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Year 3 - Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Rheumatoid arthritis - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Chronic autoimmune inflammatory condition
- Autoantibodies attack the synovial membranes of joints, bursa and tendon sheaths, leading to chronic inflammation (synovitis)

Typical patient:
- Middle age onset
- (3x) F > M
- Family history of RA

Presentation:
- Joint pain / swelling / stiffness, particularly of the small/distal joints
- Symmetrical and affects many joints
- Onset can be sudden or more gradual
- Pain is worse in the morning and worse on rest
- May have some signs in the hands
Systemic symptoms:
- Fatigue
- Weight loss
- Flu-like illness
- Myalgia and weakness

Investigations:
Diagnosis is clinical but want back up of:
- Specific bloods for rheumatoid factor (RF) and then anti-CCP if RF negative
- Routine bloods e.g. FBC, ESR, CRP
- X-rays hands and feet
- Ultrasound of joints to confirm synovitis if unsure

Management:
1. One early DMARD (disease modifying anti-rheumatic drugs) e.g. Methotrexate, Leflunomide or Sulfasalazine
2. Two DMARDs
3. Methotrexate + biologic (e.g. TNF inhibitor Infliximab)
4. Methotrexate + Rituximab (Anti-CD20)
- Use of steroids to settle first presentation and for flares
- Surgery can be used to improve joint complications of RA but not used as much now due to early interventions

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2
Q

List some signs in the hands of someone with established rheumatoid arthritis

A
  • Ulnar deviation of fingers (at MCP joints)
  • Bouchard nodes (flexed PIP and extended DIP)
  • Swan neck deformity (extended PIP and flexed DIP)
  • Z shaped deformity of thumb
    + rheumatoid nodules on elbows
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3
Q

List some extra-articular manifestations of rheumatoid arthritis (3 CAPS)

A

(3)CAPS

3 C’s:
- Carpal tunnel syndrome
- Cardiovascular disease (increased risk)
- Cord compression (atlanto-axial subluxation)

3 A’s:
- Anaemia of chronic disease (normochromic and normocytic)
- Amyloidosis
- Arteritis

3 P’s:
- Pulmonary disease e.g. fibrosis, bronchiolitis obliterans, bronchiectasis
- Pleural disease
- Pericarditis

3 S’s:
- Sjogren’s syndrome (secondary)
- Scleritis / episcleritis
- Splenomegaly (Felty’s syndrome if with neutropaenia)

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4
Q

List the x-ray changes seen in rheumatoid arthritis

A

LESS!

Loss of joint space
Erosions
Soft tissue swelling
See-through bones (osteopenia)

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5
Q

Outline the DAS28 score for rheumatoid factor and what it’s used for

A

DAS 28 score - disease activity score of 28 joints
Points given for:
- Swollen joints
- Tender joints
- ESR / CRP level

Useful for monitoring disease activity and response to treatment

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6
Q

List some side effects of Methotrexate

A
  • GI upset e.g. N&V and diarrhoea
  • Pulmonary fibrosis
  • Mouth ulcers and mucositis
  • Bone marrow suppression / leukopenia
  • Thrombocytopenia
  • Teratogenic
  • Hepatotoxic
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7
Q

List some side effects of NSAIDs

A
  • Indigestion
  • Peptic ulcer disease
  • VTE e.g. DVT/PE
  • Peripheral oedema
  • Slight increased risk of stroke and heart attack
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8
Q

List some side effects of corticosteroids e.g. Prednisolone

A
  • Immunosuppression
  • Diabetes mellitus
  • Osteoporosis
  • Suppression of HPA axis
  • Teratogenic
  • Increased BP
  • Cataracts and glaucoma
  • Oedema

Cushing’s syndrome
- Thin skin, easy bruising
- Obesity distributed centrally
- Increased hair growth (hirsutism)
- Striae

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9
Q

List some side effects of Sulfasalazine

A
  • Myelosuppression
  • Nausea
  • Rash
  • Oral ulcers
  • Infertility / decreased sperm count
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10
Q

List some side effects of Biologic therapy (e.g. Adalimumab)

A
  • Immunosuppression
  • Reactivation of TB
  • Allergic reaction / reaction at infusion site
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11
Q

Systemic lupus erythematosus (SLE) - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Systemic autoimmune condition targeting the connective tissue
- Characterised by ANA antibodies (anti-nuclear) against own cell nuclei in proteins
- Often has a relapsing-remitting course

