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MSK/ Elderly/ Neuro > Rheum fifth yr > Flashcards

Rheum fifth yr Flashcards

1
Q

What is polymyalgia rheumatica?

A

an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck

strong association with GCA

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2
Q

Demographics of PMR?

A

> 50
F>M
Caucasians

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3
Q

Features of PMR?

A

core features, present for at least 2 weeks:
Bilateral shoulder pain that may radiate to the elbow
Bilateral pelvic girdle pain
Worse with movement
Interferes with sleep
Stiffness for at least 45 minutes in the morning
Rapid onset

Other features:

Systemic symptoms such as weight loss, fatigue, low grade fever and low mood
Upper arm tenderness
Carpel tunnel syndrome
Pitting oedema

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4
Q

Ix of PMR?

A

Diagnosis is mainly based on the clinical presentation and the response to steroids

Need to exclude other conditions:
Full blood count
Urea and electrolytes
Liver function tests
Calcium can be raised in hyperparathyroidism or cancer or low in osteomalacia
Serum protein electrophoresis for myeloma and other protein disorders
Thyroid stimulating hormone for thyroid function
Creatine kinase for myositis
Rheumatoid factor for rheumatoid arthritis
Urine dipstick
Additional investigations to consider:

Anti-nuclear antibodies (ANA) for systemic lupus erythematosus
Anti-cyclic citrullinated peptide (anti-CCP) for rheumatoid arthritis
Urine Bence Jones protein for myeloma
Chest xray for lung and mediastinal abnormalities
EMG normal

Inflammatory markers (ESR, plasma viscosity and CRP) are usually raised however normal inflammatory markers do not exclude PMR

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5
Q

Differentials of PMR?

A

Osteoarthritis
Rheumatoid arhtirits
Systemic lupus erythematosus
Myositis (from conditions like polymyositis or medications like statins)
Cervical spondylosis
Adhesive capsulitis of both shoulders
Hyper or hypothyroidism
Osteomalacia
Fibromyalgia

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6
Q

Tx of PMR?

A

Steroid regime

Initially patients are started on 15mg of prednisolone per day.

Assess 1 week after starting steroids. If there is a poor response in symptoms it is probably not PMR and an alternative diagnosis needs to be considered. Stop the steroids.

Assess 3-4 weeks after starting steroids. You would expect a 70% improvement in symptoms and inflammatory markers to return to normal to make a working diagnosis of PMR.

If 3-4 weeks of steroids has given a good response then start a reducing regime with the aim of getting the patient off steroids:

15mg until symptoms are fully controlled then
12.5mg for 3 weeks then
10mg for 4-6 weeks then
Reduce by 1mg every 4-8 weeks

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7
Q

Additional measures for patients taking long term steroids?

A

Don’t STOP
DON’T – Make them aware that they will become steroid dependent after 3 weeks of treatment and should not stop taking the steroids due to the risk of adrenal crisis if steroids are abruptly withdrawn
S – Sick Day Rules: Discuss increasing the steroid dose if they become unwell (“sick day rules”)
T – Treatment Card: Provide a steroid treatment card to alert others that they are steroid dependent in case they become unresponsive
O – Osteoporosis prevention: Consider osteoporosis prophylaxis whilst on steroids with bisphosphonates and calcium and vitamin D supplements
P – Proton pump inhibitor: Consider gastric protection with a proton pump inhibitor (e.g. omeprazole)

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8
Q

What is SLE?

A

an inflammatory autoimmune connective tissue disease. It is “systemic” because it affects multiple organs and systems and “erythematosus” refers to the typical red malar rash that occurs across the face. It presents with varying and non-specific symptoms

often takes a relapsing-remitting course, with flares and periods where symptoms are improved. The result of chronic inflammation means patients with lupus often have shortened life expectancy. Cardiovascular disease and infection are leading causes of death.

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9
Q

Demographics of SLE?

A

more common in women and Asians + Afro-Caribbean, and usually presents in young to middle aged adults (20-40) but can present later in life.

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10
Q

Pathophysiology of SLE?

