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Year 3 Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Which seronegative spondylarthrioathies is most likely to cause enthesitis (inflammation of the joint capsules, tendons and ligaments join into the bone)?

A

Ankylosing spondylitis

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2
Q

What is the classical triad of primary Sjorgen syndrome?

A

Dry mucosa
Fatigue
Joint pain
(Active arthritis may be seen but arthralgia is more common)

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3
Q

Arthralgia VS arthritis?

A

In the strictest sense, arthralgia simply refers to joint pain. Arthritis is inflammation in the joints, which also causes symptoms such as pain and stiffness.

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4
Q

How is temporal arteritis diagnosed?

A

Biopsy, showing features of inflammation of which are typical of giant cell arteritis.
Normal biopsy does not r/o - skip lesions, suboptimal sample

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5
Q

What are the clinical features of polymyositis?

A

Proximal muscle weakness and pain
No skin involement
As disease progresses, and other muscles become involved:
Pharangeal or oesophageal muscles leading to dysphonia and dysphagia
Respiratory muscles can lead to poor ventilation with type 2 respiratory failure

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6
Q

What will be seen on biopsy of muscle affected by polymyositis (gold standard diagnostic investigation)?

A

Endomysial inflammatory infiltrates

Muscle necrosis and atrophy

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7
Q

What score is used to measure disease activity in RA?

A

DAS-28
Doctor looks at 28 joints to decide if they are tender or swollen
A patient global health assessment from 0 to 100
ESR and CRP can be added into the formula
Low score indicated remission, higher score suggests patient has more active disease

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8
Q

Bechet’s disease symptoms/features?

A

CT changes of an acute venous sinus thrombosis, on a background of recalcitrant oral ucleration
Recurrent ocular events (relapising anterior uveitis)
Genital ulceration may provide further support for the diagnosis

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9
Q

Features of anti-phospholipid syndrome?

A

Commonly occurs secondary to SLE
Causes arterial and vebous thromboembolism, thrombocytopenia and livedo reticularis (a mottled, lace-like appearence on the legs)

One or more of the follow positive blood tests on more than two ocassions, more than two weeks apart required to diagnose APS:

  1. Anti-cardiolipin antibodies
  2. Anti-beta 2-GPI antibodies
  3. Positive lupus anticoagulant assay
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10
Q

How does methotrexate work?

A

Folate antagonist, binds to dihydrofolate reductase impairing the synthesis of DNA and therefore cell replication (therefore common side effect is folic acid deficiency and subsequently a macrocytic anaemia)

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11
Q

How does cerebral lupus present?

A

Unremitting headache
Psychosis
Features of active lupus (prominent rash, raised ESR, low complement levels)

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12
Q

What is CREST syndrome?

A

Limited cutaneous form of systemic sclerosis
Calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia (dilation of capillaries causing red marks on the skin)
Pulmonary hypertension presenting as right sided heart failure is a well known complication of systemic sclerosis associated with CREST syndrome subtype of systemic sclerosis

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13
Q

What lung complication does diffuse cutaneous SSc tend to cause?

A

Pulmonary fibrosis

as opposed to pulmonary HTN in limited SSc

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14
Q

How should you monitor for pulmonary HTN in systemic sclerosis?

A

Echocardiogram or diffusing capactiy on spirometery

Can be confirmed with right heart catherisation

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15
Q

What conditions is anterior uveitis associated with?

A

Associated with HLA-B7

Autoimmune disease: IBD, ankylosing spondylitis, reactive arthritis, Betchet’s disease

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16
Q

What is uveitis?

A

Inflammation of the anterior portion of the uvea, which includes the iris and ciliary body.
Patients present with a red and painful eye +/- photophobia, blurred vision, lacrimation and a hypopyon (inflammatory cells in the anterior chamber)

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17
Q

How do patients with reactive arthritis tend to present?

A

Dysuria
Iritis/conjunctivitis
Arthralgia

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18
Q

Pathophysiology of RA?

A

Citrullination of self antigens which are then recognised by T and B cells which then produce antibodies (rheumatoid factor (Fc portion of IgG), anti-CCP).
Stimulated macrophages and fibroblasts release TNFalpha.
Inflammatory cascade leads to proliferation of synoviocytes (boggy swelling)
These grow over the cartilage and lead to restriction of nutrients and cartillage is damaged.
Activated macrophages stimulate osteoclast differentiation contributing to bone damage.

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19
Q

Typical history for RA?

A 
Female (3:1)
30-50 years
Presents with progressive, peripheral and symmetrical polyarthritis.
Affects MCPs/PIPs/MTPs
Spares DIPs
History of > 6 weeks
Morning stiffness >30 mins duration
Commonly c/o fatigue/malaise
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20
Q

What may be seen on examination of a patient with RA?

A

Soft tissue swelling and tenderness
Ulnar deviation/ Palmar sublucation of MCPs
Swan neck and Boutonniere deformity to digits
Rheumatoid nodules
Check median nerve for carpal tunnel association

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21
Q

Investigations for RA?

A 
Rheumatoid factor
Anti-CCP antibodies
FBC (normocytic anaemia of chronic disease)
WCC if concerned about septic arthritis
ESR/CRP - elevated 
X-ray changes (established disease)
USS/MRI (early disease)
PFTs HRCT if chest and lung involvement (e.g. pulmonary fibrosis)
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22
Q

How does (progressed) RA appear on an X ray?

A

Loss of joint space
Erosions (periarticular)
Soft tissue swelling
Subluxation

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23
Q

Treatment of RA?

A

Initially DMARD monotherapy (methotrexate)
Combination DMARDs (leflunomide, hydroychloroquine, sulfasalazine)
Steroids (actutely) - PO/IM or intra articular
Symptom control with NSAIDs + PPI cover
If still severe after combination DMARDs, biologics (anti-TNFs such as entanercept)
OT/PT podiatry psychological

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24
Q

Extra-articular manifestations of RA?

A

3Cs - Carpal tunnel syndrome, elevated Cardiac risk (CVD), Cord compression (atlanto-axial subluxation)
3As- Anaemia (normochromic & normocytic), Amyloidosis (rare, can cause nephrotic syndrome and CKD), Arteritis (rare)
3Ps - Pericarditis (uncommon), Pleural disease (common), Pulmonary disease (common) e.g. bronchiectasis, bronchiolitis obliterans fibrosis
3Ss - Sjogren’s (common), Scleritis/episcleritis (uncommon), Splenic enlargement (together with neutropaenia = Felty’s syndrome, rare)

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25
Q

What is Giant cell arteritis and who is affected?

A

Chronic vasculitis of the large and medium sized vessels
Occurs among individuals over 50 years of age
Median age of onset is 72
Most commonly causes inflammation of arteries originating from the arch of the aorta
Occlusive arteries can result in anterior ischemic optic neuropathy
Visual symptoms are an opthalmic emergency
Inflammation of arteries supplying the muscles of mastication results in jaw claudication and tongue discomfort
GCA may present as CVA

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26
Q

Risk factors for GCA?

A 
Increasing age
2-4 more times common in women
Caucasion
Strong association with PMR
Genetic predisposition - HLA-DRA
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27
Q

How does GCA present?

A

Headache: localised, unilateral, boring, lancinating in quality over the temple
Tounge or jaw claudication upon mastication
Constitutional symptoms
Visual symptoms (may develop weeks to months following the other symptoms): amaurosis fugax, blindness, diplopia and blurring
Scalp tenderness, especially over the temporal artery

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28
Q

How is GCA diagnosed?

