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Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What are some risk factors for Osteoarthritis?

A
  • Obesity
  • Age
  • Occupation
  • Trauma
  • Female
  • Family history
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2
Q

What is osteoporosis thought to be caused by?

A

Imbalance between the cartilage being worn down and the chondrocytes repairing it

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3
Q

What are the 4 key Xray changes for osteoporosis?

A

LOSS

Loss of joint space

Osteophytes

Subarticular sclerosis

Subchondrial cysts

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4
Q

How does OA present?

A

Joint pain and stiffness (worsened with activity in contrast to inflammatory arthritis)

Deformity

Instability

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5
Q

What are some commonly affected joints for OA?

A
  • Hips
  • Knees
  • Sacro-iliac joints
  • DIPJ
  • Wrist
  • Cervical spine
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6
Q

What are some signs in the hands for OA?

A

Herbeden’s nodes (DIP)

Bouchard’s nodes (PIP)

Squaring at base of thumb at carpo-metacarpal joint

Weak grip

Reduced range of motion

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7
Q

What are the management options for OA?

A

Lifestyle: weight loss, physio to inprove strength. OT and orthotics

Analgesia: Paracetamol and topical NSAIDs (PPI for protection) or topical capsaicin (chilli pepper extract), THEN opiates e.g. codeine and morphine

Intra-articular steroid injections temporary reduction in inflammation

Joint replacement

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8
Q

What is rheumatoid arthritis?

A

Autoimmune condition resulting in chronic inflamamtion of the synovial lining of joints, tenson sheaths and burse

It’s an inflammatory arthritis

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9
Q

How is the inflammation in RA distributed?

A

Symmetrical distribution affecting muliple joints

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10
Q

What is the genetic association of RA?

A

HLA DR4

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11
Q

What is Rheumatoid Factor?

A

Autoantibody targetting the Fc portion of the IgG antibody.

The Fc portion is used to bind to cells of the immune system

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12
Q

What is the result of RA?

A

Activation of the immune system against the patients own IgG causing systemic inflammation.

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13
Q

What class of immunoglobulin is Rheumatoid Factor?

A

Usually IgM

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14
Q

What antibodies are more sensitive and specific to RA than rheumatoid factor?

A

Anti-CCP antibodies

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15
Q

How does RA present?

A

Symmetrical distal polyarthropathy: pain, stiffness, swelling

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16
Q

What are the key symptoms of RA?

A

Pain

Swelling

Stiffness

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17
Q

What are the associated systemis symptoms of RA?

A

Fatigue

Weight loss

Flu like illness

Muscle aches and weakness

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18
Q

What is palindromic rheumatism?

A

Self limiting short episodes of inflammatory arthritis with joint pain, stiffness and swelling (only lasting 1-2 days then completely resolving)

Having RF and anti-CCP may indicate progression to full RA

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19
Q

Which joints are commonlmy affected by RA?

A

PIP joints, MCP joints (DIPJ almost never affected)

Wrist and ankle

Metatarsophalangeal joints

Cervical spine

Large joints can be affected e.g. knee, hips and shoulders

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20
Q

Are the distal IPJ ever affected by RA?

A

No - it will be OA

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21
Q

What is atalantoaxial subluxation?

A

The axis and atlas shift caused by local synovitis

Sublaxation can cause spinal cord compression and is an emergency

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22
Q

What are the hand symptoms of RA?

A

Z shaped thumb

Swan neck deformity

Boutonnieres deformity

Ulnar deviation of the fingers at knuckle

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23
Q

How does Boutonnieres deformity occur?

A

Teat in the central slip of the extensor components of the fingers. This means that when the patient tries to straighten their finger, the lateral tendons that go around the PIP (called the flexor digitorum superficialis tendons) pull on the distal phalynx without any other supporting structure, causing the DIPs to extend and the PIP to flex

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24
Q

What are some extra articular manifestations of RA?