A

ANA
antibodies to proteins within the persons own cell nucleus. This causes the immune system to target theses proteins - causing inflammatory response
Type 3 hypersensitivity reaction - thought to be caused by immune system dysregulation leading to immune complex formation

Associated with HLA B8, DR2, DR3

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11
Q

Presentation of SLE?

A

Fatigue
Weight loss
Arthralgia (joint pain) and non-erosive arthritis
Myalgia (muscle pain)
Fever
Photosensitive malar rash. This is a “butterfly” shaped rash across the nose and cheek bones that gets worse with sunlight.
Lymphadenopathy and splenomegaly
Shortness of breath
Pleuritic chest pain
Mouth ulcers
Hair loss
Raynaud’s phenomenon

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12
Q

Ix of SLE?

A

Autoantibodies:
ANA - non specific
anti-dsDNA - specific to SLE

Full blood count (normocytic anaemia of chronic disease)
C3 and C4 levels (decreased in active disease)
CRP and ESR (raised with active inflammation)
Immunoglobulins (raised due to activation of B cells with inflammation)
Urinalysis and urine protein:creatinine ratio for proteinuria in lupus nephritis
Renal biopsy can be used to investigate for lupus nephritis

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13
Q

Diagnosis of SLE?

A

SLICC Criteria or the ACR Criteria

involves confirming the presence of antinuclear antibodies and establishing a certain number of clinical features suggestive of SLE

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14
Q

Complications of SLE?

A

Cardiovascular disease - HTN and CAD

Infection - as part of disease but also secondary to immunosuppressants

Anaemia of chronic disease - normocytic anaemia, due to bone marrow inflammation, can also get leucopenia, neutropenia, thrombocytopenia

Pericarditis

Pleuritis

Interstitial lung disease - leads to pulmonary fibrosis

Lupus nephritis - ssessed urine protein:creatinine ratio and renal biopsy. The renal biopsy is often repeated to assess response to treatment. Can lead to ESRF

Neuropsychiatric SLE - optic neuritis (inflammation of the optic nerve), transverse myelitis (inflammation of the spinal cord) or psychosis.

Recurrent miscarriage, intrauterine growth restriction, pre-eclampsia and pre-term labour.

VTE - antiphospholipid syndrome occurring secondary to SLE

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15
Q

Treatment of SLE?

A

anti-inflammatory and immunosuppression to reduce Sx and complications

First line treatments are:

NSAIDs
Steroids (prednisolone)
Hydroxychloroquine (first line for mild SLE)
Suncream and sun avoidance for the photosensitive malar rash

Other commonly used immunosuppressants in resistant or more severe lupus: Methotrexate, Mycophenolate mofetil, Azathioprine, Tacrolimus, Leflunomide, Ciclosporin

Biological therapies: Rituximab (MAB target CD20 on B cells), Belimumab (MAB target B-cell activating factor)

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16
Q

Drug-induced lupus features?

A

arthralgia
myalgia
skin (e.g. malar rash) and pulmonary involvement (e.g. pleurisy) are common
ANA positive in 100%, dsDNA negative
anti-histone antibodies are found in 80-90%
anti-Ro, anti-Smith positive in around 5%

renal and nervous system involvement being unusual

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17
Q

Causes of drug-induced lupus?

A

Most common causes
procainamide
hydralazine

Less common causes
isoniazid
minocycline
phenytoin

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18
Q

What is polymyositis?

A

inflammatory disorder causing symmetrical, proximal muscle weakness. thought to be a T-cell mediated cytotoxic process directed against muscle fibres. Associated with malignancy

Affects middle-aged, F:M 3:1

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19
Q

Features of polymyositis?

A

Proximal muscle weakness +/- tenderness
Raynaud’s
Respiratory muscle weakness
Interstitial lung disease - fibrosis alveoli, organising pneumonia - indicates poor prognosis
Dysphagia, dysphonia

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20
Q

Investigations and management for polymyositis?