A

Presence of 2 or more in patients over 50 years:
Raised ESR, CRP, or PV
New onset of localized headache
Tenderness or decreased pulsation of temporal artery
New visual symptoms
Biopsy revealing necrotizing arteritis

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29
Q

How is GCA treated

A

60-100mg prednisolone PO per day for at least 2 weeks, then consider tapering down
Methylprednisolone IV pulse therapy (1g) for 1-3 days IF ACUTE ONSET SYMPTOMS
Low dose asprin therapy to reduce thrombotic risks

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30
Q

Most common complication of GCA?

A

Permanent visual loss

20-50% of patients go blind if untreated

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31
Q

What is Polymyalgia Rheumatica?

A

Clinical syndrome characterized by pain and stiffness of the shoulder, hip girdles, and neck. Patients may use the term stiffness and pain interchangeably,
Primary impacts the elderly
Associated with morning stiffness
Elevated inflammatory markers

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32
Q

How is affected by PMR?

A

70-80 years
Very rare under 50
Association with GCA

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33
Q

Symptoms of PMR?

A

New sudden onset proximal limb pain and stiffness (neck, shoulders, hip)
Night time pain
Systemic symptoms (25%) fatigue, weight loss, low-grade fever
Difficulty rising from chair, combining hair (proximal muscle involvement)

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34
Q

How might the physical examination of a patient with PMR be?

A

Decreased ROM of shoulders, neck and hips
Muscle strength is usually normal - may be limited by pain/stiffness
Muscle tenderness

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35
Q

How is PMR diagnosed?

A

Examination
ESR or PV, CRP - will almost always be raised, although not proportional to severity of the symptoms
Consider temporal artery biopsy if symptoms of GCA
Dramatic response within 5 days of starting prednisolone

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36
Q

What other conditions may present with PMR symtpoms?

A

Cancer

RA

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37
Q

Treatment of PMR?

A

15mg of prednisolone daily, taper down slowly. Most patients require 18 months of treatment.
In relapsing patients methotrexate can be steroid-sparing

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38
Q

What is the presence of HLA-B27 associated with?

A

Spondyloarthropathies

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39
Q

What are the spondyloarthropathies?

A

Ankylosing spondylitis (most common)
Enteropathic arthritis
Psoratic arthritis
Reactive arthritis

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40
Q

Common clinical features of the spondyloarthropathies?

A

Sacroiliac/axial disease - back/buttock pain
Inflammatory arthopathy of peripheral joints
Enthesitis (inflammation at tendon insertions)
Extra-articular features (skin/gut/eye)

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41
Q

Ankylosing spondylitis clincal features

A

Usually presents in young men (teens to mid therties)
Presentation with bilateral buttock pain, chest wall and thoracic pain
Examination is often normal, loss of lumbor lordosis in later disease
Exaggerated thoracic kyphosis in later disease
Positive Schober’s test in later disease
Reduced chest expanison in later disease
Raised or normal CRP

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42
Q

How would you investigate Ankylosing Spndylitis?

A

CRP (may be normal)
MRI spine and SI joints
HLA-B27

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43
Q

How is ankylosing spondylitis managed?

A

NSAIDs
Physio
TNF inhibitors (e.g. infliximab)
IL-17 inhibitors (brodalumab,

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44
Q

Clinical features of psoriatic arthritis?

A

Psoriasis
Oligo-arthritis with dactylitis (sausage digit)
Symetrical or mono-arthritis
Severe disease: arthritis mutilans
Central erosions seen on USS or MRI, leading to pencil in cup x-ray appearence

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45
Q

How is psoriatic arthritis managed?

A 
NSAIDs
DMARDs
TNF inhibitors 
IL-17 inhibitors
IL 12/23 inhibitors
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46
Q

When does reactive arthritis occur?

A

Distant infection
Post dysentery (Salmonella/Shigella/Campylobacter)
Urethritis/cervicitis (Chlaymidya trachomatis)

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47
Q

How long after infection dose reactive arthritis occur?

A

Days-2 weeks post infection

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48
Q

What is reactive arthritis?

A

Sterile synovitis developing after a distant infection

Acute asymmetrical lower limb arthritis

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49
Q

Extra-articular features of reactive arthritis?

A

Skin: circinate balanitis, keratoderma blennorrhagica
Eye: conjunctivitis, uveitis
MSK: enthesitis
Urogential: urethritis

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50
Q

What investigations should be undertaken in suspected reactive arthritis?

A

Serology/microbiology
Raised inflammatory markers
Join asp to rule out septic arthritis/gout
HLA-B27

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51
Q

How should reactive arthritis be treated?

A

Treat underlying infection (this may not improve arthritis)
NSAIDs, joint injections
If not resolved in 2 years (most will) may need DMARDs

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52
Q

What is type 1 peripheral enteropathic arthritis?

A

Oligoarticular, asymmetric and has a correlation with IBD flares

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53
Q

What is type 2 peripheral enteropathic arthritis?

A

Polyarticular symettrical and has less correlation with IBD flares

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54
Q

10-20% of patients with IBD develop arthropathy. Which is more common, peripheral arthritis or axial disease?

A

Peripheral arthritis

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55
Q

What treatment should be considered in enteropathic arthritis?

A 
Consider DMARDs (NSAIDs may flare IBD)
TNF inhibitors will treat IBD and arthritis
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56
Q

Extra-articular manifestations of Ankylosing spondylitis?

A 
Anterior uveitis 
Aortic incompetence
AV block
Apical lung fibrosis
Amyloidosis
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57
Q

Features of inflammatory back pain?

A 
Insidious onset
Pain at night (improves on getting up)
Age at onset <40
Improvement with exercise
No improvement with rest
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58
Q

What is lupus?

A

Autoimmune disease
Inadequate T cell supressor activity with increased B cell activity
Most patients have antibodies to certain cell nucleus components
Complex multisystem disease with variable presentations
Characterized by remissions and flares
Can be famillial

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59
Q

Common signs and symptoms of SLE?

A

Serositis (pleurisy, pericarditis)
Oral ulcers, usually painless, palate is most specific
Arthritis - small joints, non errosive
Photosensitivity
Blood disorders: low WCC, lymphopenia, thrombocytopenia, haemolytic anemia
Renal invovlement - glomerularnephritis
Autoantibodies (90% of cases ANA +)
Immunologic tests e.g. low complements
Neurologic disorders - seizures, psychosis

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60
Q

What blood test abnormalities may be present in patients with SLE?

A

Most patients will have a raised ESR or plasma viscosity
Anaemia and leukopenia
ANA positive (90%)
Anti-Ro, Anti-La are common
Anti-dsDNA (rises with disease activity)
Maybe be antiphospholipid antibodies (these increase the risk of pregnancy loss and thrombosis)
C3 and C4 fall with disease activity

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61
Q

What can be used to monitor SLE?

A

Anti-dsDNA - titre rises with disease activity
C3 and C4 - both fall with disease activity
Urinalysis for detecting renal disease
Renal biopsy- diagnosis and prognosis
Skin biopsy - can be diagnostic

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62
Q

How is SLE treated?

A

Sun protection
Lifestyle risk reduction of CVD
Hydroxychloroquine is helpful for rash and arthralgia
Mycophenolate mofetil, azathioprine and rituximab are commonly used
Short courses of prednisolone for flares

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63
Q

When is the peak onset of SLE?

A

Early adulthood

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64
Q

Why is lupus 9x more common in women?

A

Estrogens are thought to be permissive for autoimmunity.

