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Medicine block > Rheumatology medicine block > Flashcards

Rheumatology medicine block Flashcards

1
Q

What is the pathogenesis of rheumatoid arthritis?

A
  • Ab to RF and anti CCP
  • Activate macrophages = TNFa which stimulates inflam cascade
  • Proliferation of synoviocytes = on cartilage, restrict nutrients and cause damage
  • Increased osteoclast differentiation so more bone damage
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2
Q

Describe the typical history of RA

A
  • Female, 30-50
  • Progressive, peripheral, symmetrical arthritis
  • > 6 weeks morning stiffness more than 30 mins
  • Also malaise and fatigue
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3
Q

What joints are affected in RA?

A

Any joint can be affected but usually PIPs, MCPs and MTPs w DIPs usually spared

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4
Q

What are the findings on examination of someone with RA?

A
  • Soft tissue swelling and tenderness
  • Swan neck and Boutonniere’s deformity
  • Rheumatoid nodules, most commonly on elbow - aggressive disease, +ve RF Ab
  • Z thumb
  • PIPJ synovitis
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5
Q

Draw the difference between swan neck and Boutonniere’s deformity

A

Answers on ipad

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6
Q

What are the Ix in RA?

A
  • RF and anti CCP Ab (this is more specific than RF)
  • FBC = normocytic anaemia due to ACD
  • Increased inflam markers
  • XR changes in established disease
  • PFTs if pulm fibrosis
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7
Q

What is the treatment of RA?

A
  • DMARD therapy, start w methotrexate
  • In severe disease use combination DMARD eg. + sulfasalazine or hydrochloroquine
  • NSAIDs for sx control w PPI cover
  • If DMARD combination not working try biologicals eg. anti TNFs
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8
Q

What are the extra articular manifestations of RA?

A
  • 3Cs - CVD, CTS, cord compression
  • 3Ps - pleural disease, pulm disease, pericarditis
  • 3As - anaemia, amylordosis, arteritis
  • 3Ss - Sjogren’s, scleritis, splenomegaly
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9
Q

What is Felty’s syndrome?

A

Splenomegaly + neutropenia + RA

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10
Q

What are the XR features of RA?

A

Loss of joint space
Erosions
Soft tissue swelling
Subluxation

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11
Q

What is giant cell arteritis?

A

Chronic vasculitis of med and large vessels originating off the arch of the aorta.
Age is the biggest RF, pt almost always >50.

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12
Q

What are the arteries that originate from the arch of the aorta?

A
  • Brachiocephalic artery = R common carotid and R subclavian
  • L common carotid
  • L subclavian
    Go to supply the head and arms.
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13
Q

What are the symptoms of GCA?

A
  • Headache = localised, over temples, unilateral
  • Jaw and tongue claudication, pain eating and talking
  • Visual disturb = amourosis fugax, diplopia, blind due to occlusion of artery = AION
  • Scalp tenderness over temporal artery
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14
Q

What is AION?

A

Ant ischaemic optic neuropathy

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15
Q

What is the diagnostic criteria for GCA?

A

> 50 yo pt w 2 or more of the following:

  • Raised inflam markers
  • Tenderness/reduced pulsation in temporal artery
  • New onset headache or visual symptoms
  • Biopsy shows necrotising arteritis
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16
Q

How do you treat GCA?

A
  • Prednisolone 60-100mg OD for 2 weeks and then consider reducing
  • IV methyprednisolone for 1-3 days for acute visual sx
  • Baby aspirin to avoid thrombotic events
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17
Q

What is polymyalgia rheumatica?

A

Pain and stiffness in the shoulder, hip and neck in the elderly, presentation normally at 70-80yo.
Is associated w morning stiffness, raised inflam markers and GCA.

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18
Q

How do you diagnose polymyalgia rheumatica?