A

Elevated CK - usually >1000
Other muscle enzymes (LDH, aldolase, AST and ALT)
EMG
Muscle biopsy
Anti-synthetase antibodies - anti-Jo-1

Tx - high-dose corticosteroids, azathioprine as steroid-sparing agent, IV immunoglobulins, biologics (infliximab/etanercept)
PT/OT to help muscle strength and function

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21
Q

What is dermatomyositis?

A

an inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions

can be idiopathic, associated with CTD or underlying malignancy (ovarian, breast, lung)

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22
Q

Features of dermatomyositis?

A

photosensitive
macular rash over back and shoulder
heliotrope rash in the periorbital region
Gottron’s papules - roughened red papules over extensor surfaces of fingers
‘mechanic’s hands’: extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
nail fold capillary dilatation
proximal muscle weakness +/- tenderness
Raynaud’s
respiratory muscle weakness
interstitial lung disease: e.g. Fibrosing alveolitis or organising pneumonia
dysphagia, dysphonia

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23
Q

Ix of dermatomyositis?

A

CK - usually >1000
Majority are ANA positive
Antibodies to aminoacyl-tRNA synthesase - anti-Jo-1, SRP, anti-Mi-2 antibodies

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24
Q

What is fibromyalgia?

A

syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites. The cause of fibromyalgia is unknown.

Women 5 times more affected
30-50 yrs old

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25
Q

Features of fibromyalgia

A

chronic pain: at multiple site, sometimes ‘pain all over’
lethargy
cognitive impairment: ‘fibro fog’
sleep disturbance, headaches, dizziness are common

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26
Q

Diagnosis and treatment of fibromyalgia?

A

Diagnosis is clinical and sometimes refers to the American College of Rheumatology
classification criteria which lists 9 pairs of tender points on the body. If a patient is tender in at least 11 of these 18 points it makes a diagnosis of fibromyalgia more likely

Management tailored to individual patient. Psychosocial and MDT approach.
Explanation
Aerobic exercise
CBT
Medication - pregabalin, duloxetine, amitriptyline

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27
Q

What is gout + features of gout?

A

type of crystal arthropathy and inflammatory arthritis. associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint causing it to become hot, swollen and painful. Gout flares

Gouty tophi are subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears. The DIP joints are most affected in the hands.

typically presents with a single acute hot, swollen and painful joint. Typical joints - metatarsophalangeal, wrists, carpometacarpal - also knee and ankle

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28
Q

Risk factors for gout?

A

Male
Obesity
High purine diet (e.g. meat and seafood)
Alcohol
Diuretics
Existing cardiovascular or kidney disease
Family history
increased production of uric acid - myeloproliferative, cytotoxic drugs, severe psoriasis
Lesch-Nyhan syndrome

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29
Q

Diagnosis of gout?

A

diagnosed clinically or by aspiration of fluid from the joint. Excluding septic arthritis is essential as this is a potential joint and life-threatening diagnosis.

uric acid - checked once acute episode settled down (2wks later)

Aspirated fluid - no bacterial growth, needle shaped, negatively birefringement of polarised light, monosodium urate crystals

X-ray - joint space maintained, lytic lesions in bone, punched out erosions with sclerotic borders and overhanging edges

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30
Q

Management of gout?

A

Acute:
NSAIDs, colchicine, steroids
colchicine - SE diarrhoea

Prophylaxis:
Allopurinol (xanthine oxidase inhibitor) - reduces uric acid levels
Lifestyle changes

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31
Q

What is pseudogout?

A

form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium

Cause hot, swollen, stiff, painful knee - or shoulder, wrist, hip

Associated with increasing age. If younger (<60) then usually have underlying risk factor (haemochromatosis, hyperparathyroidism, low Mg, low phosphate, acromegaly, Wilsons)

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32
Q

Ix of pseudogout?

A

joint aspiration: weakly-positively birefringent rhomboid-shaped crystals

x-ray: chondrocalcinosis
in the knee this can be seen as linear calcifications of the meniscus and articular cartilage

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33
Q

Management of pseudogout?

A

aspiration of joint fluid, to exclude septic arthritis

NSAIDs or intra-articular, intra-muscular or oral steroids as for gout

Joint washout in severe cases

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34
Q

What is osteoporosis?