Estradiol may prolong the life of autoreactive B and T lymphocytes

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65
Q

How does UV light rigger SLE?

A

Alters the structure of DNA in the dermis which renders it more immunogenic

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66
Q

Examples of drugs which can trigger an SLE-like syndrome include?

A

Isoniazid
Minocycline
TNF inhibitors

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67
Q

What will the CRP in a patient with SLE be?

A

Normal

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68
Q

What will FBC be in most patients with SLE?

A

Abnormal

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69
Q

OA vs RA in terms of morning stiffness?

A

OA - no morning stiffness

RA - morning stiffness

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70
Q

OA vs RA in terms of effect of activity?

A

OA - worse with activity

RA - improves with activity

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71
Q

Most common joints effected by OA?

A

Knee
Hip
Hand

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72
Q

What joint is most commonly affected by gout?

A

First metatarsophalangeal joint

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73
Q

How do patients with gout typically describe the pain?

A

Anything touching the affected joint will cause discomfort
Inflammation develops within a few hours
Pain disturbs their sleep

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74
Q

What antibody is likely to be raised in drug induced lupus?

A

Anti-histone antibody

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75
Q

How does polymyositis initially present?

A

Bilateral, proximal (hip and shoulder girdle) muscle weakness, developing over weeks to months.
Muscle pain and tenderness sometimes present
Muscle bulk and reflexes are preserved (until very late)

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76
Q

What happens in progressive disease in polymyositis?

A

Pharyngeal or oesophogeal muscle involvement, leading to dysphonia and dysphagia
Respiratory muscles involvement, leading to poor ventilation and type 2 respiratory failure

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77
Q

What will be seen on joint aspiration in gout?

A

Negatively birefringent needle-shaped crystals

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78
Q

What arthritis can be caused by tumour lysis syndrome (renal involvement)?

A

Gout

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79
Q

A patient taking methotrexate for RA should be advised how when she wishes to become pregnant?

A

Wash out of at least 6 months before conception

Low dose steroids in the event of a disease flare

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80
Q

Classic signs of OA?

A

Heberden’s nodes

Bouchard’s nodes

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81
Q

What are Heberden’s nodes?

A

Swelling of the distal interpharangeal joint

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82
Q

What are Bouchard’s nodes?

A

Swelling of the proximal interpharangeal joints

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83
Q

What hand deformities may be seen in RA?

A

Ulnar deviation
Swan neck deformity
Boutinnieres deformity
Z deformity of the thumb

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84
Q

What are the most commonly affected joints in RA?

A

PIP: proximal interpharangeal joints
MCP: metacarpopharangeal joints of the fingers

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85
Q

What might be the caused of bilateral, proximal muscle pain and stiffness without a rise in CK levels?

A

PMR

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86
Q

What are the most commonly affected joints in ankylosing spondylitis?

A

Sacroilliac, hence the most common presenting complaint is lower back pain

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87
Q

What should be ruled out in a patient with dermatomyositis?

A

Mallignancy - dermatomyositis can present as a paraneoplastic phenominum

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88
Q

What is Anterior ischemic optic neuropathy and which rheumatological conditions is it associated with?

A

GCA/PMR with GCA
AION is infarction of the posterior cillary arteries which supply the optic nerve
Most common mechanism if visual loss in GCA
Classic findings: on fundus examination include a swollen, chalky white, optic disc

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89
Q

What findings indicate a diagnosis of Churg-Strauss sydnrome?

A 
Esonophillia
Poorly controlled asthma 
CXR findings indicative of granulomatous change
Renal involvement
Elevated ESR
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90
Q

What is Chaugg-Strass syndrome also known as?

A

Churg-Strauss vasculitis, eosinophilic granulomatosis with polyangiitis (EGPA), and allergic angiitis.

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91
Q

First line treatment for knee or hand OA?

A

TOPICAL NSAID

+ Paracetomol

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92
Q

Serious side effects of methotrexate?

A

Drug induced pulmonary fibrosis
Abortive/tetragenic
Liver chirrosis
Leucopenia

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93
Q

What is Schirmer’s test used to diagnose and how is it performed?

A

Sjorgen’s syndrome
Place filter paper on eye for 5 mins
Positive is less than 10 mm of moisture on the filter paper in 5 minutes

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94
Q

What rehumatological conditions is Raynaud’s phenomenon associated with?

A

Scleroderma
SLE
Dermatomyosis and polymoyositis
Sjorgen’s syndrome

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95
Q

Over what age should a patient developing symptoms of Raynaud’s phenomenon alert you to likely underlying disease?

A

30 years

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96
Q

What are the possible physical causes of raynauds phenomenon?

A

Use of heavy vibrating tools
Cervical rib
‘sticky’ blood - cryoglbuniaemia

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97
Q

What common drug class can induce Raynaud’s phenomenon?

A

Beta blockers

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98
Q

What is Raynaud’s phenomenon?

A

Condition caused by vasospasm of hand digits.
Painful
May be precipitated by stress
Characterized by a typical sequence of colour changes in response to a COLD STIMULUS: white, blue, red

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99
Q

What is the colour sequence and what is occuring at each stage in Raynaud’s phenomenon?

A

White - inadequete blood flow
Blue - venous stasis
Red - re-warming hyperaemia

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100
Q

What is Raynaud’s syndrome?

A

Idiopathic Raynaud’s phenomenon
Usually improves with age
May be familial
Treatment comprises measures including keeping warm, avoiding smoking

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101
Q

Pharmacological management of Raynaud’s phenonomenon?

A

Calcium-channel blockers are first line

Phosphodiesterase-5 inhibitors and prostacyclins are usually effective

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102
Q

Complications of RP?

A

Digital ulcers
Severe digital ischemia
Infection
Gangrene

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103
Q

Pattern of symptoms in Raynaud’s syndrome vs RP secondary to underlying disease?

A

RS: Pattern symettrical and bilateral, lasts minuites
RP: Asymettrical pattern, only a few digits affected, may last hours

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104
Q

What test can be used in the diagnosis of RP?

A

Nail-fold capilaroscopy

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105
Q

What is vasculitis?

A

Inflammatory blood vessel disorder
Clinical features result from the damage of blood vessel walls with subsequent thrombosis, ischemia, bleeding and/or aneurysm formation.

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106
Q

Important aspects of vasculitis history?

A

Age, gender, ethnicity
Comprehnesive drug history
FHx
Constitutional symptoms: fever, weight loss, malaise, fatigue, diminished apperitie, sweats
Glove and sweater approach
RP
MSK: arthralgia, myalgia, proximal muscle weakness
CNS/PNS: headaches visual loss, tinnitus, stroke seizure encephalopathy
Heart/lung: percarditis, cough, chest pain, hemoptysis, dyspnea
GI: abdominal pain
Renal haematuria
Limbs: Neuropathy. digital ulcers/ischemia

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107
Q

How should you examine a patient with suspected vasculitis?

A

Vital signs: BP ?HTN, Pulse ?irregular ?rate
Skin: palpable purpura, livedo reticularis, nodules, digital ulcers, gangrene, nail bed capillary changes
Neurologic: cranial nerve exam, sensorimotor exam
Ocular exam: visual fields, scleritis, uveitis episcleritis
Cardiopulmonary exam: Crackles, pleural rubs, murmurs, arrhythmias
Abdo exam: tenderness, organomegaly

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108
Q

What are the primary vasculitides (small-vessel)?

