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Year 3 Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Using the mnemonic CHIMP, name the drugs that can cause Drug Induced Lupus

A
  • Carbamazepine/Chlorpromazine
  • Hydralazine
  • Isoniazid/Infliximab
  • Minocycline
  • Penicillamine/Procainamide/Pyrazinamide
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2
Q

Name the two ‘special tests’ for Carpal Tunnel Syndrome

A

Tinnel’s test Phalen’s test

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3
Q

Give two rheumatological causes of Neutropenia

A
  1. SLE
  2. DMARD Toxicity (neutropenic sepsis)
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4
Q

Name three inflammatory markers and what they indicate

A

ESR - Erythrocyte Sedimentation Rate (reflects presence of fibrinogen and immunoglobulins) PV - Plasma Viscocity (same as above) CRP - Short lived protein good for monitoring progression

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5
Q

Give 4 subtypes of ANA and what they’re raised in

A
  • Anti DsDNA - SLE
  • Anti RO - Sjogren’s
  • Anti Centromere - Systemic Sclerosis
  • Anti Jo-1 - Polymyositis
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6
Q

what anti body is associated with Sjogren’s?

A

anti-RO and anti-LA

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7
Q

what antibodies are associated with SLE?

A

anti-dsDNA

anti RO and anti LA

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8
Q

which antibodies are associated with Systemic sclerosis?

A

anti cantromere and anti Scl70

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9
Q

which antibody raises with disease activity?

A

anti-dsDNA

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10
Q

what antibody is associated with Polymyositis?

A

anti Jo-1

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11
Q

What is ANCA?

A

Anti Neutrophil Cytoplasmic Antibody

  • antibodies directed against enzymes present in neutrophils
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12
Q

what condition are patients ANCA positive?

A

GPA - Granulomatosis with Polyangiitis

(aka Wegener’s granulomatosis)

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13
Q

What is HLA - B27 and what conditions is it associated with?

A

class 1 surface antigen associated with:

  • Ankylosing Spondylitis
  • Iritis
  • Juvenile Arthritis
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14
Q

What 2 conditions is urinalysis mandated in?

A

SLE

vasculitis

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15
Q

what 2 conditions must synovial fluid analysis be done and what may be seen on polarized light microscopy?

A
  • septic arthritis - gram stain and culture before Abx
  • crystal arthropathy
    • negatively birefringent needle shaped crystals in gout
    • positively birefringent rhomboid shaped crystals in pseudo gout
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16
Q

What is Polymyositis?

A

Inflammation of striated muscle

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17
Q

How does Polymyositis present?

A

Insiduous Onset (Painless)
May be myalgia (muscle pain)
Proximal Muscle Weakness
Raynauds
Dysphagia/Dysphonia/Resp Weakness

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18
Q

How does Dermatomyositis present?

A

Muscle and Skin signs, Skin Signs being

  • Helitrope Rash (lilac rash around eyes)
  • Shawl Sign (macular rash)
  • Nail Fold Infarcts
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19
Q

Describe the 5 Diagnostic Criteria of (Dermato)Myositis, and how many is required for each

A
  • Symmetrical Proximal Muscle Weakness
  • Raised serum muscle enzyme levels (CK,ALT,AST)
  • Electromyograph showing fibrillatory changes
  • Biopsy evidence
  • PM requires 3
  • DM requires 2 + Skin Changes
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20
Q

Name 4 investigations you could do for Polymyositis and what they would show

A

Bloods - Raised ALT (normal LFTs)
Bloods - Raised ANA - Anti Jo1
Electromyograph - Fibrillatory Changes
Muscle MRI - Muscle Oedema

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21
Q

How is Polymyositis managed?

A

Initial - High dose Prednisolone Followed by DMARDs if resistant

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22
Q

How is Dermatomyositis managed long term?

A

Hydroxychloroquine and sun protection

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23
Q

What is Fibromyalgia?