A

Condition where there is reduction in the density of bones. Osteopenia is less severe reduction than osteoporosis. Means bone is less strong and more prone to fractures

Osteoporotic vertebral fracture - loss of height, kyphosis, localised tenderness on palpation of spinous processes at fracture site

35
Q

Risk factors for osteoporosis?

A

Older age
Female
Reduced mobility and activity
Low BMI (<18.5 kg/m2)
Rheumatoid arthritis
Alcohol and smoking
Long term corticosteroids. NICE suggest the risk increases significantly with the equivalent of more than 7.5mg of prednisolone per day for more than 3 months)
Other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogens
Post menopausal - as oestrogen is protective against osteoporosis

36
Q

Investigations for osteoporosis?

A

FRAX assessment on patients at risk: women >65, men >75, Younger patients with risk factors such as a previous fragility fracture, history of falls, low BMI, long term steroids, endocrine disorders and rheumatoid arthritis.

FRAX outcome without a BMD result will suggest one of three outcomes:
Low risk – reassure
Intermediate risk – offer DEXA scan and recalculate the risk with the results
High risk – offer treatment

FRAX outcome with a BMD result will suggest one of two outcomes:
Treat
Lifestyle advice and reassure

Lab values all normal (calcium, phosphate, ALP, PTH)

37
Q

Management for osteoporosis?

A

Lifestyle - activity and exercise, healthy weight, adequate calcium and vitamin D, avoid falls, stop smoking, reduce alcohol consumption

calcium supplementation with vitamin D in patients at risk of fragility fractures with an inadequate intake of calcium - e.g., calcichew D3. If adequate calcium intake but lack sun exposure - vit D supplementation

Bisphosphonates - reduce osteoclast activity and preventing the reabsorption of bone. E.g., alendronate, risedronate, zoledronic acid. SE - reflux, oesophageal erosions, atypical fractures, osteonecrosis of jaw and external auditory canal

Denosumab is a monoclonal antibody that works by blocking the activity of osteoclasts.

Strontium ranelate is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction.

Raloxifene is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus.

Hormone replacement therapy should be considered in women that go through menopause early.

Follow up for low risk patients, and pt’s on bisphosphonates should have repeat FRAX and DEXA scan after 3-5 years. Consider treatment holiday if BMD improved and no fractures.

38
Q

Summary of FRAX tool

A

Gives prediction of the risk of a fragility fracture over the next 10 hears

Input information (age, BMI, co-morbidities, smoking, alcohol, FHX, and also BMD if available). Gives percentage risk of 10 year probability of major osteoporotic fracture and hip fracture

in patients 40-90

QFracture tool - pts 30-90, larger group of RFs included

39
Q

Summary of bone mineral density and DEXA

A

BMD measured using DEXA (dual energy X-ray absorptiometry)

Reading at hip used for classification and management of osteoporosis

Bone density can be represented as a Z score or T score. Z scores represent the number of standard deviations the patients bone density falls below the mean for their age. T scores represent the number of standard deviations below the mean for a healthy young adult their bone density is.

WHO classification - T score > -1 is normal, -1 to -2.5 is osteopenia, less than -25 is osteoporosis, less than -2.5 plus fracture is severe osteoporosis

40
Q

Investigations for secondary causes of osteoporosis?

A

Blood cell count, sedimentation rate or C-reactive protein, serum calcium,
albumin, creatinine, phosphate, alkaline phosphatase and liver transaminases

Thyroid function tests

Bone densitometry ( DXA)

Other procedures, if indicated:
Lateral radiographs of lumbar and thoracic spine/DXA-based vertebral imaging
Protein immunoelectrophoresis and urinary Bence-Jones proteins
25OHD
PTH
Serum testosterone, SHBG, FSH, LH (in men),
Serum prolactin
24 hour urinary cortisol/dexamethasone suppression test
Endomysial and/or tissue transglutaminase antibodies (coeliac disease)
Isotope bone scan
Markers of bone turnover, when available
Urinary calcium excretion

41
Q

What is osteomalacia?