Typical patient:
- Women
- Young-middle age
- Asian

Presentation:
- Usually young-middle aged adults
- F > M and Asians
- Photosensitive malar rash
- Systemic features: fatigue, weight loss, fever
- Hair loss
- Joint pain and inflammatory arthritis
- Myalgia
- Mouth ulcers
- Lymphadenopathy
- Raynaud’s
- SOB
- Chest pain

Investigations:
Criteria used based on clinical features and presence of anti-nuclear antibodies
- Specific bloods for ANA and anti-dsDNA antibodies
- Routine bloods e.g. FBC, ESR, CRP
- Further bloods e.g. C3, C4, immunoglobulins
- Urinalysis and protein:creatitine ratio to test for kidney involvement
- Renal biopsy if lupus nephritis suspected

Management:
First line:
- Hydroxychloroquine
- NSAIDs
- Prednisolone (steroids)
- Skin protection e.g. suncream
If not responding/severe:
- Immunosuppressants e.g. Methotrexate, Mycophenolate mofetil
- Biologics e.g. Rituximab

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12
Q

List some complications of SLE

A

Cardiovascular disease (HTN and coronary artery disease) = LEADING CAUSE OF DEATH

  • Infection (disease + immunosuppressants)
  • Lupus nephritis (inflammation in kidneys)
  • Anaemia of chronic disease (bone marrow suppression)
  • Pericarditis
  • Pleuritis
  • Interstitial lung disease (fibrosis)
  • Neuropsychiatric (optic neuritis, transverse myelitis or psychosis)
  • Recurrent miscarriages
  • Antiphospholipid syndrome, leading to VTE
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13
Q

Gout - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Crystal arthropathy which occurs as a result of chronic hyperuraemia
- Sodium urate crystals are deposited in the joint causing joint to become painful, swollen and hot

Typical patient:
- Male
- Obese
- Family history
- Existing cardiovascular or renal disease

Presentation:
- Single painful, swollen and hot joint
- Acute, severe onset
Key differential should be septic arthritis

Investigations:
- Diagnosed clinically or by joint aspiration
- X-ray of affected joint
KEY = exclude septic arthritis

Management:
Acute attack
- NSAIDs
- Colchicine
- Steroids
Prophylaxis/prevention
- Allopurinol (only once acute attack has resolved)
- Lifestyle changes e.g. lose weight, hydration, limit alcohol and limit purine-based foods

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14
Q

List some risk factors for gout (modifiable and non-modifiable)

A

Modifiable
- Alcohol intake / high purine diet
- Obesity
- Diuretics

Non-modifiable
- Male
- Family history
- Existing cardiovascular or renal disease

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15
Q

List some typical joints that are affected in gout

A
  • Base of the big tole (MTP)
  • Base of thumb (MCP)
  • Bigger joints e.g. knee and ankle
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16
Q

List 3 things seen in a joint aspiration from a gouty joint

A
  • Monosodium urate crystals (needle-shaped)
  • Negative birefringent of polarised light
  • Absence of bacteria
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17
Q

List 2 things that x-ray of a gout joint will show

A
  • Punched out erosions (with overhanging edges and sclerotic margins)
  • Lytic bone lesions

Joint space is generally maintained

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18
Q

Outline how pseudogout differs from gout

A

Pseudogout involves calcium pyrophosphate (rather than monosodium urate) crystals being deposited into joints

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19
Q

Osteoporosis - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Reduced density of bones (low bone mass) leading to reduced bone strength
- Increased risk of fractures

Typical patient
- Post-menopausal women
- White / south asian

Presentation:
- Generally not symptomatic
- Often discovered upon an unusual fracture e.g. low energy fracture

Investigations:
- FRAX assessment to assess risk
- DEXA scan to confirm (dual energy x-ray absorptiometry)

Management:
Based on results from a FRAX prediction or DEXA scan
Conservative
- Weight bearing exercise
- Limit alcohol intake
- Stop smoking
- Increase dietary calcium
Medical
- Vitamin D and calcium supplements (AdCal D3)
- Oral bisphosphonates (IV if not tolerated)
- Then Denosumab 2nd line

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20
Q

List the risk factors for developing osteoporosis (modifiable and non-modifiable)

A

Modifiable:
- Low mobility (non-weight bearing)
- Low calcium diet / low sun exposure (vitamin D deficiency)
- Smoking
- Excess alcohol intake
- Low BMI/weight
- Corticosteroids

Non-modifiable:
- Female
- Post-menopausal
- Family history of osteoporosis
- Increased age
- White or south asian
- Premature menopause

