Rheumatology Flashcards

(47 cards)

1
Q

Definition of Osteoarthritis

A

Age related degenerative synovial joint disease & degenerative of articular cartilage leading to structural changes, pain & reduced function

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2
Q

Aetiology & Risk Factors - OA

A

primary - unknown, secondary - predisposing factor which accelerated degeneration (trauma, congenital abnormalities, inflammatory e.g. RA)

Risk factors: obesity, female sex, occupation, genetic factors, age

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3
Q

Clinical Features - OA

A

Joint pain
Stiffness - <30mins in morning
Better at rest/worse with exercise
Reduced function

Joint Deformities

- Heberden's nodes - DIP
- Bouchard's nodes - PIP
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4
Q

Investigations & Findings - OA

A

X-ray - LOSS

loss of joint space, osteophytes, subchondral cysts & subchondral sclerosis

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5
Q

Management - OA

A

Conservative
• Patient education
• Lifestyle advice - weight loss, stretching, exercise

Medical
• Paracetamol - safest & often helps w/ symptoms
• NSAIDs - topical & remember PPI/risks in elderly
Steroid Injections

Surgical
• Arthroscopy - not routine, if loose body or mechanical locking
• Joint replacement - consider ‘shelf life’, when impacting QOL significantly,

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6
Q

Definition of Rheumatoid Arthritis

A

an inflammatory arthritis - autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths & bursa

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7
Q

Aetiology& Risk Factors - RA

A

Autoimmune of unknown cause/trigger
a/w other AI conditions e.g. Raynaud’s, Sjogren’s
HLA-DR1 & HLA-DR4 haplotypes

Female sex, lower socioeconomic status, family history, other AI conditions, smoking

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8
Q

Clinical Features - RA

A
Gradual onset (occasionally rapid)
Joint pain & swelling - symmetrical & many (MCP > Wrists > PIP > knee > MTP)

Morning stiffness >30mins, better with movement/worse with rest

Constitutional symptoms: myalgia, fatigue, low-grade fever, weight loss, and low mood

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9
Q

Investigations - RA

A
Bloods
	• FBC, U&Es, bone profile, vit D, LFTs, ESR & CRP (normal in 40%), autoimmune screen
	• Rheumatoid factor & anti-CCP
Imaging
	• X-rays - hands & feet
	• CXR - extra-articular manifestations
	• USS - for effusions
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10
Q

Management options - RA

A

Symptom control - NSAIDs, occupational & physio

DMARDs - methotrexate (1st line + bridging therapy of steroids for first 2-3mths)

Biologics - Anti-TNF e.g. infliximab, Rituximab: anti-CD20, Tocilizumab: anti-IL-6

Acute flares - steroids

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11
Q

Definition of Osteomalacia

A

Vitamin D or calcium deficiency leads to defective bone mineralisation in adult remodelling bones; bones become soft
When this occurs in children (before growth plate closure) it leads to condition called Ricket’s

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12
Q

Aetiology of osteomalacia

A

Aetiology & Risk factors:
• Vit D deficiency - poor diet, malabsorption or lack of exposure to sunlight
• Renal osteodystrophy - due to AKI/CKD
• Inherited Vit D resistance
• Anticonvulsants
• Malignancy - tumour induced osteomalacia

* Lots of time indoors
* Ethnicity - darker skin
* Live in colder climates 
* Malabsorption conditions
* Renal issues
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13
Q

Clinical presentation - Osteomalacia

A

Patients often present w/ bone pain, muscle weakness/aches, pathological or abnormal fractures
• Looser zones are fragility fractures that go partially through the bone.

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14
Q

Investigations - Osteomalacia

A
Bloods
	• Serum Vit D (75mmol/L or more is optimal)
	• Calcium
	• Phosphate
	• PTH - secondary HPTH may be present 
Imaging
	• X-ray; shows radiolucent bones 
	• DEXA; will show low mineral density
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15
Q

Treatment - Osteomalacia

A

Vit D supplements

• Correct deficiency (loading regime) followed by maintenance dose

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16
Q

Definition of Osteoporosis

A

Reduction in bone mineral density

less than 2.5 standard deviations below mean peak mass of healthy adult (T score)

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17
Q

Risk factors - Osteoporosis

A

Older age - as we age osteoclasts activity is not matched by osteoblasts
Female sex - especially post menopausal women
Alcohol & Smoking
Long term corticosteroid use
Other medications inc SSRIs, PPIs, anti-epileptics, anti-oestrogens
Rheumatoid arthritis
Low BMI <18.5
Reduced mobility & activity

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18
Q

Assessment tools & Investigations - Osteoporosis

A

Assessment tools e.g. FRAX calculate the overall 10yr risk of having a major fracture
• If high risk - offer DEXA
• Intermediate risk - DEXA
Low - optimise RFs & repeat after 5yrs

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19
Q

DEXA interpretation

A

• T score - standard deviations below that of a healthy adult
○ >-1 = normal
○ -1 to -2.5 = osteopenia