A

a condition where there is defective bone mineralisation causing “soft” bones. Results from insufficient vitamin D.

Vitamin D is essential in calcium and phosphate absorption from the intestines and kidneys. Vitamin D is also responsible for regulating bone turnover and promoting bone reabsorption to boost the serum calcium level. Causes low Ca and phosphate and hence defective bone mineralisation.

Low Ca causes secondary hyperparathyroidism, so more PTH and increased reabsorption from bones.

42
Q

Presentation of osteomalacia?

A

May be asymptomatic
Fatigue
Bone pain
Muscle weakness - proximal myopathy > waddling gait
Muscle aches
Pathological or abnormal fractures - especially femoral neck
Looser zones

43
Q

Investigations of osteomalacia?

A

Serum 25-hydroxyvitamin D is the laboratory investigation for vitamin D. The interpretation of the results is as follows:
<25 nmol/L – vitamin D deficiency
25 – 50 nmol/L – vitamin D insufficiency
75 nmol/L or above is optimal

Low Ca, low phosphate, increased ALP, increased PTH

X-rays - osteopenia (more radiolucent)

DEXA - low BMD

44
Q

Risk factors for osteomalacia?

A

Darker skin
Low exposure to sunlight
Live in colder climates
Spend a lot of time indoors
CKD
Drug induced - anticonvulsants
Inherited - hypophosphatemic rickets
Liver disease - cirrhosis
Coeliac disease

45
Q

Treatment of osteomalacia?

A

supplementary vitamin D (colecalciferol) - several regimes 50,000 IU once weekly for 6 weeks, 20,000 IU twice weekly for 7 weeks, 4000 IU daily for 10 weeks

maintenance supplementary dose for of 800 IU or more per day should be continued for life after the initial treatment

46
Q

What is psoriatic arthritis?

A

inflammatory arthritis associated with psoriasis that is within the seronegative spondyloarthropathy group.

Often precedes the development of skin lesions. It occurs in 10-20% of patients with psoriasis and usually occurs within 10 years of developing the skin changes. It typically affects people in middle age but can occur at any age.

Associations
Eye disease (conjunctivitis and anterior uveitis)
Aortitis (inflammation of the aorta)
Amyloidosis

47
Q

Features of psoriatic arthritis?

A

Not a single pattern of affected joints:
symmetrical poly arthritis - similar to RA, more common in women, hands, wrists, ankles, DIP, MCP less commonly (unlike RA)
asymmetrical pauciarthritis - mainly digits and feet, only few joints
spondylitic pattern - more common in men, back stiffness, sacroilitis, atlanto-axial joint involvement
also: spine, achilles tendon, plantar fascia

Plaques of psoriasis
Pitting of nails
Onycholysis
Dactylitis
Enthesitis - points of insertion of tendon to bone

Arthritis mutilans - most severe form of psoriatic arthritis occurring in phalanxes - osteolysis (destruction) of the bones around the joints in the digits. This leads to progressive shortening of the digit. The skin then folds as the digit shortens giving an appearance that is often called a “telescopic finger”.

48
Q

Investigations of psoriatic arthritis?

A

PEST tool - nvolves several questions asking about joint pain, swelling, a history of arthritis and nail pitting. A high score triggers a referral to a rheumatologist.

X-ray:
Periostitis is inflammation of the periosteum causing a thickened and irregular outline of the bone
Ankylosis is where bones joining together causing joint stiffening
Osteolysis is destruction of bone
Dactylitis is inflammation of the whole digit and appears on the xray as soft tissue swelling
Pencil-in-cup appearance - central erosions of the bone beside the joints

49
Q

Management of psoriatic arthritis?

A

Similar to RA - coordinated between dermatologists and rheumatologists.

NSAIDs
DMARDs
Anti-TNF (etanercept, infliximab, adalimumab)
Ustekinumab - last line - monoclonal antibody that targets interleukin 12 and 23

50
Q

Summary of Ehlers-Danlos syndrome?