A

Disorder of central pain processing characteised by widespread pain in all 4 quadrants of the body, associated with Allodynia (painful response to non painful stimulus), and Hyperaesthesia (exaggerated response to mildly painful stimulus)

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24
Q

Describe three different aetiological ideas for Fibromyalgia

A

Sleep Deprivation - Hyperactivation in response to painful stimuli Patient CSF - Increased Substance P and decreased NA and Serotonin PET Scan - Abnormal central dopamine response to pain

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25
Q

Give presentations of Fibromyalgia

A
  • Widespread Pain
  • Profound fatigue
  • Unrefreshed Sleep
  • Migraines
  • Numbness
  • Depression
  • Joint/Muscle Stiffness
  • IBS/iritable bladder syndrome
  • poor concentration and memory (fibrofog)
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26
Q

what is seen on examination of fibromyalgia?

A
  • no physical abnormalities to the MSK
  • no neurological symptoms
  • tender points on palpation of their muscles
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27
Q

Fibromyalgia is purely a clinical diagnosis, how could you manage it?

A
  • Physio
  • CBT
  • Low dose Amitryptyline/Pregabalin
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28
Q

what is significant about a diagnosis of fibromyalgia?

A

it is a diagnosis of exclusion

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29
Q

What is Giant Cell Arteritis? aka temporal arteritis

A

Chronic vasculitis in large and medium sized vessels occurring in over 50s

most commonly causes inflammation of the arteries originating from the arch of the aorta

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30
Q

Why do you get Jaw Claudication in GCA?

A

Inflammation of arteries supplying the muscles of mastication results in jaw clauducation and tongue discomfort following chewing and talking at length

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31
Q

Give 5 presentations of GCA

A
  • Headache (unilateral over temple)
  • Scalp Tenderness - over temporal artery
  • Jaw Claudication (+tongue)
  • Amaurosis Fugax, blindness, diplopia, blurring
  • Malaise + constitutional symptoms
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32
Q

Name three investigations you could do for GCA. What would they show?

A
  • Bloods - Raised ESR and CRP
  • Temporal Artery Biopsy - Necrotising arteritis (skip lesions)
  • Doppler - Decreased pulsation of temporal artery
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33
Q

Name three risk factors for GCA

A
  • Age (>60)
  • Female
  • White
  • strong association with PMR
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34
Q

How is GCA diagnosed?

A

diagnosed if 2 or more of the following:

  1. raised ESR, CRP, PV
  2. new onset localised headache
  3. tenderness/decreased pulsation of temporal artery
  4. new onset visual symptoms
  5. biopsy revealing necrotising arteritis
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35
Q

How would you manage GCA?

A
  1. Prednisolone 60-100mg for 2 weeks before tapering
    1. If visual symptoms consider 1g methylprednisolone IV pulse therapy for 1-3 days
  2. Low-dose aspirin to reduce thrombotic risks
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36
Q

What is Gout? And which joint is most commonly affected?

A

Accumulation of Monosodium Urate crystals in joints and soft tissues causes an inflammatory arthritis

1st MTP (metatarsophalangeal) joint

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37
Q

Give two long term manifestations of Gout

A

Urate Nephropathy

Uric Acid Nephrolithiasis

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38
Q

how does gout present?

A

sudden, severe attacks of pain, swelling, redness and tenderness in the joints, often the joint at the base of the big toe

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39
Q

Give 2 modifiable and some non modifiable risk factors of Gout

A

Non Mod = >40 yo & Male

Mod

  • Increased Alcohol
  • Thiazide Diuretics
  • high purine intake
  • hypertension
  • DM
  • obesity
  • smoking
  • dyslipidaemia
  • CAD
  • renal disease
  • organ transplant
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40
Q

how can gout be prevented?

A
  • maintain optimal weight
  • regular exercise
  • diet modification
  • smoking cessation
  • decrease alcohol
  • increase fluid intake
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41
Q

What would a synovial fluid sample show of Gout? What would you see for pseudogout?