A

Microscopic polyangitis
Granulomatosis with polyangitis - GPA (wegner’s granulomatosis)
Eosinophillic granulomatosis with polyangitis EGPA (churg-strauss syndrome
Iga vasculitis (Henoch-Schonlein purpura)

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109
Q

What are the primary vasculitides (medium-vessel)?

A 
Polyarteritis nodosa (PAN)
Kawasaki disease (KD)
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110
Q

What are the primary vasculitides (large-vessel)?

A 
Takayasu arteritis (TAK)
Ginat cell arteritis (GCA)
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111
Q

Vasculitis is normally secondary, what may it be caused by if this is the case?

A

Infection
Drugs
Mallignancy
Connective tissue disease

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112
Q

Why is urinalysis important in vasculitis?

A

Renal involvement often silent

Urinalysis to identify any underlying GN

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113
Q

What initial tests should be ran in suspected vasculitis?

A 
FBC, U&Es, LFTs, CRP, PV< ESR
Specific serology: ANA, ANCA, RF
Complement levels: C3, C4
Hep screen for B and C
HIV screen
Cryoglobins
Serum and urine protein elctrophoresis
CK, blood cultures, ECG, CXR, CT scan, MRI
arteriography
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114
Q

What is a common cause of skin vasculitis caused by medications?

A

Hypersensitivity vasculitis

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115
Q

Artial Myxomas can present with a vasculitis like syndrome, what test can exclude it?

A

ECHO

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116
Q

How is vasculitis managed?

A

R/o / treat any infection
Stop any offending drugs
1st line corticosteroids
2nd line cytotoxic medications, immunomodulatory or biologic agents (cyclophosphamide, methotrexate, azathioprine, leflunomide, mycophenolate mofetil, rituximab, IVIG

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117
Q

What are dermatomyositis and polymyositis?

A

Rare idiopathic muscle disease characterized by the inflammation of striated muscle.
M:F is smilar and peak age of onset is 40-50 years

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118
Q

How do dermatomyositis and polymyositis normally present?

A

INsideous onset of muscle proximal weakness
Ofetn painless
SOB/Rash
Often normal inflammatory markers, some raised
Normal FBC,
Kidney function not affected
Raised ALT from muscle but ALP and AST normal
80% antinuclear anitbody positive
Well demonstrated myositis on MRI

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119
Q

What is the diagnostic criteria for polymositis?

A 
3 or more of
Symetrical proximal muscle weakness
Raised serum muscle enzyme levels 
Typical electromyographic changes 
Biopsy evidence of myositis
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120
Q

What is the diagnostic criteria for dermatomyositis?

A

Typical rash of dermatomyositis and 2 of

Symmetrical proximal muscle weakness
Raised serum muscle enzymes
Typical electromyographic changes

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121
Q

How are Dematomyositis and Polymyositis treated?

A

Mainstay of treatment for first few weeks are high dose corticosteroids.
Long term control with methotrexate or azathioprine.
Rituximab can be effective
IV immunoglobin also effective
Sun protection in DM is important HCQ may be required to reduce the rash

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122
Q

How are Dermatomyositis and Polymyositis monitored?

A

Monitoring and disease activity can be difficult but the inflammatory markers and CK are often used
EMG studies/MRI or biopsy may be needed

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123
Q

Complications of dermatomyositis and polymyositis?

A

Involvement of the striated muscle of the oesophogus - swallow difficulty and aspiration pneumonia
DIaphragmatic involvement - respiratory failure
Inflammatory lung disease
Increased risk of malignancy 2-3 years before and after diagnosis of dermatomyositis
DM: rash is photosensitive and often leads to post inflammatory hyper- or hypo- pigmentation in areas that are light exposed (scalp, face, neck)
Linear plaques on dorsal aspect of the hands (Gottron’s papules)
DIlated nail fold capillaries
Dry cracked palms and fingers
Periorbital oedema
Heliotrope rash to eye lids (violet rash)

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124
Q

What other rheumatological conditions can lead to myositis?

A

Scleroderma

SLE

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125
Q

What is systemic sclerosis?

A

Multisystem autoimmune disease
Also known as scleroderma
Increased fibroblast activity resulting in abnormal growth of conncective tissue which leads to vascular damage and fibrosis

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126
Q

What are the two main subtypes of SSc?

A

limited

diffuse

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127
Q

What is limited scleroderma normally preceded by?

A

Many years of Raynaud’s phenomenon

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128
Q

Which subtype of SSc is more common

A

Limited (CREST syndrome)

129
Q

What complication often develops after aprox. ten years of the onset of symptoms of crest syndrome?

A

PA hypertension

130
Q

What is diffuse scleroderma?

A

Less common subtype of SSc with higher mortality,

Characterised by the sudden onset of skin involvement and is proximal to the elbows and knees

131
Q

How would you investigate SSc?

A 
Inflamatory markers - usually normal
X-ray hands - calcinosis
CXR, HRCT, PFT - pulmonary disease
ECG and ECHO - PA HTN, HF myocarditis and arrhythmias
Antibody serology
132
Q

What antibodies may be found in a patient with SSc?

A

Positive ANA (90%)
Anti-centromere antibody strongly associated with limited SSc
Scl-70 (topisomerase) and anti RNA polymerase III antibodies strongly associated with diffuse SSc

133
Q

How is systemic sclerosis treated?

A

Calcium antagonist/sildenafil/iloprost infusion for Raynaud’s symptoms
Methotrexate and mycophenolae mofetil may reduce skin thickening
ACEi prevent HTN crisi and reduce mortality from renal failure
Short course of prednisolone for flares
Proton pump inhibitors for GI symptoms
Psychological support

134
Q

What is the localized form of scleroderma called?

A

Morphoea

135
Q

Which sex is more commonly affected by SSc?

A

Women 5 times more affected

136
Q

What does vascular involvement of SSc invlude?

A

Raynaud’s phenomenon
Ischemic digital ulcer
HTN crisis
Pulmonary arterial HTN

137
Q

How does SSc cause kidney problems?

A

Scleroderma renal crisis is a serious condition with features of accelerated HTN, which can lead to renal failure.
Seen early in the course of disease in patients with diffuse SSc

138
Q

What is Sjogren’s syndrome?

A

Chronic autoimmune inflammatory disorder
Characterized by diminshed lacrimal and salivary gland secretion
Primary form - no association with other disease
Secondary form - association with another rheumatic disease
Most pts female

139
Q

Common signs and symptoms

A 
MADFRED
Myalgia
Arthralgia
Dry mouth 
Fatigue
Raynaud's phenomenon
Enlarge parotids
Dry eyes
140
Q

What antibodies are positive in most patients with Sjorgen’s syndrome?

A

Anti Ro
Anti La
90%

141
Q

What less common antibodies might be seen in a patient with Sjorgen’s syndrome?

A

RF and anti ds-DNA

142
Q

What biopsy may be needed to diagnose Sjorgen’s syndrome and what will be seen?

A

Salivary gland

Focal lymphocytic infiltration

143
Q

How is Sjorgen’s syndrome treated?

A 
Avoid dry or smoky atmostpheres 
Dry eyes- artfical dear
Dry mouth - artifical saliva 
Skin emoillents, vaginal lubricants
Immunosupressents/Steroids rarely required
144
Q

What are the most common diseases associated with Sjorgens syndrome?

A

RA
SLE
ALso: coeliac, primary bilary cirrhosis, autoimmune thyroid disease

145
Q

What haemotological condition are patients with Sjogren’s syndrome more at risk of?

A

B cell lymphoma

146
Q

What are the risks pregnant women with Sjogren’s syndrome might need to know about?