A

AD CTD
Mostly affects type III collagen
Tissue more elastic than normal - causing joint hyper mobility and increased elasticity of the skin

Features -
elastic, fragile skin
joint hypermobility: recurrent joint dislocation
easy bruising
aortic regurgitation, mitral valve prolapse and aortic dissection
subarachnoid haemorrhage
angioid retinal streaks

mild can be managed in GP
MDT - PT, CBT, symptom relief, genetic counselling, celiprolol to prevent Aortic dissection, care with wound healing

51
Q

Summary of Marfan’s syndrome?

A

AD CTD
Defect in FBN1 gene on chromosome 15 that codes for protein fibrillar-1
1 in 3000 people

Features
tall stature
high arched palate
arachnodactyly
Pectus excavatum
pes planus
scoliosis of >20 degrees
heart - dilation of aortic sinuses (aortic aneurysm, aortic dissection, aortic regurgitation), MV prolapse
lungs - repeated pneumothoraces
eyes - upwards lens dislocation, blue sclera, myopia
dural ectasia

Ghent criteria
Thumb and wrist sign

regular ECHO
beta-blocker and ACEi therapy
aortic dissection and CVD problems are leading cause of death

52
Q

Summary of Raynauds phenomenon?

A

characterised by an exaggerated vasoconstrictive response of the digital arteries and cutaneous arteriole to the cold or emotional stress.

It may be primary (Raynaud’s disease) or secondary (Raynaud’s phenomenon). Raynaud’s disease typically presents in young women (e.g. 30 years old) with bilateral symptoms. Secondary causes = CTD (scleroderma, RA, SLE), leukaemia, type 1 cryoglobulinaemia, cold agglutinins, use of vibrating tools, drugs (OCP, ergot), cervical rib

Management
- if suspected secondary then referral to secondary care
first-line - calcium channel blocker (nifedipine)
IV prostacyclin (epoprostenol) infusions: effects may last several weeks/months

53
Q

Summary of anti-phospholipid syndrome?

A

an acquired disorder characterised by a predisposition to both venous and arterial thromboses, recurrent fetal loss and thrombocytopenia.

Primary or secondary, commonly from SLE. Also other AI disorders, lymphoproliferative disorders, phenothiazines

Causes paradoxical rise in APTT - due to an ex-vivo reaction of the lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade

54
Q

Features of APS?

A

venous/arterial thrombosis

recurrent fetal loss

livedo reticularis

other features: pre-eclampsia, pulmonary hypertension

Libmann-Sacks endocarditis is a type of non-bacterial endocarditis where there are growths (vegetations) on the valves of the heart. The mitral valve is most commonly affected.

55
Q

Ix for APS?

A

Antibodies = anticardiolipin, ant-beta2 glycoprotein, lupus anticoagulant

Thrombocytopenia

Prolonged APTT

56
Q

Management for APS?

A

Primary thromboprophylaxis = low-dose aspirin

Secondary thromboprophylaxis = initial venous thromboembolic events: lifelong warfarin with a target INR of 2-3

recurrent venous thromboembolic events: lifelong warfarin; if occurred whilst taking warfarin then consider adding low-dose aspirin, increase target INR to 3-4

arterial thrombosis should be treated with lifelong warfarin with target INR 2-3

Pregnancy - LMWH plus aspirin. Warfarin CI’ed in pregnancy

57
Q

What is Behcet’s disease?

A

complex inflammatory condition. presumed autoimmune-mediated inflammation of the arteries and veins

It characteristically presents with recurrent oral and genital ulcers.

It can also cause inflammation in a number of other areas such as the skin, gastrointestinal tract, lungs, blood vessels, musculoskeletal system and central nervous system.

There is a link with the HLA B51 gene. This is a prognostic indicator of severe disease.

relapsing remitting condition

more common in eastern Mediterranean (Turkey) and men

58
Q

DDx for mouth ulcers?

A

Simple aphthous ulcers are very common

Inflammatory bowel disease (particularly Crohn’s disease)

Coeliac disease

Vitamin deficiency (B12, folate or iron)

Herpes simplex ulcers

Hand, foot and mouth disease (coxsackie A virus)

Squamous cell carcinoma

59
Q

Features of Behcet’s disease?