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21
Q

Outline how a DEXA scan is used to diagnose osteoporosis

A

DEXA scan is gold standard for diagnosis of osteoporosis
- Assesses the bone mineral density using x-rays
- Measures how much radiation is absorbed by the bones, which indicates how dense the bones are
- Reading taken at the hip is key
- T score used (can also use Z score)

T score < - 2.5 = osteoporosis
T score > -1 = normal
T score between those two is osteopenia

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22
Q

Briefly outline how the FRAX score is calculated and it’s use in osteoporosis

A

FRAX score gives a risk of fragility fracture in the next 10 years (assess risk of osteoporosis)

Performed on individuals at risk of osteoporosis
- Women over 65
- Men over 75
- Anyone at increased risk e.g. low BMI, long-term steroids

Calculated using information e.g. age, BMI, co-morbidities, smoking, alcohol and family history
Can also enter results of a DEXA scan for a more accurate result

Overall gives a 10 year risk of having either:
- Major osteoporotic fracture
- Hip fracture

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23
Q

Osteomalacia - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Condition of ineffective bone mineralisation (soft bones)
- Caused by insufficient vitamin D

Presentation:
- Rickets if happens in childhood
May not have any symptoms!
- Bone pain
- Muscle pain / weakness
- Fatigue
- Fractures

Investigations:
- Serum vitamin D (25-hydroxyvitamin D)
- X-ray / DEXA scan showing osteopenia
Blood tests may also reveal
- Hypocalcaemia
- Hypophosphataemia
- Secondary hyperparathyroidism

Management:
- Vitamin D3 supplements (initial treatment followed by a life-long maintenance dose)

24
Q

List some risk factors for developing osteomalacia

A
  • Darker skin tone
  • Reduced UV radiation exposure (lack of sunlight)
  • Malabsorption disorders e.g. IBD, coeliac disease
25
Q

Polymyalgia rheumatica (PMR) - state the following:
- Pathophysiology
- Typical patient
- Presentation
- How diagnosis is made
- Management

A

Pathophysiology:
- Inflammatory condition leading to pain and stiffness in: shoulders, pelvic girdle and neck
- Closely associated with GCA

Typical patient:
- Over 50
- Female
- Caucasian
- Association with GCA

Presentation:
- Pain and stiffness in: shoulders, pelvic girdle and neck
- Worse on movement
- Interferes with sleep
- Stiffness for > 45 mins in morning
- Systemic features e.g. weight loss, fatigue
- Upper arm tenderness
- Carpal tunnel syndrome
- Peripheral oedema

How diagnosis is made:
- Clinical diagnosis based on symptoms plus response to steroids
- May need to exclude other conditions
- Inflammatory markers usually raised also (ESR, CRP and plasma viscosity)

Management:
- Steroids e.g. Prednisolone (then assess response)
- Check after 1 week: if poor response, probably not PMR
- Check after 1 month: should expect 70% improvement, then start to wean off

26
Q

Outline the mnemonic ‘don’t STOP’ for long-term steroid use

A

don’t stop steroids suddenly

Sick day rules (double dose)
Treatment card (steroid card)
Osteoporosis
PPI cover (gastric protection)

27
Q

Ankylosing spondylitis - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigation and special test
- Management

A

Pathophysiology:
- Inflammatory condition mainly affecting the spine
- Leads to progressive pain and stiffness in mainly the sacroiliac joints and the vertebral column joints
- Can progress to fusion of sacroiliac joints and spine
- Seronegative spondyloarthropathy: related to reactive arthritis and psoriatic arthritis (HLA-B27 gene)

Typical patient:
- Young male
- Late-teens or 20’s

Presentation:
- Gradual development > 3 months
- Lower back pain and stiffness
- Buttock/sacroiliac pain
- Worse with rest, better on movement
- Worse in morning and at night, can wake from sleep
- > 30 min early morning stiffness
Symptoms can fluctuate with flares

Investigation and special test:
- Blood tests e.g. CRP, ESR
- HLA B27 genetic test
- X-ray spine and sacrum
- MRI spine may show bone marrow oedema in early disease
- Special test: Schober’s test

Management:
Conservative
- Physiotherapy
- Avoid smoking
- Surgery if deformity
Medical
- NSAIDs to help with pain
- Steroids for flares
- MAB e.g. Adalimumab or Infliximab or Anti-TNF e.g. Etanercept

28
Q

List some x-ray changes seen in ankylosing spondylitis (including the main one)