A

anti Ro/SS A antibodies - higher risk of fetal loss, complete heart block in fetus, neonatal lupus syndrome of the newborn

147
Q

What is Hypermobility Spectrum disorder?

A

This is a pain syndrome in people with joints that move beyond normal limits.
No precise definition - joint mobility is a graduated phenomenon.
Due to laxity of ligaments, capsules and tendons
Is thought that the origin of pain is from microtrauma

148
Q

Complication of Hypermobility Spectrum Disorder?

A

Recurrent subluxations or dislocations

149
Q

Symptoms and signs of hypermobility spectrum disorder?

A 
Pain around the joints
Worse after activity
Genralized and fatigue
Soft tissue rheumatism e.g. epicondylitis 
Abnormal skin: papyraceous scars, hyperextensible, thin, striae 
Marfanoid habitus
Arachnodactlyly 
Drooping eyelids, myopia
Hernias and uterine/rectal prolapses
150
Q

Treatment of hypermobility spectrum disorder?

A

This is the mainstay of treatment is non drug therapy
Strengthening exercises to reduce joint subluxation
Work on posture and balance may also be needed
Splinting and even surgical interventions may be needed
Advice on pacing and goal setting
Specialist pain management input is often needed
Paracetamol should be mainstay

151
Q

What score is used to measure extent of hypermobility spectrum disorder?

A

Beighton score

152
Q

What are the heritable connective tissue disorders?

A

HSD
Marfan syndrome
Ehlers Danlos syndrome

153
Q

What is osteoarthritis?

A

Degenerative joint disorder where there is a progressive loss of articular cartillage accompanied by new bone formation and capsular fibrosis

154
Q

Aetiology of OA?

A

Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of cartilage due to defective stiffened subchondral bone passing more load to it

155
Q

Key features of cartillage in OA?

A

Loss of elasticity with a reduced tensile strength

Cellularity with proteoglycan content are reduced

156
Q

What provokes pain in OA?

A

Pain
Weight baring
Activity

Starts intermittently, progresses to constant

157
Q

X ray changes in OA?

A

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

158
Q

Pharmacological therapy?

A 
Regular paracetomol is first choice
NSAIDs short term orally
Topical NSAIDs and topical rubefacients 
Capsaicin 
Intra-articular corticosteroids can be offered
159
Q

Where may pain in OA emanate from?

A

Any tissue except cartilage which is avascular and aneural
It may be due to microfractures of the subchondral bone, or from low grade synovitis, capsular distention or muscle spasam

160
Q

What is strongly associated with the development of knee OA?

A

Nodal OA

161
Q

What is fibromyalgia?

A

Common disorder of central pain processing charcterized by chronic widespread pain in all 4 quadrants of the body - both sides, above and below the waist. Allodynia, as heightened, painful response to innoculous stimuli is often present.

162
Q

Signs and symptoms of fibromyalgia?

A 
Joint/muscle stiffness
Profound fatigue
Unrefreshed sleep
Numbness
Headaches
Irritable bowel/bladder
Depression and anxiety
Poor concentration and memory 
Tender points on palpation of their muscles
163
Q

What is the underlying pathogenesis of fibromyalgia?

A

Can be induced by deliberate sleep deprivation - reduced REM sleep and delta wave sleep.
Hyper-activation in response to noxious stimuli
Neural activation in brain regions associated with pain perception and response to non-painful stimuli

164
Q

Risk factors for fibromyalgia?

A

Female (9:1)
Peak age of onset 40-50 years
Trigger - emotional distress, physcial pain e.g. arthritis, sleep deprivation

165
Q

Treatment for fibromyalgia is based on pain intentsity, function, and associated features such as depression, fatigue, and sleep disturbance. What may it include?

A

Education - explanation of their symproms
Physical - exercise
CBT
Pharmacology - low dose amitryptiline, pregablin may be effective (OPIATES NOT RECCOMENDED)

166
Q

What blood tests should be undertaken in a suspected diagnosis of fibromyalgia to exculde other pathologies?

A 
ESR
CRP
FBC
U&E
LFT
Ca
CK
TFT
167
Q

What are the non modifiable risk factors for osteoperosis?

A 
Advancing age (>65)
Female gender
Caucasion or south asian
Family history
History of low trauma fracture (fall from standing height or less at walking speed or less)
168
Q

What are the modifiable risk factors for osteoperoisis?

A 
Low body weight (58 kg or BMI<21)
Premature menopause
Calcium/vit D deficiency
Inadequete physical activity
Cigarette smoking
Excessive alcohol intake (>3 drinks/day)
Iatrogenic: e.g. corticosteroids, aromatase inhibitors
169
Q

Gold standard to diagnose osteoperosis?

A

DEXA (Dual energy x-ray absorptiometry) of the lumbar spine and hip is considered the gold standard

170
Q

Below what T score is considered osteoperosis?

A

2.5 or less

171
Q

What is a normal bone marrow density T-score?

A

Greater than or equal to -1

172
Q

What T score indicates osteopenia?

A

-1 and -2.5

173
Q

What is T score?

A

Number of SDs from the mean bone density of persons of the same gender at age of peak density (25)

174
Q

What is a Z score?

A

Z-score is a comparison of the patient’s BMD with an age- & gender matched population

175
Q

What should a Z score of less than -2 prompt?

A

Evaluation for causes of secondary osteoperosis?

176
Q

What are plain radiographs not used to diagnose osteoperosis? What might they show that is indicative of osteoperosis?

A

Lack sensitivity
May show rib fractures or vertebral compression fractures without trauma history - this prompts evaluation for osteoporosis

177
Q

How is osteopenia treated?

A

Treatment should focus only on risk modification:
Weight bearing exercise
Vitamin D2 supplementation (800-2000 IU/day)
Limiting alcohol
Smoking cessatopm
Dietary advice regarding calcium intake

178
Q

How is osteoperosis treated?

A

Vitamin D +/- calcium supplementation, AND
1st line: oral bisphosphonates - Alendronic Acid
2nd line: Denosumab or teriparatide

179
Q

What are secondary causes of osteoperosis?

A 
Coeliac disease
Eating disorders
Hyperparathyroidism 
Hyperthryoidism 
Multiple myeloma
Men: hypogonadism
180
Q

What instructions and advise should be given to patients who are taking bisphosphonates?

A

Take on empty stomach at least 30 mins before food with full glass of water
Serious side effects are very rare
Patients (or their carers) should be advised to stop taking alendronic acid and to seek medical attention if they develop symptoms of oesophageal irritation such as dysphagia, new or worsening heartburn, pain on swallowing or retrosternal pain.

181
Q

What is gout?

A

Inflammatory arthritis related to a hyperuricemia (although this is not the only determining factor)

182
Q

What complication is gout associated with?

A

High risk of CVD

183
Q

What is the pathogenisis of gout?

A

Deposition of monosodium urate (MSU) crystals accumulate in joints and soft tissues
Result in chronic arthritis, tophi (soft tissue masses), urate nephropathy, and uric acid nephrolithiasis

184
Q

Within what time period will most patients have a second flare of gout following the initial flare?

A

1 year

3/4 within 2

185
Q

What are the non-modifiable risk factors for gout?

A

Age>40 years

Male gender

186
Q

What are the modifiable risk factors for gout?