A

Yellow and Turbid Polarised Light Microscopy - Negatively bifringent needles

pseudogout = Positively berefringent romboid shaped crystals made of calcium pyrophosphate

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42
Q

What would an Xray of Gout show?

A

Early stage = swelling

Late = normal joint space, soft tissue swelling and periarticular erosions

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43
Q

how is gout diagnosed?

A

2 of the following

  • typical Hx
  • tophi
  • increased serum urate
  • crystals in joint
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44
Q

Give 3 pharmacological options to TREAT Gout - acute

A
  • NSAIDs (Diclofenac, Naproxen)
  • Steroids
  • Colchicine (good when NSAIDs CI) its an antimitotic drug and decreases inflammation caused by uric acid crystals
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45
Q

Give 2 pharmacological options to PREVENT Gout. What should you tell the patient?

A
  • Allopurinol and Febuxostat (XANTHINE OXIDASE INHIBITORS)
  • Do not start the drugs in an acute attack
  • Cover with NSAIDs once started as they may precipitate an attack
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46
Q

Give 4 contraindications to the use of NSAIDs

A

BARS

  • B- Bleeding
  • A - Asthma
  • R - Renal Dysfunction
  • S - Stomach (Peptic Ulcer or Gastritis)
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47
Q

What is the pathophysiology of Pseudogout?

A
  • Calcium Pyrophosphate crystals
  • Positive bifringent rods
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48
Q

What is Hypermobility Spectrum Disorder?

A

Pain syndrome in people with joints that move beyond normal limits

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49
Q

Give 5 presentations of Hypermobility Spectrum Disorder

A

Pain around joints (worse after activity)
Hernias
Drooping Eyelids
Recurrent dislocations
Marfans/EDS

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50
Q

What gene is defective in Marfans?

A

Fibrillin

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51
Q

Describe 3 aetiologies of OA

A
  1. Failure of normal cartilage due to prolonged abnormal or excessive loading
  2. Damaged cartilage failing under normal conditions
  3. Cartilage breaks up due to defective bone putting on more weight
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52
Q

Describe the cartilage of OA on a microscopic level

A
  • Decreased elasticity
  • Decreased cellularity
  • Decreased tensile strength
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53
Q

The pain of OA cannot originate from the cartilage itself as it is avascular and aneural, therefore where does it originate from?

A
  • Microfractures of bone
  • Low grade synovitis
  • Capsular distension
  • Muscle spasm
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54
Q

Give 4 presentations of OA

A
  • Pain and Crepitus on movement
  • Joint Gelling
  • Background Ache at rest
  • Joint Swelling
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55
Q

Describe the XRay findings of OA

A

Loss of joint space

Osteophytes

Subchondral Sclerosis

Subchondral Cysts

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56
Q

Give 2 conservative and 2 pharmacological managements of OA

A

Conservative - Movement and Strengthening exercises, Walking stick Management - Paracetamol, Topical NSAIDs and Capsaicin

57
Q

What is Osteoporosis?

A

Low bone mass, deterioration of bone tissue and disruption of bone architecture leading to reduces bone strength and increased fracture risk

58
Q

What are the two types of Osteoporosis?

A

1 - Post menopausal women, oestrogen withdrawal increases osteoclast activity 2 - Increased age reduces osteoblast function

59
Q

Using the mnemonic SHATTERED, what are the risk factors for Osteoporosis?

A
  • Steroids
  • Hyperthyroidism
  • Alcohol and Tobacco
  • Thin
  • Testosterone
  • Early Menopause
  • Renal Failure
  • Erosive Bone Disease (Myeloma)
  • Dietary Malabsorption
60
Q

Suspected Osteoporosis patients are given a DEXA scan, to produce a T and Z score, what are they?