A

Main: bamboo spine (due to spine fusion)

  • Squaring of vertebral bodies
  • Subchondral sclerosis and erosions
  • Syndesmophytes
  • Ossification of ligaments, discs and joints
  • Fusion of sacroiliac and facet/costovertebral joints
29
Q

Osteoarthritis - state the following:
- Pathophysiology
- Typical patient
- Presentation
- How diagnosis is made
- Management

A

Pathophysiology:
- General wear and tear of joints (non-inflammatory)
- Imbalance of cartilage wearing down and chondrocyte repair
- Occurs in synovial joints

Typical patient:
- Female
- Increased age
- Obese
- Family history

Presentation:
- Joint pain, worse on movement
- Joint stiffness, worse throughout the day
- May have signs of OA in the hand
- History of risk factors

How diagnosis is made:
- Can be made without any investigations
- May do an x-ray to confirm

Management:
Conservative
- Patient education
- Weight loss
- Activity modification / physiotherapy
Medical
- Paracetamol / NSAIDs (topical or oral)
- Opiates e.g. Co-codamol or Morphine
- Intra-articular joint replacement
- Surgery joint replacement

30
Q

Outline x-ray changes seen in osteoarthritis

A

LOSS!

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

However, x-ray findings don’t always correlate with clinical symptoms

31
Q

List some risk factors for osteoarthritis

A
  • Increased age
  • Female
  • Obesity
  • Previous trauma leading to articular damage
  • Occupation
  • Family history
32
Q

List commonly affected joints in osteoarthritis

A
  • Hips
  • Knees
  • Sacroiliac joints
  • MCP (thumb)
  • DIPs (hands)
  • Wrist
  • Cervical spine
33
Q

List signs of osteoarthritis in the hands

A
  • Squaring of base of thumb
  • Heberden’s nodes (DIPs)
  • Boucharde’s nodes (PIPs)
  • Weak grip
  • Reduced ROM
34
Q

Fibromyalgia - state the following:
- Pathophysiology
- Typical patient
- Presentation
- How diagnosis is made
- Management

A

Pathophysiology:
- Disorder of central pain processing
- Can be triggered by a traumatic event or sleep deprivation

Presentation:
- Chronic widespread pain in all 4 quadrants of the body
- Allodynia (heightened and painful response to innocuous stimuli)
- Unrefreshed sleep
- Fatigue
- Numbness
- Headaches
- IBS / bladder syndrome
- Fibro-fog
- Depression and anxiety

How diagnosis is made:
- No specific diagnostic test
- May have tender points on palpation, but otherwise no abnormalities
- May want to rule out other differentials with blood tests

Management:
Conservative
- Improve sleep hygiene
- Increase physical activity levels
- CBT
Medical
- Low dose Amitriptyline
- Pregabalin or Gabapentin

35
Q

List some risk factors for fibromyalgia

A
  • Female (9:1)
  • 40-50
  • Obvious triggers e.g. emotional or physical event
36
Q

Psoriatic arthritis - state the following:
- Pathophysiology
- 3 typical patterns of affected joints
- Presentation
- Investigation
- Management

A

Pathophysiology:
- An inflammatory arthritis associated with psoriasis
- Varies in severity, from mild pain/stiffness to complete joint destruction (arthritis mutilans)
- Occurs in 10% of patients with existing psoriasis
- Seronegative spondyloarthropathy: related to reactive arthritis and ankylosing spondylitis (HLA-B27 gene)

3 typical patterns of affected joints:
1. Symmetrical polyarthritis - similar to RA but MCP joints less likely
2. Asymmetrical pauciarthritis - mainly digits of hands and feet
3. Spondylotic pattern - back stiffness, sacroiliitis and atlantoaxial joint

Presentation:
- Joint pain/stiffness (as described previously)
- Psoriatic plaques
- Nail pitting
- Onycholysis
- Dactylitis (sausage fingers)
- Inflammation of tendon insertion points
- Anterior uveitis or conjunctivitis

Investigation:
- Routine bloods including CRP
- X-ray showing pencil-in-cup (central erosions of bone beside joints)

Management:
- Similar to RA management
- NSAIDs
- DMARDs
- TNF inhibitors

37
Q

Reactive arthritis - state the following:
- Pathophysiology
- Presentation
- Investigation
- Management

A

Pathophysiology:
- Inflammation of synovial joint, as a reaction to a recent infective trigger
- Seronegative spondyloarthropathy: related to reactive arthritis and ankylosing spondylitis (HLA-B27 gene)