A
  • Typical hx and exam + raised inflam markers

- Can do a temporal artery biopsy if sx of GCA

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19
Q

What is the typical hx of a pt w polymyalgia rheumatica?

A
  • Sudden onset proximal joint pain and stiffness
  • Difficulty rising from a chair and brushing hair
  • Night time pain
  • 25% of pt have systemic sx
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20
Q

What can you find on examination in polymyalgia rheumatica?

A
  • Reduced ROM in shoulders, neck and hips

- Normal muscle strength but tenderness

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21
Q

How do you treat polymyalgia rheumatica?

A

Has a dramatic response within 5 days to prednisolone, 15 mg OD.
Then taper it down slowly, too quick = relapse.
Can use methotrexate for steroid sparing in a relapsing pt.

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22
Q

What are spondyloarthropathies?

A

Conditions that affect the spine and peripheral joints w an association w HLA-B27.

  • Psoriatic arthritis
  • Ankylosing spondylitis
  • Reactive arthritis
  • Enteropathic arthritis
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23
Q

What are the common clinical features of all spondyloarthropathies?

A
  • Sacro iliac/axial disease = back and buttock pain
  • Inflam arthopathy of peripheral joints
  • Enethesis - inflam of tendon insertions
  • Extra articular features
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24
Q

What is the presentation of ankylosing spondylitis?

A

Younger man, pain in chest wall, thorax and bilateral buttocks

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25
Q

Ankylosing spondylitis:

  • Exam
  • Ix
  • Treatment
A

Exam - often normal but later on = thoracic kyphosis, reduced chest expansion and Schober’s test
IX - MRI spine and SI joints, raised CRP
Treatments - NSAIDs, physio, TNF inhib, IL-17 inhib

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26
Q

Psoriatic arthritis:

  • Exam
  • Ix
  • Treatment
A

Exam - oligoarthritis, dactylitis = sausage digits, 10% of psoriasis pt, nail pitting
Ix - raised CRP, central joint erosion on MRI
Treatment - NSAIDs, DMARDs, TNF inhib, IL-17 inhib

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27
Q

What is the clinical hx of a pt w reactive arthritis?

A

Sterile synovitis following colitis, urethritis, cervicitis. Normally a few days-2 weeks after infection develop acute asymmetrical lower limb arthritis.

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28
Q

Reactive arthritis:

  • Exam
  • Ix
  • Treatment
A

Exam - keratoderma blenorrhagica
Ix - serology, microbiology, raised CRP, joint aspiration to exclude septic/crystal arthritis
Treatment - treat infection, NSAIDs, joint infection, if doesn’t resolve w/i 2 years = DMARDs

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29
Q

What is the history of enteropathic arthritis and the types?

A

Hx = 10-20% of pt w IBD get arthropathy.
Type 1 - oligoarthritis, asymmetrical, correlates w IBD flares
Type 2 - polyarthritis, symmetrical, doesn’t correlate w flares

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30
Q

How do you treat enteropathic arthritis?

A

Don’t use NSAIDs as they cause flares. TNF inhib treat IBD and arthritis, can used DMARDs.

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31
Q

What are the common signs and symptoms of lupus?

A 
A RaSH POINts Medical Dx:
Arthritis
Renal abnorm
Serositis
Haem abnorm
Photosensitivity
Oral ulcers
Immunological abnorm
Neuro abnorm
Malar/discoid rash
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32
Q

What is SLE?

A

Systemic Lupus Erythematous - autoimmune disease due to inadequate T cell suppressor activity w increased B cell activity. Is a multi system disease w variable presentation. Remission and flares disease.

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33
Q

What are the Ix into SLE?

A
  • ANA +ve = serology
  • Raised ESR and plasma viscosity
  • FBC = anaemia + leukopenia v common
  • Urinanalysis to see if renal disease
  • Diagnostic skin and renal biopsy
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34
Q

What is the treatment of SLE?