A

T score - Number of standard deviations from the mean bone density of a healthy person. above -1 SD is normal between -1 and -2.5 SD is defined as mildly reduced bone mineral density (BMD) compared with peak bone mass (PBM) at or below -2.5 SD is defined as osteoporosis

Z Score - comparing your DEXA with someone of the same age, less than -2 SD indicates Osteoporosis

61
Q

Give 4 conservative managements of Osteoporosis

A
  • Quit smoking
  • Increase weight bearing exercises
  • Calcium and Vit D rich diet
  • limit alcohol
  • stop smoking
62
Q

What is the first pharmacological choice for managing Osteoporosis? What should you advise the patient with this medication?

A
  • Oral Bisphosphonates such as Alendronic Acid
  • Stay upright and wait 30 mins before food after taking
  • Possible SE include Jaw Osteonecrosis and GI Upset
63
Q

Other than Bisphosphonates, describe two other pharmacological options for Osteoporosis (2nd line)

A

Teriparatide - Recombinant PTH

Denosumab - MAB decreasing bone reabsorption given subcut biannually

64
Q

What is Polymyalgia Rheumatica?

A

Idiopathic inflammatory condition characterised by severe bilateral pain and morning stiffness of shoulder/neck/pelvic girdle

65
Q

What other rhumatological condition does PMR commonly co-exist with?

A

50% association with GCA

66
Q

Give 3 symptoms of PMR

A
  • Subacute (<2wks) proximal limb pain and stiffness
  • Difficulty rising from chair/combing hair
  • Night time pain
  • (systemic symptoms)
67
Q

what is seen on examination of PMR

A
  • decreased ROM - shoulder, neck and hips
  • muscle strength is usually normal - limited by pain and/or stiffness
  • muscle tenderness
68
Q

What is the difference in presentation between PMR and Polymyositis?

A
  • PMR - No weakness, just pain
  • Polymyositis - Generally no pain, just weakness
69
Q

how is PMR diagnosed?

A

tyical history and exam supported by raised inflammatory markers - CRP, ESR and PV

consider temporal artery biopsy if symptoms of GCA

70
Q

How would you manage PMR?

A

15mg Prednisolone daily before tapering, adjusting to symptoms (dramatic response within 5d)

also bisphosphonates, vit D and calcium

71
Q

what drug is used in relapsing patients with PMR?

A

methotrexate - steroid sparing

72
Q

What is Raynaud’s Phenomenon?

A

Painful vasospasm of digits resulting in colour changes in response to cold stimulus

73
Q

What is the difference between Raynaud’s Syndrome and Raynaud’s Phenomenon/Disease?

A
  • Syndrome - Idiopathic, Symmetrical and Bilateral
  • Disease - Asymmetrical and lasts longer
74
Q

What are the three colour changes in Raynauds?

A
  • Pale (white) - Ischaemia - inaequate blood flow
  • Blue - Deoxygenation - venous stasis
  • Red - re-warming hyperaemia
75
Q

Describe Primary and Secondary Raynauds. How can you differentiate between?

A
  • Primary - young female and generally no underlying disease
  • Secondary - more severe pain, older, co-morbidities Differentiated by raised ESR in secondary only
76
Q

triggers of Raynauds

A
  • Exposure to cold
  • Medications (Beta Blockers)
  • Vasculitis
  • Heavy Vibrating Tools
  • Diseases (SLE, Scleroderma, Sjogren’s)
  • cervical rib
  • sticky blood - cryoglbulinaemia
77
Q

Give two conservative and two pharmacological treatments for Raynauds

A

Conservative - Stop smoking, avoid the cold

Pharmacological

  • 1st line = Calcium Channel blockers
  • phosphodiesterase-5 inhibitors
78
Q

Give 4 complications of Raynauds

A
  1. Digital Ulcers
  2. Digital Ischaemia
  3. Infection
  4. Gangrene
79
Q

In four steps, describe the pathophysiology of RA including the 2 main associated antibodies

A
  1. Self antigens become citrullinated and recognised by B and T cells which subsequently release RF and Anti CCP
  2. Macrophages and Fibroblasts become activated to release TNFalpha
  3. Infammatory cascade activated
  4. Synoviocytes proliferate, growing over articular cartilage, restricting nutrients and damagin cartilage
80
Q

typical history of RA

A
  • usually female
  • 30-50 yo
  • peripheral, progressive and symmetrical pain worsened by movement
  • > 6 week history
  • Morning stiffness>30 mins
  • Fatigue/malaise
81
Q

what is the S factor in RA?

