers, genital ulcers and anterior uveitis

Thrombophlebitis, DVT
Arthritis
Neuro involvement
Abdo pain, diarrhoea, colitis
Erythema nodosum
90
Q

Epidemiology of Behcet’s syndrome

A 
Eastern mediterranean (eg. Turkey)
More common in men
Typically 20-40
Associated with HLA B51
30% have positive FHx

Medicine (15 decks)

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