Presentation:
- Generally an acute monoarthritis
- Hot, swollen and painful joint

Investigation:
- Joint aspiration and send for gram staining and MC&S
- Crystal examination if gout suspected

Management:
- Give Abx until possibility of septic arthritis can be excluded
- Treat underlying infection
- NSAIDs
- Steroid infection into affected joint
- Systemic steroids may be needed if multiple joints affected
Most cases resolve within 6 months (may need DMARDs or anti-TNF if not)

38
Q

List 2 conditions that can commonly cause reactive arthritis

A
  • Gastroenteritis
  • Sexually transmitted infection (chlamydia or gonorrhoea)
39
Q

List some conditions associated with reactive arthritis (helpful phrase)

A
  • Balanitis
  • Anterior uveitis
  • Bilateral conjunctivitis
    + reactive arthritis

‘can’t see, can’t pee, can’t climb a tree’

40
Q

Systemic sclerosis - state the following:
- Pathophysiology (list 2 types)
- Autoantibodies (2)
- Management

A

Pathophysiology:
- Autoimmune inflammatory and fibrotic connective tissue condition
- Cause is actually unclear
- Mostly affects the skin, but also affects internal organs
2 types:
1. Limited
2. Diffuse

Autoantibodies:
- ANA antibodies
- Anti-centromere antibodies (limited mainly)
- Anti Scl-70 antibodies (diffuse mainly)
- Nailfold capillaroscopy (helps to find systemic sclerosis in patients with Raynaud’s)

Management:
Conservative
- No smoking
- Emollients
- Occupational /physiotherapy
Medical:
- Manage complications
- Can use steroids and immunosuppressants in diffuse

41
Q

List some features of limited and diffuse systemic sclerosis

A

Limited: CREST
Calcinosis
Raynaud’s
Eosophageal dysmotility
Sclerodactyly
Telangiectasia

Diffuse:
Cardiovascular problems - HTN and coronary artery disease
Lung problems - pulmonary HTN and pulmonary fibrosis
Kidney problems - glomerulonephritis

42
Q

Giant cell arteritis (GCA) - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigation
- Management

A

Pathophysiology:
- Systemic vasculitis of the medium and large arteries
- Strong link with polymyalgia rheumatica

Typical patient:
- Over 50
- Female
- Caucasian
- Association with polymyalgia rheumatica

Presentation:
- Severe unilateral temporal headache
- Scalp tenderness
- Jaw claudication
- Vision changes (blurred or double vision)
- Systemic symptoms e.g. fever, muscle aches, fatigue, loss of appetite

Investigation:
- Temporal artery biopsy which show multinucleated giant cells (although can be falsely negative)
- Bloods including ESR

Management:
Initial
- High dose steroids (Prednisolone)
- Aspirin
- PPI while on steroids
If vision changes - same day referral to ophthalmologist
If no vision changes - discuss with specialist and refer using GCA fast-track pathway
Continue on steroids until symptoms have resolved, can take years

43
Q

List some complications of giant cell arteritis (early and later)

A

Early:
- Permanent vision loss
- Stroke

Late:
- Relapse of GCA
- Long-term steroid complications
- Stroke
- Aortitis (risk of aortic aneurysm and dissection)

44
Q

Sjogren’s syndrome - state the following:
- Pathophysiology
- Typical patient
- Presentation
- Investigation
- Management

A

Pathophysiology:
- Autoimmune condition targeted against exocrine glands
- Leads to dry mucous membranes such as dry eyes, dry mouth and dry vagina
2 types:
Primary Sjogren’s: occurs alone
Secondary Sjogren’s: associated with SLE or RA

Typical patient:
- Female (80%)
- 40-50
- Caucasian

Presentation: (MADFRED)
Myalgia
Arthralgia
Dry eyes
Fatigue
Raynaud’s
Enlarged parotids
Dry mouth

Investigations:
- Specific blood tests for anti-Ro and anti-La
- Schirmer’s test (tear production/collection)
- May need salivary gland biopsy

Management:
- Artificial tears
- Artificial saliva / sugar free gum/pastilles
- Vaginal lubricants
- Hydroxychloroquine to halt disease progression

45
Q

List some complications of Sjogren’s disease

A

Eyes:
- Conjuntivitis
- Corneal ulcers

Mouth:
- Dental cavities
- Candida

Vagina:
- Sexual issues/dysfunction
- Candidiasis

46
Q

Briefly describe the pathophysiology of vasculitis

A

Pathophysiology:
- Inflammation of the blood vessels (can be arteries or veins)
- Categorised by the size of vessel affected (small, medium or large)
- Leads to damage of blood vessel walls and subsequent thrombus formation, ischaemia, bleeding or aneurysm formation