A
  • Sun protection and advise on healthy lifestyle and reduction of CVS RF
  • Hydroxychloroquine for rash and arthritis
  • Short course of prednisolone for flares
  • Can also add myeophenolate mofetil, azathioprine and rituximab
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35
Q

What does subluxation mean?

A

Partial dislocation

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36
Q

What is Raynaud’s phenomenon? How does it differ to Raynaud’s syndrome?

A

Vasospasm of the digits = pain and colour change in response to cold stimulus, often in times of stress:
- White = reduced blood flow
- Blue = venous stasis
- Red = re warming hyperaemia
Syndrome - idiopathic in young women, phenomenon = underlying disease, over 30 yo.

37
Q

What are the patterns of episodes in Raynaud’s phenomenon and syndrome?

A

Syndrome - min long, symmetrical, bilateral

Phenomenon - hours long, asymmetrical, affect few digits

38
Q

What points to a rheumatic cause of RP?

A
  • Abnormal nail fold capillaries
  • Puffy fingers
  • Photosensitive rash
39
Q

What are the diseases RP is associated with?

A
  • Scleroderma
  • SLE
  • Sjogren’s
  • Polymyositis, dermomyositis
40
Q

What are the physical and drug causes of RP?

A

Physical - cervical rib, cryoglobulinaemia, use of vibration tools
Drug - B blockers

41
Q

How is RP treated?

A
  • Advise to stop smoking and keep warm

- 1st line = CCB then phosphodiesterase 5 inhib

42
Q

What are the complications of RP?

A
  • Digital ulcer
  • Infection
  • Severe digital ischaemia
43
Q

What is the pathophysiology in vasculitis?

A

Inflam blood vessel disorder = damange to vessel wall = thrombosis = iscahemia and bleeding +/- aneurysm

44
Q

What are the glove and sweater questions for taking a hx in vasculitis?

A
  • Raynaud’s, nose bleed, ulcers
  • MSK - arthralgia, myalgia, proximal muscle weak
  • CNS - headaches, visual loss, stroke, tinnitus, seizures
  • Heart + lung - pericarditis, cough, chest pain, haemopytsis, SOB
  • Abdo pain, haematuria, neuropathy, digital ischaemia
45
Q

What are you looking for on exam in vasculitis?

A
  • General exam - BP, pulsem also look for normal findings on cardio, resp and abdo
  • Skin - palpable purpura, livedo reticularis, digital ulcer, nodules, gangrene, nail bed changes
  • Neuro - CN exam, sensorimotor exam
  • Eyes - ocular fields, scleritis, uvetitis
46
Q

What is livedo reticularis?

A

Skin symptom - redish blue web on skin, normally legs, can get worse when cold

47
Q

What are the primary vasculitides?

A
  • Small vessel = micropolyangitis, MPA
  • Med vessel = Kawasaki disease
  • Large vessel = giant cell arteritis, GCA
48
Q

What are the secondary causes of vasculitis?

A

Secondary causes - drugs, malignancy, infection, connective tissue disorders

49
Q

What are the ix into vasculitis?

A
  • Bloods - FBC, U&E, LFT, CRP, ESR
  • Serology - ANA, RF, cryoglobulins
  • Screen Hep B/C, HIV
  • CT, CXR, MRI, PET, angiography
50
Q

What is the treatment of vasculitis?

A
  • Rule out infection and stop secondary cause drugs
  • 1st line - corticosteroids
  • 2nd line - cytotoxic meds or biologicals
51
Q

What is systemic sclerosis? What are the 2 different types?

A

Multi system autoimmune disease, previously known as scleroderma.
Increased fibroblasts = abnormal connective tissue = vascular damage and fibrosis.
1. limited SSc - skin tightness distal to elbow/knee
2. diffuse SSc

52
Q

What are the signs and symptoms of limited SSc/scleroderma?