A 
Increased purine intake (meats, seafood)
Alcohol intake (especially beer)
High fructose intake
Obesity 
Congestive HF
Coronary artery disease
Dyslipidemia 
Renal disease
Organ transplantation
HTN
Smoking 
DM
Urate-elevating medications e.g. thizazides, loop diruetics, Pyrazinamide
187
Q

How is gout treated conservatively?

A

Maintain optimal weight
Regular exercise
Diet modification (purine-rich food)
Reduce alcohol consumption (beer and liquour)
Smoking cessation
Maitain fluid intake and avoid dehydration

188
Q

First line treatment for acute gout?

A

NSAIDs
oral/IM steroids
colchcine if NSAIDs not tolerated

189
Q

What medication is used to prevent gout, and how does it act?

A

Urate lowering therapy, after acute attack
Xanithine oxidase inhibitors (reduce urate formation): Allopurinol/febuxostat
Second line is benzbromarone and sulfinpyrazone are used less commonly as more side effects. They act to increase the renal excretion of uric acid.

190
Q

How will the fluid aspirate contents of a joint viewed under polarised red light in gout?

A

Negatively birefringent, needle shaped crystals

191
Q

How will the fluid aspirate contents of a joint viewed under polarised red light in pseudogout?

A

POsitively birefringent rhomboid shaped crystals

192
Q

What are crystals in pseudogout composed of?

A

Calcium pyrophosphate

193
Q

Who normally suffers from pseudogout?

A

Older women with OA

194
Q

Does hyperuricemia need treatment if asymptomatic?

A

No

195
Q

Within what time period should treatment begin for an acute gout flare?

A

within 24 hrs of onset

196
Q

What type of pathology does worsening pain with particular movements indicate?

A

Peri-articular pathology

197
Q

What MSK strucutres can pain arise from?

A 
Synovium
Join capsule
Subchondral bone
Peri-articular
Skin
198
Q

Where is pain from the glemohumeral joint or rotator cuff felt?

A

Upper arm

199
Q

Where might hip pain radiate to?

A

Groin
Buttock
Thigh
Knee

200
Q

What can cause radiculopathy?

A

Disc prolapse

201
Q

What id pain during tenosynovitis triggered by?

A

Certain movements

202
Q

Where is the pain from lateral epicondylitis felt? What makes it worse?

A

Outside of elbow joint

Worsened on resisted elbow extension

203
Q

Where is the pain felt in Achilles tendinitis?

A

Just above the heel

Worse on active plantar flexion

204
Q

Where is pain from De Quervain’s tensoynovitis felt? What makes it worse?

A

Snuffbox area of the wrist and is worse when pinching or using thumb to operate a smartphone

205
Q

What rheumatological conditions have a proximal only patten of joint/muscle involvement?

A

PMR

206
Q

What rheumatological conditions have a distal only patten of joint/muscle involvement?

A

OA
Gout
PsA

207
Q

What rheumatological conditions have a small joint only patten of joint/muscle involvement?

A

RA (early stages)

208
Q

What rheumatological conditions have a large joint only patten of joint/muscle involvement?

A

OA

209
Q

What does monoarticular mean?

A

1 joint

210
Q

What does oligoarticular mean?

A

2-4 joints

211
Q

What does polyarticular mean?

A

More than 4 joints

212
Q

Symetrical rheumatological conditions?

A

RA

213
Q

Asymetrical rheumatological diseases?

A

PsA

Gout

214
Q

Which rhematological diseases commonly involve the spine?

A

Main feature of AS

Sometimes PsA

215
Q

Causes of acute monoarthritis?

A

Infections - Staph aureus and Streptococcal most common
Crystal induced - Gout (men), pseudogout (older women with OA)
Trauma - haemarthrosis

Septic arthritis until proven otherwise

216
Q

Causes of chronic monoarthritis?

A

Infections - always consider TB
Inflammatory - Psoriatic arthritis, reactive arthritis, forigen body
Non-inflammatory - OA, Trauma (e.g. meniscal tare), osteonecrosis (associated with prednisolone use), neuropathic (Charcot’s joint)
Tumours - rare

217
Q

Causes of acute polyarthritis?

A

Inflammatory arthritis - RA, PsA, reactive arthritis
Autoimmune - SLE, vasculitis
Viral infection - HIV, chikungunya, parovirus
Crystal arthritis - uncontrolled gout

218
Q

Causes of chronic (>3 months) arthritis?

A

Inflammatory - RA, PsA, reactive
Autoimmune - SLE, vasculitis
Crystal arthrits - uncontrolled gout

219
Q

Causes of arthritis of the DIPJs?

A

Psoratic arthritis: will also be nail dystrophy in the affected digit
OA commonest - Herberden’s nodes

220
Q

What is early morning stiffness suggestive of?

A

Inflammatory arthritis e.g. RA PsA

221
Q

What is generalised stiffness more likely to be suggestive of?

A

Inflammatory arthritis e.g. RA or PsA

222
Q

Over what time period does swelling in gout tend to appear?

A

Over an hour - very actuely

223
Q

What does swelling following injury suggest?

A

Haemarhtorsis

224
Q

What kind of swelling is seen in OA?

A

Bony swelling (Heberden/Bouchard’s noads)

225
Q

What does a swelling extruding chalky material indicate?

A

Gout tophi

226
Q

What does a swelling exturding hard yellowish lumps indicate?

A

Calcinosis in systemic sclerosis

227
Q

Inflammatory vs mechnical morning stiffness?

A

> 1 hour infammatory

>30 mins mechanical

228
Q

Inflammatory vs mechnical effect of activity?

A

Better in inflammatory worse in mechanical

229
Q

Inflammatory vs mechnical effect of resting?

A

Worse in inflammatory

Better in mechanical

230
Q

Inflammatory vs mechnical fatigue?

A

Significant in inflammatory

Minimal in mechanical

231
Q

Inflammatory vs mechnical systemic invovlement?

A

Yes in inflammatory

No in mechanical

232
Q

What kind of vasculitis is caused by penicillin?

A

Cutaneous hypersensitivity (leucocytoclastic)

233
Q

Exaggerated thoracic kyphosis and loss of lumbar lordosis may suggest what?

A

Longstanding AS

234
Q

Exaggerated thoracic kyphosis and loss of lumbar lordosis may suggest what?

A

Osteoperotic fractures

235
Q

Describe antalgic gait?

A

Pain causes the patient to reduce the time spent on the affected side

236
Q

Describe Trendelenberg gait?

A

Due to poor hip abduction (weak gluteus medialis) the pelvis drops down on the opposite side when standing on the affected leg.
Seen in hip disease and after THR

237
Q

Describe senory ataxia?

A

Wide based stamping gate, an attempt to compensate for lack of sensory input.
Sight also helps to compensate, hence worse with eyes shut.

238
Q

Describe cerebellar ataxia?

A

Wide-based, staggering. Arms often flung out to try and improve balance.

239
Q

Describe hemiplegic gait?

A

Narrow-based, leg swung forward and the toes scrape the ground

240
Q

Festinant or projectile

A

Difficulty initiating walking, then a shuffling run.

Reduced arm swing.

241
Q

What causes bow legs?

A

Usually medial compartment arthritis in OA as the medial compartment takes most of the load

242
Q

How do you screen motor function of the hand?

A

The following to be performed against resistance
Wrist/finger extension - radial nerve
Finger ABduction of the index finger - ulnar nerve
Thumb ABduction - median nerve

243
Q

What is Tinel’s test?

A

This is used to help diagnose carpal tunnel syndrome (CTS), the most common peripheral neuropathy of the upper
limb. Any type of arthritis at the wrist can predispose to this.
Tap over the carpal tunnel with your index and middle fingers for 30-60 seconds. If the patient develops tingling in
the thumb and radial two and a half fingers, this suggests median nerve irritation.