A
  • swelling
  • stiffness
  • squeezing
82
Q

what is seen on examination of RA?

A
  • Soft tissue swelling - MCPs and wrists
  • Ulnar Deviation
  • Z Thumb
  • Rheumatoid Nodules (on elbows)
  • Carpal Tunnel
  • Swan Neck (DIPJ)
  • Boutonnieres (PIPJ)
  • small muscle wasting
  • 1st web space dipping
  • guttering between metacarpals
83
Q

what joints are commonly effected by RA?

A
  • wrist
  • MCP
  • PIPJ
  • elbow
  • shoulder
  • knee
84
Q

what investigations are done in suspected RA?

A
  • RF & ant-CCP
  • FBC - norocytic aneamia, WCC - septic arthritis
  • inflammatory markers - raised
  • x-ray - x ray changes in later stages of disease
  • PFTs and HRCT if chest involvement
85
Q

XRays can be used in later stages of RA, what would you see?

A
  • L - Loss of Joint Space
  • E - Erosions
  • S - Soft tissue swelling
  • S - Sublaxation
86
Q

Name a scoring system used for RA

A

ABCD

  • Joint Involvement
  • Serology
  • Acute Phase Reactants
  • Duration of Symptoms

>= 6 points = diagnostic of RA

87
Q

what is the treatment for RA?

A
  • initially DMARD monotherapy - methotrexate
    • early treatment
  • steroids acutely - PO or IM
  • symptom control with NSAIDs
  • biologics after combination DMARD therapy
  • non drug - OT, PT, podiatry, psychological
88
Q

When would you give Biologics in RA? Give 3 examples and their targets

A

When you have trialled atleast 2 DMARDs:

  • Infliximab (TNFalpha)
  • Rituximab (CD20)
  • Tocilizumab (IL6)
89
Q

Using the mnemonic CAPS, describe some extra-articular manifestations of Rheumatoid Arthritis

A
  • Carpal tunnel syndrome
  • CVD
  • Cord compression
  • Anaemia
  • Amyloidosis
  • Arteritis
  • Pericarditis
  • Pleural disease
  • Pulmonary disease
  • Sjogrens
  • Scleritis
  • Splenic anlargement
90
Q

What is Sjogren’s Syndrome?

A

Autoimmune inflammatory disorder characterised by diminished lacrimal and salivary gland secretion (lymphocytic infiltration and fibrosis of exocrine glands)

91
Q

What cancer does Sjogren’s Syndrome increase your risk of?

A

Non Hodgekin’s Lymphoma

92
Q

Using the mnemonic MADFRED, describe the signs and symptoms of Sjogrens

A
  • Myalgia
  • Arthralgia
  • Dry Mouth
  • Fatigue
  • Raynauds
  • Enlarged Parotids
  • Dry Mouth
93
Q

Name three investigations for Sjogren’s, and what a positive result would show.

A

Blood tests - Anti RO and anti LA antibodies (RF and anti-dsDNA may be seen)

Schirmer’s Test - Reduced tear volume

Salivary gland biopsy - Lymphocytic infiltration

94
Q

Management of Sjogren’s is normally conservative, give 3 examples

A

Avoid dry/smoky atmospheres

Artificial tears (hypromellose)

Artificial saliva

Skin emollients

Vaginal lubricants

95
Q

What is the risk with Anti RO antibodies in pregnancy?

A

Can cross placenta and cause heart block/foetal loss/neonatal lupus

96
Q

What are Spondyloarthropathies?