A

CREST:
Calcinosis cutis - Ca2+ deposits in the skin
Raynaud’s phenomenon
Eoseophageal dysmotility
Sclerodactyly - thickening/tight of the skin
Telangiectasia

53
Q

What are the signs and symptoms of diffuse SSc/scleroderma?

A

Much less common but a higher risk of mortality = sudden onset skin involvement proximal to the elbow and knees

54
Q

What are the ix into SSc/scleroderma?

A
  • Normal inflam markers
  • XR hands = calcinosis
  • CXR + PFT if pulm disease
  • +ve ANA
  • ECG, ECHO = HTN, HF, arrhythmia
55
Q

What are the Ab that suggest limited SSc and what are the Ab that suggest diffuse?

A

Limited - anti centromere Ab

Diffuse - anti RNA polymerase or anti topoisomerase

56
Q

What is the treatment for SSc/scleroderma?

A

No cure, have to treat symptoms and psychological support may be needed:

  • CCB for Raynaud’s
  • Methotrexate/mycophenolate mofetil to reduce skin thickening
  • ACEi to prevent HTN crisis and reduce mortality
  • Short courses prednisolone for flares
  • PPI for GI sx
57
Q

What are the common signs and sx of Sjogren’s?

A 
MADFRED
Myalgia
Arthralgia
Dry mouth
Fatigue
Raynaud's phenomenon
Enlarged parotids
Dry eyes
58
Q

What are the ix of Sjogren’s?

A
  • Salivary gland biopsy
  • Anti Ro and anti La Ab in 90% of people
  • Schirmer’s test = measures tear vol
59
Q

What is the treatment of Sjogren’s?

A
  • Dry eyes = artificial tears - hydromellose
  • Dry mouth = artificial saliva, sugar free gym/gummies
  • Skin emollient, lube
  • Avoid smokey/dry atmospheres
60
Q

What is hypermobility spectrum disorder?

A

Pain syndrome that results in joints moving excessively due to lax ligaments, capsules and tendons. Pain usually caused by microtrauma.

61
Q

Who does hypermobility affect?

A
  • 10% of the population but most are asymptomatic
  • Presents in childhood and adulthood
  • Subluxation and dislocations recurrent
62
Q

What are the signs and sx of hypermobility?

A
  • Pain around joints worse after activity, can be generalised
  • Soft tissue rheumatism
  • Myopia, abnormal skin, drooping eyes
  • Rectal prolapse and hernias
  • Arachnodactylyl
63
Q

What is the treatment of hypermobility?

A
  • No evidence for pharmacology except paracetamol for pain
  • Strengthening exercises to reduce subluxation
  • Posture and balance training
  • Specialist pain mangement
  • Splinting and surgical intervention
64
Q

What is the score used in hypermobility?

A

Beighton’s score

65
Q

What is fibromyalgia?

A

Disorder of central pain processing = chronic widespread pain in all 4 quadrants of the body. Most have allodynia.

66
Q

What is allodynia?

A

Heightened and painful response to harmless stimuli

67
Q

What is the underlying pathophysiology of fibromyalgia?

A

Induced by sleep deprivation = reduced REM sleep and increased D wave.
Neural activation in the pain processing area of the brain in response to non painful stimuli and increase activation in painful stimuli.

68
Q

What are the signs and symptoms of fibromyalgia?

A
  • Pain and numbness
  • Depression and anxiety
  • Joint pain and stiffness
  • IBD, irritable bladder
  • Unrefreshing sleep, fatigue, headaches
  • Poor concentration and memory
  • No signs on exam but may have ‘tender points’
69
Q

What are the RF and demographics of fibromyalgia?

A
  • Female:male = 9:1
  • Onset ~ 40-50
  • 5% of the population affected
  • Triggered eg. emotional or physical like painful arthritits
70
Q

What is the treatment of fibromyalgia?

A
  • Pt improves w an explanation of their sx and measures to improve sleep and activity level
  • Low dose amitriptyline or pregabalin
  • CBT
71
Q

What is amitriptyline?