20
Q

Management of Osteoporosis

A

Lifestyle & risk factors modification - good diet & weight, smoking, alcohol, exercise

Vit D & Ca supplements

Bisphosphonates - alendronate 70mg weekly

Denosumab - ab

HRT - in premature menopause

Follow up - repeat FRAX & DEXA 3-5yrs

21
Q

Considerations for Bisphosphonates

A

Taken weekly, on empty stomach & sitting upright for 30mins

SE inc: reflux/oesophageal erosions, atypical fractures, osteonecrosis of jaw & external auditory canal

22
Q

Definition of Paget’s Disease of Bone

A

Increased bone turnover is due to the excessive activity of both osteoclasts & osteoblasts. However turnover isn’t co-ordinated or regulated leading to patchy areas of high density (sclerosis) and low density (lysis). This makes the bones structurally weak, deformed & overall enlarged. Particularly affects axial skeleton (head & spine).

Aetiology unknown

23
Q

Clinical Presentation - Paget’s Disease

A
Typically affects older adults & p/w 
	• Bone pain
	• Bone deformity
	• Hearing loss - if affects bones of ear
Pathological fractures
24
Q

Investigations - Paget’s Disease

A
Bloods
	• Raised ALP - other LFTs normal
	• Calcium - normal
	• Phosphate - normal
Imaging - X-ray
	• Enlarged & deformed bones
	• Osteoporosis circumscripta describes well defined osteolytic lesions that appear less dense compared with normal bone
	• Cotton wool appearance of skull
	• V shaped defects in long bones -  osteolytic bone lesions within the healthy bone
25
Management - Paget's Disease
• Bisphosphonates - interfere with osteoclast activity & return normal bone metabolism, improve sx • Vit D & Calcium supplementation • NSAIDs for bone pain Monitor ALP & symptoms
26
Complications - Paget's Disease
Two key complications are osteosarcoma (at increased risk) & spinal stenosis/spinal cord compression
27
Examples of Crystal Arthropathies
Gout - deposition of urate crystals in joints | Pseudogout - calcium pyrophosphate crystals
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Risk factors - Gout
``` High purine diet - meat, seafood Alcohol Diuretics Existing CVD or renal dysfunction Family hx Male ```
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Clinical presentation - Gout
Red hot swollen painful joint Gouty tophi on hands, elbows & ears ``` typical joints: base of the big toe (metatarsophalangeal joint) Wrists Base of thumb (carpometacarpal joints) Also knee and ankle ```
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Differentials for hot swollen joint
SEPTIC ARTHRITIS Gout Pseudogout Bleeding into joint
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Investigations - Red, hot joint
Bedside • Observations - considering if systemically unwell • Joint examination - red, hot, swollen, ROM ``` Bloods • FBC - Hb, WBC • U&Es • LFTs • ESR/CRP - ESR may be high • Cultures - exclude sepsis ``` Imaging • X-ray - assessing for joint damage, signs of OA etc Specialist • Joint aspiration & microscopy/culture - gold standard for diagnosis of crystal arthropathies ○ Gout - negatively birefringent needles Pseudogout - positive birefringence, rhomboid/brick shaped crystals • Cell count > 50,000 cell/cm3 - think septic arthritis!
32
Management of Gout
• Acute attacks - NSAIDs (1st line) --> colchicine (2nd or if CA) --> intraarticular corticosteroids (3rd line) • Prophylaxis - allopurinol (xanthine oxidase inhibitor), lifestyle changes Start allopurinol after acute attack has settled
33
Risk factors - septic arthritis
``` Diabetes Advancing age Prothesis Immunodeficiency/suppression IVDU ```
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Clinical Features - septic arthritis
``` Symptoms • Pain • Swelling • Fevers Inability to weight bear ``` ``` Signs • Pain on active and passive movement • Reduced ROM (range of motion) • Erythema • Warmth • Joint effusion ```
35
Management - Septic Arthritis
Antibiotics - typically at least 6 week course (flucloxacillin 200-500mg 4x times a day, 2week IV then 6 week oral), liase w/ microbiology Joint aspirate/washout
36
Reactive Arthritis - Definition
Definition: Synovitis occurs in joints as a reaction to recent infective trigger (one of the spondyloarthropathies) Typically causes acute monoarthritis, affecting a single joint in the lower limb (most often the knee) presenting with a warm, swollen and painful joint.
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Triggers - Reactive Triggers
The most common infections that trigger reactive arthritis are gastroenteritis or sexually transmitted infection. Chlamydia is the most common sexually transmitted cause of reactive arthritis. Gonorrhoea commonly causes a gonococcal septic arthritis.
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Management - Reactive Triggers
Management of reactive arthritis when septic arthritis is excluded: • NSAIDs • Steroid injections into the affected joints Systemic steroids may be required, particularly where multiple joints are affected
39
Anklylosing Spondylitis - definition & clinical features