A

Group of conditions affecting spine and peripheral joints associated with HLA - B27 Includes: Ankylosing Spondylitis, Psoriatic Arthritis, Reactive Arthritis, Enteric Arthritis

97
Q

What is Ankylosing Spondylitis?

A

Chronic inflammation of spine and sacroiliac joint

98
Q

What is the ‘typical’ clinical picture of Ankylosing Spondylitis?

A
  • Man less than 30y/o Progressive back pain
  • Worse at night with morning stiffness, improving throughout the day
  • Reduced spinal movement and chest expansion
99
Q

What happens to the curves of the back with Ankylosing Spondylitis?

A

Loss of lumbar lordosis Increasing thoracic kyphosis Extreme cases - Q mark

100
Q

Using the 5A’s mnemonic, name the extra articular features of Ankylosing Spondylitis

A
  1. Anterior Uveitis
  2. Aortic Incompetence
  3. AV Block
  4. Apical Lung Fibrosis
  5. Amyloidosis
101
Q

Name two clinical tests and two radiological investigations for Ankylosing Spondylitis

A
  • Schober’s Test - mark 10cm above and 5cm below the PSIS and ask the patient to bend forward. In a normal patient this distance should increase to atleast 20cm
  • Forced external hip rotation - pain
  • MRI - Bone marrow oedema (more sensitive than X-ray)
  • XRay - Bamboo Spine
102
Q

What is the mainstay of treatment for Ankylosing Spondylitis?

A

NSAIDs and Physio

103
Q

What are the conditions for starting biologic therapy in Ankylosing Spondylitis? And what can be started?

A

Had to have tried 2 NSAIDs, for 6 weeks each

VAS>4 (Visual Analogue Scale)

BASDAI>4 (Bath Ankylosing Spondylitis Disease Activity Index)

TNF inhibitors, IL-17 inhibitors

104
Q

Describe the presentation of Psoriatic Arthritis

A

Oligoarthritis with Dactylitis (Sausage FIngers)

Can be symmetrical

10% pt with psoriasis

105
Q

how is psoriatic arthritis treated?

A
106
Q

What would imaging of Psoriatic Arthritis show in it’s early and late stages?

A

Early - joint erosions (USS or MRI)

Late - Pencil in a cup (XRay)

107
Q

What is Reactive Arthritis?

A

Arthritis occurs as a result of infection elsewhere in the body (eg post dysentry or post chlamydia)

108
Q

Describe the clinical presentation of Reactive Arthritis

A

Occurs 2d-2w post infection Involves conjunctivitis and urethritis (cant see cant pee cant bend at the knee)

other features - circinate balanitis, keratoderma blannorrhagica, conjunctivitis, uveitis, enthesitis

109
Q

How would you manage Reactive Arthritis?

A

Treat underlying infection

NSAIDs and joint injections

If not resolved in 2 years then consider DMARDs

110
Q

Describe the two types of Enteropathic Arthritis

A
  1. Oligoarticular, Asymmetric, Responds to flares
  2. Polyarticular, Symmetric, Doesn’t respond to flares
111
Q

How would you manage Enteropathic Arthritis?

A
  • Avoid NSAIDs (as they may precipitate an IBD flare)
  • Use Infliximab (as it can treat both the IBD and the Arthritis)
112
Q

Using the mnemonic IPAIN, describe the 5 classical features of inflammatory back pain

A
  • Insiduous Onset
  • Pain at night
  • Age of onset<40
  • Improved by exercise
  • No improvement with rest
113
Q

Describe the pathophysiology of SLE

A

Inadequate supression of T cells, and excessive B cell activity (along with production of antibodies against certain nuclear components)

114
Q

Using the mnemonic SOAP BRAIN describe the signs and symptoms of SLE

A
  • Serositis
  • Oral Ulcers
  • Arthritis
  • Photosensitivity - malar or discoid rash
  • Blood disorders (lymphopenia)
  • Renal involvement (glomerulonephritis)
  • Autoantibodies
  • Immunulogic tests (low C3 and C4)
  • Neurologic Disorders (seizures, psychosis)
115
Q

What 3 investigations would you do with a blood sample for SLE?