244
Q

What is Phalen’s test?

A

If the history suggests carpal tunnel syndrome, Phalen’s test may be used..
Ask the patient to hold their wrist in complete and forced flexion (pushing the dorsal surfaces of both hands
together) for 60 seconds. If the patient’s symptom develop then the test is positive

245
Q

Where is the sensory supply to the hand by the median nerve?

A

Skin over thenar eminence
Lateral 2/3 of palm
Palmar aspect of lateral 3 1/2 fingers
Dorsal fingertips of lateral 3 1/2 fingers (thumb, index, middle and half of ring finger)

246
Q

Why is the skin over the thenar eminence spare in CTS?

A

Preservation of the palmar cutaneous branch

247
Q

Motor supply to the hand: median nerve

A

All muscles of anterior compartment of forearm EXCEPT flexor carpi ulnaris and the medial two parts of flexor
digitorum profundus
pronator teres and pronator quadratus – pronate forearm
flexor carpi radialis – flexes and abducts wrist
palmaris longus – flexes wrist and tenses palmar aponeurosis
flexor digitorum superficialis – flexes fingers at PIPJs
lateral two parts of flexor digitorum profundus – flex index and middle fingers at DIPJs
flexor pollicis longus – flexes thumb at IPJ
intrinsic muscles of hand – LOAF muscles
lateral two lumbricals – flex MCPJs and extend IPJs of index and middle finger
opponens pollicis – opposes thumb
abductor pollicis brevis – abducts thumb
flexor pollicis brevis – flexes thumb at MCPJ

248
Q

Clinical features of a median nerve palsy?

A

History of wrist trauma/pathology
Numbeness in the hand in a median nerve distribution (palm spared, unless damage in the arm)
Weakness of thumb opposition and abduction (move upwards away from palm, touch thumb to little finger)
Thenar eminance wasting (late feature)
If damage to arm: weak finger flexion put preservation of the ring finger and little finger DIPJs (ulnar nerve)

249
Q

Sensory nerve supply to the hand - ulnar nerve?

A

Skin over the hypothenar eminence
Medial 1/3 of the hand
Palmar aspect of the lateral 1 1/2 fingers
medial 1/3 dorsum of the hand
dorsal aspect of the medial 1.5 fingers (little finger and half of ring finger)

250
Q

Motor nerve supply to the hand: ulnar nerve

A

Two muscles of the forearm:
flexor carpi ulnaris - flexes and adducts wrist, medical two parts of flexor digitorum profundus
flex ring and little fingers at the DIPJs
Most of the intrinsic muscles of the hand - interossei and the adductor pollicis

251
Q

Clinical features of ulnar nerve palsy?

A

These include numbness over the hypothenar eminence and in the ulnar nerve distribution of the hand
Paralysis of flexor carpi ulnaris causes weak wrist flexion and adduction
Paralysis of most of the intrinsic muscles of the hand results in weak MCPJ flexion and IPJ extension of the ring and little fingers, loss of finger abduction and adduction and loss of opposition of little finger
Paralysis of medial two parts of flexor digitorum profundus causes weak flexion of ring and little finger DIPJs

252
Q

What is Froment’s test?

A

To test adductor pollicis, ask the patient to grip a piece of card between the thumb and the side of the
index finger

IN ulnar nerve palsy the IPJ and MCPJ of the thumb will flex as the patient tries to grib the card

253
Q

WHat should be tested for un suspected ulnar nerve palsy?

A

To test adductor pollicis, ask the patient to grip a piece of card between the thumb and the side of the
index finger (Froment’s test). In ulnar nerve palsy, the IPJ and MCPJ of the thumb will flex as the patient
tries to grip the card. Test adduction by asking the patient to grip the card between the little and ring
fingers whilst holding the fingers extended. Test the first dorsal interosseus muscle by asking the patient to
abduct the extended index finger against resistance.

254
Q

What is a Claw Hand deformity?

A

Present in ulnar nerve palsy
Fixed flexion of the IPJs and hyperextension of the MCPJs of the ring and little fingers, hyperextension of the MCPJs of the ring and little fingers due to unopposed median nerve function
Most pronounced when the nerve is injured at the wrist

255
Q

Interpreting blood tests in rheumatic diseases?

A

Hb - anaemia of chronic disease most common in RA, Fe deficiency may be used to NSAIDs
Platelets - rise with inflammation or bleeding, fall in SLE
Neutrophils - rise with inflammation, sepsis and prednisolone usage, Fall in SLE or with DMARD toxicity
Lymphocytes - fall in SLE or DMARD induced
U&E - Rise due to NSAIDs, renal disease in lupus/vasculitis or gout
Uric acid - Elevated in gout, but falls with inflammation
LFTs - hepatitic rise due to DMARD toxicity
CK, ALT, LDH - rise in myositis

256
Q

Which inflammatory marker is affected by anaemia?

A

ESR - rises

257
Q

What can Anti-dsDNA antibodies suggest?

A

SLE

258
Q

What can Anti RO and anti-LA antibodies indicate?

A

SLE

Sjorgren’s

259
Q

What can anti centromere and anti Scl70 antibodies indicate?

A

Systemic scelrosis

260
Q

What can anti Jo-1 antibodies indicate?

A

Polymyositis

261
Q

Which antigen is associated with AS?

A

HLA-B27

262
Q

What might C ANCA indicate?

A

GPA, infection, neoplasia

263
Q

What might P ANCA indicate?

A

Microscopic polyangitis
Infection
Neoplasia

264
Q

Potential side effects of methotrexate?

A 
Nausea - most common
Oral ulcers, hair thinning
Hepatitis, cirrhosis 
Pneumonitis
Bone marrow suppression
265
Q

Potential side effects of hydroxychloroquine?

A

GI disturbance - most common
Retinal pigmentation and loss of vision – rare but
screening needed
No blood tests needed

266
Q

Side effects of sulfasalazine?

A

GI upset -most common
Rash
Hepatitis
Bone marrow suppression

267
Q

Side effects of azathioprine?

A

GI upset - most common

Bone marrow suppression

268
Q

Side effects of cyclophosphamide?

A

Bone marrow suppression
Infertility
Increased cancer risk

269
Q

Side effects of ciclosporin?

A

Renal impairment

HTN

270
Q

Side effects of leflunomide?

A

GI Upset
HTN
Bone marrow suppression
Hepatitis

271
Q

What is Schober’s test and what is a positive result?

A

To test for this decreased spine mobility, many doctors use the Schober Test, in which they draw two lines on the patient’s spine, 10 cm apart. Then, the patient leans forward and the doctor measures how much the distance increases between the two lines. An increase below 5 cm is positive and indicates AS, while an increase of 5 cm and above is negative and does not indicate AS.

272
Q

Where does Paget’s disease of the bone typically affect?

A

The skull, spine/pelvis, and long bones of the lower extremities

273
Q

What should patients with anti-phospholipid syndrome who haven’t had a thrombosis previously be treated with?

A

Low-dose aspirin

274
Q

A positive femoral nerve stretch test in the context of hip pain?

A

Reffered lumbar spine pain

275
Q

What treatment of osteoperosis may increase the risk of an atypical stress fracture of the proximal femoral shaft?

A

Bisphosphonates are associated with an increased risk of atypical stress fractures

276
Q

What should be ruled out prior to commencing azathioprine?