Chronic multi-system inflammatory disorder characterised by inflammation of the sacroiliac joints & axial skeleton. Part of the SpA group & a/w HLA-B27 - tends to present in young men as chronic back pain, morning stiffness & eventually spinal deformity • Back pain - worse w/ rest, better w/ exercis • Neck pain • Alternating buttock pain • Morning stiffness • Fatigue • Arthritis • Enthesitis (inflammation at the insertion of tendons and ligaments) • Positive Schöber test (assesses decrease in lumbar spine flexion) Spinal deformity (seen in advanced disease)
40
Ankylosing Spondylitis - Extra-atricular Manifestations
○ Aortitis - can lead to aortic regurgitation ○ Anterior uveitis - unilateral red eye, pain & photophobia ○ AV block ○ Apical lung fibrosis ○ Amyloidosis IgA nephropathy
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Ankylosing Spondylitis - investigations & management
Modified New York criteria - clinical & radiological criteria Bloods - FBC, U&Es, LFTs,CRP & ESR, HLA-B27 Imaging - Plain SIJ XR OR MRI SIJ & whole spine if XR normal ``` Management - Non-pharmacological Treatments • Patient Education • Smoking Cessation • Input from PT & Ots • Psychological support Pharmacological • NSAIDs - naproxen, ibuprofen, celecoxib ○ Along w/ PPI ○ Relieve symptoms & help w/ physio DMARDs - tend to be ineffective ```
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Clinical Features & Complications - Systemic Sclerosis
• Thickening of skin in 2 distinct subtypes: ○ Limited (distal elbows, knees & neck) or diffuse • Raynaud's phenomenom • Digital ulceration • ILD • Renal disease - accelerated HTN & proteinuria • Pulmonary hypertension Investigations & Diagnosis: Auto-antibodies • ANA, Scl-70, anticentromere, anti-RNA polymerase Others - investigations for complications • Lung (pulmonary fibrosis) - CXR, pulmonary function tests, high resolution CT scan Heart (pericariditis) - ECG, echo
43
ClinicalFeatures of SLE
``` 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 ```
44
Giant Cell Arteritis - definition, S&S, investigations & management
Definition: Large vessel vasculitis which is sight-threatening Inflammation of medium & large sized arteries - preferential involvement of branches of carotid (Temporal, ophthalmic & occipital) Presentation/Clinical Features: • Unilateral headache - usually temporal • Scalp pain • Jaw/tongue claudication • Visual symptoms - blurring, amaurosis fugax (temporary monocular blindness), diplopia • Constitutional symptoms: fever, weight loss, fatigue Investigations & Diagnosis: Suspected GCA should be assessed immediately w/ urgent referrals to rheumatology & ophthalmology team Bloods • FBC • U&E • LFT • ESR/CRP: typically elevated but may be normal at presentation (<5%). Keep a high index of suspicion Temporal artery biopsy Sampling of a small piece of tissue from the temporal artery. Due to the presence skip lesions, a negative biopsy does not exclude GCA Management: Immediate management • Start steroids immediately - do not wait for investigations ○ 40mg OD if no visual sx or jaw/tongue claudication ○ 60mg OD if those sx are present ○ Consider IV steroids if signs of cerebral ischaemia or visual loss Ongoing management • Regular monitoring - ESR & CRP • Steroid reducing plans ○ + protection i.e. bone, PPI cover
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Examples & Clinical Features of Small Vessel Vascultitides
o Granulomatosis w/ polyangiitis – small vessel vasculitis which affects respiratory tract & kidneys, a/w cANCA  Epistaxis, crusty nasal secretions, hearing loss & sinusitis  Cough, wheeze, haemoptysis, ILD  Glomerulonephritis  Rashes o Eosinophilic granulomatosis with polyangiitis – small & medium vessel vasculitis, a/w pANCA  Lung & skin manifestations but can affect other organs inc kidneys  Often presents w/ severe asthma in late teenage years or adulthood  Elevated eosinophil levels on FBC o
46
Sjogren's Syndrome - definition, clinical features & management
o Autoimmune disease which attacks exocrine glands, resulting in  Dry eyes, dry mouth, dry vagina & dry skin o Extra-glandular features: dysphagia, ILD, sensory neuropathy, arthralgia, CNS complications o Can also cause gland swelling – but if persists think about lymphoma Substitute lubricants for dry eyes & mouth, steroids & immunosuppressants can be used for systemic disease
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Types of Inflammatory Myositis - S&S & management
Polymyositis & dermatomyositis are autoimmune disorders where there is inflammation in the muscles (myositis) ® Polymyositis – chronic inflammation of muscles ® Dermatomyositis – is a CTD where there is chronic inflammation of the skin and muscles • Clinical Features: muscle pain, fatigue, weakness ○ Occurs bilaterally & typically affects proximal muscles ○ Mostly affects shoulder & pelvic girdle Develops over weeks Can be a paraneoplastic syndrome for ovarian, lung, breast & gastric cancers • Corticosteroids are the first line treatment of both conditions. • Other medical options where the response to steroids is inadequate: • Immunosuppressants (such as azathioprine) • IV immunoglobulins Biological therapy (such as infliximab or etanercept)