A

Triad - mouth ulcers, genital ulcers, anterior uveitis

Mouth ulcers - at least 3 episodes, painful, red halo, oral mucosa, heal over 2-4 weeks

Genital ulcers - similar appearance to oral ulcers, ‘kissing ulcers’

Skin - Erythema nodosum, Papules and pustules (similar to acne), Vasculitic type rashes

Eyes - need emergency review by ophthalmology - Anterior or posterior uveitis, Retinal vasculitis, Retinal haemorrhage

MSK - morning stiffness, arthralgia, oligoarthritis (knee/ankle)

GI system - inflammation and ulceration

CNS - Memory impairment, Headaches and migraines, Aseptic meningitis, Meningoencephalitis

Veins - inflamed veins causing vein thrombosis - Budd Chiari, DVT, PE, cerebral venous sinus thrombosis

Lungs - pulmonary artery aneurysms

60
Q

Ix and Tx for Behcet’s disease?

A

Clinical diagnosis

Pathergy test - abrasion on forearm, creates weal - positive in Behcets, Sweets syndrome and pyoderma gangrenosum

Tx:
Topical steroids to mouth ulcers (e.g. soluble betamethasone tablets)
Systemic steroids (i.e. oral prednisolone)
Colchicine is usually effective as an anti-inflammatory to treat symptoms
Topical anaesthetics for genital ulcers (e.g. lidocaine ointment)
Immunosuppressants such as azathioprine
Biologic therapy such as infliximab

61
Q

What is ankylosing spondylitis?

A

HLA-B27 associated spondyloarthropathy

M>F (3:1)

aged 20-30

62
Q

Features of ankylosing spondylitis?

A

Young man with lower back pain

Stiffness of insidious onset

Stiffness worse in AM - improves with exercise

Pain at night - improves on getting up

63
Q

Features of ankylosing spondylitis on examination?

A

Reduced lateral flexion

Reduced forward flexion - Schober’s test

Reduced chest expansion

64
Q

Other features of ankylosing spondylitis? (A’s)

A

Apical fibrosis

Anterior uveitis

Aortic regurgitation

Achilles tendonitis

AV node block

Amyloidosis

and cauda equina syndrome

peripheral arthritis (25%, more common if female)

65
Q

Investigations for ankylosing spondylitis?

A

Inflammatory markers raised

HLA-B27 - little use in Dx

Plain X-ray of sacroiliac joints:
sacroilitis - subchondral erosions, sclerosis
squaring of lumbar vertebrae
bamboo spine - late, uncommon
syndesmophytes - due to ossification of outer fibres of annulus fibrosus
CXR - apical fibrosis

If still suspicion and -ve X-ray - MRI - shows bone marrow oedema

Spirometry - restrictive defect - pulmonary fibrosis, kyphosis and ankylosis of costovertebral joints

66
Q

Management of ankylosing spondylitis?

A

Lifestyle - encourage regular exercise, NSAIDs, physiotherapy, avoid smoking, bisphosphonates if osteoporosis, treatment of complications

Steroids in flares

DMARDs - e.g., sulphasalazine - only useful if peripheral joint involvement

Anti-TNF therapy is persistently high disease activity despite conventional treatments - etanercept, MAB’s (infliximab, adalimumab)

Surgery - deformities of spine/joints

67
Q

What is reactive arthritis?

A

Synovitis due to a recent infective trigger

Acute mono arthritis - usually knee. No infection in joint

Link with HLA B27

Part of seronegative spondyloarthropathy

68
Q

Infections that trigger reactive arthritis?

A

Gastroenteritis - shigella, salmonella, campylobacter

STI - chlamydia

69
Q

Features of reactive arthritis?

A

Acute mono arthritis - within 4 weeks of initial infection

Bilateral conjunctivitis

Anterior uveitis

Circinate balanitis

Keratoderma blenorrhagica

70
Q

Management of reactive arthritis?

A

ABx until septic arthritis excluded

NSAIDs

Steroid injections

Systemic steroids - if multiple joints

Most resolve within 6 months and don’t recur. Recurrent cases may require DMARDs or anti-TNF medications

71
Q

Ix of reactive arthritis?