A

Azathioprine - check thiopurine methyltransferase deficiency (TPMT) before treatment

277
Q

What type of hypersensitivity reaction is SLE?

A

Type 3

Type 3 is characterised by antigen-antibody complexes. The pathogenesis of SLE involves cellular remnants containing nuclear material being transferred to lymphatic tissues. They are then presented to T cells which in turn stimulate B cells to produce autoantibodies. IgG autoantibodies are primed to attack DNA and other nuclear material which results in antigen-antibody complexes causing damage in various areas.

278
Q

What is trochantaric bursitis also known as?

A

Greater trochanteric pain syndrome is now the preferred term for trochanteric bursitis.

279
Q

What is trochanteric bursitis?

A

Due to repeated movement of the fibroelastic iliotibial band
Pain and tenderness over the lateral side of thigh
Most common in women aged 50-70 years

280
Q

Course of reactive arthritis?

A

Reactive arthritis is not typically acute - it can develop up to 4 weeks after precipitating infection and can run a relapsing-remitting course over several months

281
Q

What other rheumatology drug does azathioprine severely interact with?

A

Azathioprine and allopurinol have a severe interaction causing bone marrow suppression

282
Q

Why should visual acuity be monitored for patients taking hydroxycholoroquine?

A

May result in severe and permananent retinopathy

283
Q

Why might corticosteroids cause a patient to have reduced power of the shoulders, biceps and hip flexors/extensors

A

A patient is complaining of a proximal muscle weakness that matches a proximal myopathy. The prolonged course of steroids could be causing this.

284
Q

What common rheumatological treatment can induce neutrophillia?

A

Corticosteroid treatment (e.g. prednisolone)

285
Q

Why must a chest X-ray be performed before starting biologicS?

A

Can cause chest infection

286
Q

How should GCA be managed if there is visual loss?

A

IV methylprednisolone 500mg-1g three days OD

287
Q

A patient with osteoperosis, who has an intermidate risk but has not have a DEXA scan, should be managed how?

A

FRAX score recalculated with a dexa scan

288
Q

When diagnosing PMR, what does normal CK rule out?

A

Myopathy

MND

289
Q

What should be prescribed alongside long term steroids?

A

Bisphosphonates

PPI

290
Q

Psoratic arthritis features

A 
Joint pain DIP involvement - random distribution, oligoarthritis
Skin changes
Nail changes
Enthesis (AT) - pains around the joints
SERONEGATIVE
HLAB-27 associated
291
Q

DIstrubution of AS?

A

axial mainly

peripheral + illiosacral joints

292
Q

How can Ankylosing spondylitis lead to heart block?

A

Fibrosis of the conductive system of the heart

293
Q

Ankylosing spondylitis X ray findings?

A

Bamboo spine
Dagger spine (fusion of spinous processes)
Sacroilitis
(Apical chest fibrosis - bad prognosis)

294
Q

When can DMARDs be considered in Ankylosing spondylitis?

A

In peripheral disease - no evidence for axial disease

295
Q

What are the seronegative arthritis’?

A

Psoratic artheritis
Enteropathic arthritis (alongside IBD)
Ankylosing spondylitis
Reactive arthritis

296
Q

Which gene are serongeatives arthritis’ associated with?

A

HLA B27

297
Q

Poor prognostic factors for RA?

A 
RF positive
anti-CCP antibodies
poor functional status at presentation
X-ray: early erosions (eg after less than two years)
extra articular factors e.g. nodules
HLA DR4
insideous onset
298
Q

What X-ray features might be present in a joint affected by gout?

A

Joint effusion - early sign
well defined ‘punched out’ errosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
relative preservation of joint space until late disease
eccentric errosions
soft tissue tophi may be seen

299
Q

What might be seen on x-ray of a joint affected by pseudogout?

A

Chondrocalcinosis

in the knee this may be seen as linear calcifications of the meniscus and articular cartilage

300
Q

What are risk factors for pseudogout?

A

Haemochromatosis
Hyperparathyroidism
Low magnesium, low phosphate
Acromegaly, Wilson’s disease

301
Q

What is P ANCA associated with

A

P-ANCA is most strongly associated with microscopic polyangiitis and ulcerative colitis.

302
Q

Ankylosing spondylitis - x-ray findings

A

subchondral erosions, sclerosis

and squaring of lumbar vertebrae

303
Q

Features of stills disease?

A

arthralgia
elevated serum ferritin
rash: salmon-pink, maculopapular
pyrexia
typically rises in the late afternoon/early evening in a daily pattern and accompanies a worsening of joint symptoms and rash
lymphadenopathy
rheumatoid factor (RF) and anti-nuclear antibody (ANA) negative

304
Q

Epidemiology of stills disease?

A

has a bimodal age distribution - 15-25 yrs and 35-46 yrs

305
Q

Joint aspitrate in RA?

A

Joint aspirate in rheumatoid arthritis shows a high WBC count, predominantly PMNs. Appearance is typically yellow and cloudy with absence of crystals

306
Q

Ankylosing spondylitis - x-ray findings

A

subchondral erosions,
sclerosis
and squaring of lumbar vertebrae

307
Q

What is used in a new diagnosis of RA?

A

Methotrexate and pred

For the methotrexate monitor every 3 months - FBC U&Es and LFTs (nephrotoxic, myelosupression and heaptoxicity)

308
Q

Special insturctions methotrexate

A

Once a week injection
Folate 5mg every day (methotrexate competitively inhibits dihydrofolate reductase (DHFR), an enzyme that participates in the tetrahydrofolate synthesis) BUT NOT ON DAY OF METHOTREXATE
3 monthly monitoring of U&Es (nephrotoxic), LFTs (hepatotoxicity) and FBC (myelosupression)

309
Q

First line imperial abx in suspected septic arthritis?

A

IV flucloxacillin

310
Q

Gout management in severe renal disease?

A

Steroids

310
Q

Polymyocitis vs PMR?

A

Polymyositis: raised CK, Raised LDH AST ALT, weakness and tenderness
In PMR tenderness only and raised CRP

311
Q

How many criteria to diagnose SLE?

A

4/11 of the criteria

312
Q

What is livedo reticularis associaed?

A

Rash associated with antiphospholipid syndrome (can be 2 to lupus)
Mottled appearance

313
Q

What is antiphospoholipid synydrome?

A 
Primary disorder or associated with SLE
Coagulation defect - raised APTT
Livedo reticularis
Obestertic complications 1st trimester miscarriage - pre eclampsia
Thrombocytopenia
314
Q

Anti-coagulation in antiphospholipid syndrome?

A 
Initial VTE (INR) 2-3, 6 months warfarin
Recurrent VTE, INR 2-3, lifelong
Recurrent VTE on warfarin INR target 3-4

If pregnant LMWH+aspirin

DOACs no licsensed in this syndrome

315
Q

Most SPecific marker for RA?

A

Anti-CCP

316
Q

OA vs mallignsncy

A

Malignancy - radiolucent lesions

317
Q

Gout vs pseudogout?

A

Crystals: Gout uric acid, pseudogout calcium phosphate
Crystial shape: Gout - needle like Pseudogout rhomboid like
Bifringency; Gout - Negative Pseudogout - weaklypositive
Joint affected: Gout - 1st MCP Pseudogout - Knee
Radiography Gout - rat bite erosions, pseudogout - white lines of chondocalcinosis

318
Q

What DMARD requires visual acuity testing?

A

Hydroxychloroquine - may result in a severe and permanent retinopathy

Year 3 Medicine (8 decks)

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