A
  • Anti DsDNA titres (1:1600 - have to dilute 1600 times before undectable)
  • Low C3 and C4
  • Raised ESR and PV
116
Q

Why is sun protection especially important in SLE?

A

UV alters the DNA making it more immunogenic

117
Q

What medication would be used for the rash and arthralgia in SLE?

A

Hydroxychloroquine

118
Q

what treatment is used for SLE?

A
  • sun protection
  • advice on healthy living - increased cardiovascular risk
  • mydroxychloroquine - rash and arthralgia
  • mycophenolate mofetil, azothioprine and rituximab
  • short course prednisolone for flares
119
Q

Why is SLE more common in Women?

A

Oestrogen promotes autoimmunity by prolonging life of autoreactive B and T cells

120
Q

Describe the pathophysiology of Systemic Sclerosis (AKA Scleroderma)

A

Increased fibroblast activity resulting in abnormal CT growth, fibrosis and vascular damage 90% ANA positive

121
Q

Describe the presentation of LIMITED Scleroderma

A

CREST

Calcinosis Cutis

Raynauds Phenomenon

Esophageal Dysmotility

Sclerodactyly

Telangiectasia

Pulmonary HTN

122
Q

Describe the presentation of DIFFUSE Scleroderma

A

Sudden onset skin involvement proximal to elbows and knees

123
Q

What would you expect to find when testing the serum of a Systemic Sclerosis patient?

A
  • Normal inflammatory markers
  • +ve Anti Centromere antibodies in Limited
  • Scl-70 and anti RNA polymerase iii in diffuse
124
Q

How would you manage Systemic Sclerosis?

A

No cure - Psychological support

Nifedipine - Raynauds

Skin thickening - Methotrexate and Mycophenolate

ACE i to prevent hypertensive crisis

short course prednisolone for flares

PPI gi symptoms

125
Q

What is a Morphea?

A

Localised Scleroderma

126
Q

State the four subtypes of small vessel vasculitis and their respective markers

A
  • Granulomatosis with Polyangitis (c-ANCA)
  • Microscopic Polyangitis (p-ANCA)
  • Eosinophilic Granulomatosis (p-ANCA)
  • IgA Vasculitis (IgA)
127
Q

State two subtypes of medium vessel vasculitis

A

Polyarteritis Nodosa

Kawasaki

128
Q

Describe two subtypes of large vessel vasculitis

A

GCA

Takayasu Arteritis

129
Q

Describe four skin changes you might see in Vasculitis

A
  • Palpable Purpura
  • Digital Ulcers
  • Gangrene
  • Nail Bed Capillary Changes
130
Q

Some ocular changes you might see in Vascultiis include: Scleritis, Uveitis and Episcleritis. How would these present?

A

Scleritis - Pain and photophobia

Uveitis - Photophobia

Episcleritis - Red and watery

131
Q

What might be mistaken for vasculitis?

A

Atrial Myxoma (benign tumour in atria)

132
Q

Describe the first and second line treatment of Vasculitis

A

1) Corticosteroids
2) DMARDs

133
Q

Name 4 Seronegative Spondyloarthropathies, using the mnemonic PEAR

A
  • Psoriatic Arthritis
  • Enteropathic Arthritis
  • Ankylosing Spondylitis
  • Reactive Arthritis
134
Q

What is Polyarteritis Nodosa?

A

Necrotising vascularise affecting small and medium size vessels

Not associated with ANCA

135
Q

What is Polyarteritis Nodosa associated with?

A

Hep B

136
Q

How would Polyarteritis Nodosa present?

A

Mononeuritis Multiplex Purpura/Subcut nodules/ Ulcers Post Prandial Abdo Pain (MI)

137
Q

How is Polyarteritis Nodosa treated?

A

Steroids +/- Azathioprine or Cyclophosphamide

138
Q
A

Year 3 Medicine (15 decks)

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