A

Aspirate joint - gram staining, C&S, crystal examination

72
Q

RFs for osteoarthritis?

A

Obesity

^ age

Occupation

Trauma

Female

FHx

Hypermobility

73
Q

What is osteoarthritis?

A

Disease of ‘wear and tear’

Causes - genetic, overuse, injury

Synovial joints

Imbalance between cartilage being worn down and chondrocytes repairing it - causing structural issues in joint

74
Q

Features of osteoarthritis?

A

CMC + DIP joint

Squaring of thumb base

Episodic joint pain - worse with movement, relieved by rest

Stiffness - few mins in AM

Painless nodes - Bouchards and Heberdens

Commonly affected joints - hips, knees, sacro-iliac joints, DIP, CMC, wrist, cervical spine

75
Q

Ix for osteoarthritis?

A

If typical features = clinical Dx (over 45 and no stiffness)

Plain X-rays - LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

X-ray changes don’t correlate with Sx

Oxford Hip score

76
Q

Management of osteoarthritis?

A

Patient education

Lifestyle changes - WL, local muscle strenghening exercises, aerobic fitness

PT, OT, orthotics

Stepwise analgesia:
1 - paracetamol + topical NSAID (knee/hand)

2 - oral NSAID (+PPI)

3 - opiates (codeine/morphine)

Intra-articular steroid injections

Supports/braces

TENS

Shockin absorbing soles and shoes

Joint replacement - if severe

77
Q

What is rheumatoid arthritis?

A

Autoimmune condition causing chronic inflammation of synovial lining of joints, tendon sheaths and bursa

Inflammatory and symmetrical polyarthritis

78
Q

RFs for rheumatoid arthritis?

A

F>M

Middle age

FHx

Genetic associations - HLA DR4, HLA DR1

79
Q

Features of rheumatoid arthritis?

A

Symmetrical distal polyarthropathy - PIP, MCP, wrist/ankle, MTP, cervical spine, large joints

Pain, swelling, stiffness (>1 in AM

Z-shaped thumb

Ulnar deviation of fingers at knuckle

+ve squeeze test

Swan neck + boutonniere

Systemic Sx - fatigue, WL, flu-like illness, muscle aches

Palindromic RA - self-limiting short episodes, affecting few joints

Atlantoaxial subluxation - can cause SCC - emergency

80
Q

Extra-articular manifestations of RA?

A

Pulmonary fibrosis w/ pulmonary nodules (Caplan’s)

Bronchiolitis obliterans - small airway obstruction

Felty’s (RA, neutropenia, splenomegaly)

Secondary Sjogrens

Anaemia of chronic disease

CVD

Episcleritis + scleritis

Rheumatoid nodules

Lymphadenopathy

CTS

Amyloidosis

81
Q

Dx of rheumatoid arthritis?

A

Clinical

American College of Rheum Criteria - joints involved, serology, inflammatory markers, duration

82
Q

Ix of rheumatoid arthritis?

A

RF

Anti-CCP

Inflammatory markers

X-rays of hand:
Loss of joint space
Erosions (periarticular)
Subluxation
Soft tissue swelling
Juxta-articular osteoporosis

HAQ - functional ability of pt

NICE referral - persistent synovitis even if -ve serology, urgent if >3m

83
Q

Management of rheumatoid arthritis?

A

Initial - DMARD +/- short course of bridging prednisolone

Flares - corticosteroids (oral + IM)

Surgery - if significant problems

DMARDS - methotrexate (monitor FBC + LFT), sulfasalazine, leflunomide, hydroxychloroquine

TNF-i - etanercept, infliximab, adalimumab - if inadequate response to 2 DMARDs

Abatacept - causes decreased T-cell proliferation and cytokine production

Monitoring Tx response - CRP and disease activity - DAS28

84
Q

Poor prognostic features for RA?

A

RF +ve, anti-CCP +ve

Poor function at presentation

X-ray early erosions <2 years

HLA DR4

Insidious onset

Extra-articular features

Female

MSK/ Elderly/ Neuro (8 decks)

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