47
Q

Briefly describe the pathophysiology of vasculitis

A

Pathophysiology:
- Autoimmune condition resulting in inflammation of the blood vessels (can be arteries or veins)
- Categorised by the size of vessel affected (small, medium or large)
- Leads to damage of blood vessel walls and subsequent thrombus formation, ischaemia, bleeding or aneurysms

48
Q

Give 2 examples of each type of vasculitis
- Small vessel vasculitis
- Medium vessel vasculitis
- Large vessel vasculitis

A

Small vessel vasculitis
- Granulomatosis with polyangiitis (Wegner’s)
- Microscopic polyangiitis

Medium vessel vasculitis
- Kawasaki disease
- Polyarteritis nodosa

Large vessel vasculitis
- Giant cell arteritis
- Takayasu’s arteritis

49
Q

List some generic features of most types of vasculitis

A
  • Purpura (small purple spots under skin)
  • Peripheral neuropathy
  • Renal impairment
  • HTN
  • Anterior uveitis
  • Scleritis
  • Joint and muscle pain
  • GI disturbance

Systemic features
- Fatigue
- Weight loss
- Fever
- Loss of appetite

50
Q

List investigations for vasculitis including antibodies

A

Bloods:
- Inflammatory markers (CRP and ESR raised)

Antibodies:
- ANCA (anti-neutrophil cytoplasmic antibodies)

51
Q

Describe the general medical approach to managing vasculitis

A

Steroids:
- Tailor administration route to target affected areas
- Oral / IV / nasal / inhaled

Immunosuppressants:
- Cyclophosphamide
- Methotrexate
- Azathioprine
- Rituximab / other MAB

52
Q

Hypermobility spectrum disorder - state the following:
- Pathophysiology
- Presentation
- Investigation
- Management

A

Pathophysiology:
- Pain syndrome in people whose joints move beyond normal limits
- Due to laxity of ligaments, tendons and capsules
- Can affect any number of joints

Presentation:
- Pain around joints, worsens after activity
- Abnormal skin
- Marfan qualities e.g. arachnodactylyl
- Hernias and prolapses

Investigations:
- Do a Beighton’s score to assess likelihood

Management:
Aim to reduce pain and reduce disability
- Analgesia (Paracetamol)
- Physiotherapy
- Splinting
- Surgical interventions

53
Q

Raynaud’s syndrome - state the following:
- Pathophysiology
- Presentation (including classic pattern)
- Management

A

Pathophysiology:
- Vasospasm of the blood vessels of the digits
- Precipitated by cold or stress
- Common in young women (may be familial)

Presentation:
- Painful cold fingers
Classic pattern
- White (inadequate blood flow)
- Blue (venous stasis)
- Red (re-warming hyperaemia)

Management:
Conservative
- Avoid cold / keep hands warm
- Avoid smoking
Medical
- CCB
- Phosphodiesterase-5 inhibitors
- Prostacyclins

54
Q

List some diseases associated with Raynaud’s disease

A

If symptoms develop < 30 years old, suspect underlying disease

  • SLE
  • Systemic sclerosis
  • Sjogren’s syndrome
  • Dermatomyositis and polymyositis
    PLUS
  • Cervical rib
  • Coagulopathies (sticky blood) e.g. cryoglobulinemia
55
Q

List a physical cause and a drug that causes Raynaud’s

A

Physical cause:
- Use of heavy vibrating tools

Drug:
- Beta blockers

56
Q

List 3 complications of Raynaud’s phenomenon

A
  • Digital ulcers
  • Severe ischaemia
  • Infection
57
Q

Behcet’s disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Rare multi-organ disease caused by a systemic vasculitis

Presentation:
- Recurrent oral ulcers
- Recurrent genital ulcers
- Uveitis
- Erythema nodosum

Investigations:
- No specific test for Behcet’s
- Usually aim is to rule out other differentials e.g. rheumatoid factor, ANA or ANCA
- Can use Pathergy test for exaggerated skin injury after minor trauma, however is unreliable
- May investigate system related to specific symptoms

Management:
- Immunosuppressive treatment with biologic drugs, corticosteroids, Colchicine, Azathioprine or Methotrexate
- Some need treatment of flares only, some need ongoing treatment

Year 3 - Medicine (8 decks)

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