A

Tricyclic antidepressant used to treat neuropathic pain and depression. Makes pt sleepy so take at night. Blocks reuptake of NA and serotonin.

72
Q

What are the non modifiable risk factors of osteoporosis?

A
  • Age
  • Female
  • FH
  • Caucasian/SA
  • Hx low trauma fractures
73
Q

What are the modifiable RF of OP?

A
  • Smoking
  • Excess alcohol intake
  • Low levels of activity
  • Ca2+/Vit D deficiency
  • Premature menopause
  • Low BMI
  • Iatrogenic eg. corticosteroids
74
Q

How do you make a diagnosis of OP?

A
  • DEXA of lumbar spine and hips = gold standards

- T score

75
Q

What is the treatment of osteopenia?

A
  • Increase weight bearing exercise
  • Vit D supplement
  • Reduce alcohol and stop smoking
  • Increase Ca2+ intake
76
Q

What is the treatment of OP?

A
  • Vit D +/- Ca2+ supplement
  • 1st line = bisphosphonates eg.aldendronic acid = always coprescribe the supplements, take on empty stomach SE - reflux
  • 2nd line = denosumab
77
Q

What is gout and what is the pathophysiology?

A
  • Inflam arthritis related to hyperuricaemia
  • Can affect >1 joint but most commonly 1st MTP
  • Deposition of MSU crystals which accumulate in joint and soft tissue = arthritis, tophi, urate nephropathy, uric acid nephrolithiasis
  • Associated w increased risk CVD
78
Q

What are the non modifiable and modifiable RF of gout?

A 
Non modifiable = age+men
Modifiable:
- Drinking beer
- Smoking, HTN, DM
- Obesity, high fructose, lots of meat and seafood
- CHF, CAD, increased lipids
- Renal disease
- Organ transplant
79
Q

What is the conservative management of gout?

A

General prevention - good weight, reg exercise, reduce alcohol, stop smoking avoid dehydration

80
Q

What is the pharmacological management of gout?

A
  • 1st line = NSAIDs, steroids, colchicine
  • Urate lowering therapy eg. allopurinol + febuxostat
  • Benxbromarone increased renal excretion of uric acid
81
Q

What are the drug treatments used in rheumatology?

A
  • NSAIDs
  • Corticosteroids
  • DMARDs
  • Biologicals
  • Drugs for OP
  • Drugs for crystal arthritis
82
Q

Describe NSAID usage in rheum

A
  • Initial therapy and sx relief
  • SE = GI prob, renal impairment
  • Short term but long term w PPI cover
83
Q

Describe corticosteroid usage in rheum

A

For inflam arthritis used for few weeks and then reduced when DMARDs kick in. Have SE so used low dose and short as possible.
Mainstay for PMR and GCA.

84
Q

Describe DMARDs in rheum

A
  • Methotrexate, hydroxychloroquine and sulfasalazine = most common.
  • Used in RA, PsA, SLE, vasculitis.
  • SE - bone marrow suppression, hepatitis, GI upset, rash.
85
Q

Describe biologicals in rheum

A
  • Monoclonal Ab
  • Used in RA, PsA, AS, psoriasis, IBD
  • TNFa inhib
  • Rituximab - RA
  • IL-17 antagonists - AS, PsA
  • JAK kinas inhib - RA, PsA
  • SE = increased risk infection, theoretical malignancy risk, reactivation hep B and TB so screen and vaccinate
86
Q

What DMARD causes anaemia?

A

Methotrexate - causes folic acid suppression = macrocytic anaemia

87
Q

What is a common side effect of bisphosphonates?

A

Dyspepsia

88
Q

Gout vs pseudogout

A

Gout - needle shaped negatively birefringent, uric acid or monosodium urate, big toe more commonly
Pseudo gout - rhomboid shaped positively birefringent, calcium pyrophosphate, knee more commonly

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