A
  • Pulmonary fibrosis
  • Bronchiolitis obliterans (inflammation causing small airway destruction)
  • Felty’s syndrome (RA, neutropenia, splenomegaly)
  • Sjogrens syndrome AKA sicca syndrome
  • Anaemia of chronic disease
  • CVD
  • Episcleritis and scleritis
  • Rheumatoid nodules
  • Amyloidosis
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25
Q

What are the investigations for RA?

A
  • Check rheumatoid factor
  • If RF negative, check anti-CCP antibodies
  • Cehck inflammatory markers e.g. CRP and ESR
  • X ray hands and feet
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26
Q

What imaging can be used for RA?

A

Ultrasound scan to confirm synovitis - useful when clinical examinations are unclear

Xray

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27
Q

What are the Xray changes in RA?

A

Joint destruction and deformity

Soft tissue swelling

Periarticular osteopenia

Boney erosions

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28
Q

When should a referral for rheumatoid arthritis be made?

A

Adult with persistent synovitis even if negative RF, anti-CCP antibodies and inflammatory markers

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29
Q

What is the DAS28 score?

A

Disease activity score (28 joints are assessed)

Points are given for swollen joints, tender joints, ESR/CRP results

Useful in monitoring disease acitivity and response to treatment

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30
Q

Which RA patients have a worse prognosis?

A
  • Younger onset
  • Male
  • More joints and organs affected
  • Presence of RF and anti-CCP
  • Erosions seen on X-ray
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31
Q

What is the 1st line treatment for RA flare ups?

A

Short course of steroids

NSAIDS/COX 2 inhibitors (with PPI)

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32
Q

What is the stepwise progressive use of DMARDs in RA?

A

1st: Methotrexate, leflunomide or sulfasalazine (hydroxychloroquine in mild disease)

2nd: Use 2 in combination

3rd: Methotrexate plus biologic therapy e.g. TNF alpha inhibitor

4th: methotrexate plus rituximab

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33
Q

What type of drugs are infliximab, adalimumab?

A

Anti-TNF (biologic therapies)

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34
Q

What are the biologics worth remembering?

A

Adalimumab, infliximab and etanercept (all TNF inhibitors)

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35
Q

Name some other classes of biologic therapies?

A

Anti-TNF

Anti-CD20

Anti-IL6

JAK inhibitors

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36
Q

What are the risks with biologics?

A

Serious infection

Reactivation of latent TB and hep B

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37
Q

How does methotrexate work?

A

Interferes with metabolism of folate also suppressing the immune system.

Taken once a week along with 5mg folic acid on diff day to methotrexate

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38
Q

What are some side effects of methotrexate?

A
  • Mouth ulcers
  • Liver toxicity
  • Pulmonary fibrosis
  • Bone marrow suppression and leukopenia
  • Teratogenic (harmful to pregnancy)
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39
Q

How does leflunomide work?

A

Immunosuppressant - interfers with production of pyrimidine (component of RNA and DNA)

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40
Q

What are some side effects of leflunomide?

A
  • Mouth ulcers and mucositis
  • Increased blood pressure
  • Rashes
  • Peripheral neuropathy
  • Teratogenic
  • Liver toxicity
  • Bone marrow suppression and leukopenia
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41
Q

What is sulfasalazine?

A

Immunosuppressant and anti-inflammatory

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42
Q

What are some side effects of sulfasalazine?

A

Temporary male infertility (reduced sperm count)

Bone marrow suppression

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43
Q

What is hydroxychloriquine?

A

Traditionally an anti-malarial but also an immunosuppressant interferes with toll-like receptors disrupting antigen presentation

Thought to be safe in pregnancy

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44
Q

What are some side effects of hydroxychloroquine?

A
  • Nightmares
  • Reduced visual acuity
  • Liver toxicity
  • Skin pigmentation
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45
Q

How do anti-TNF drugs work?

A

Block TNF - a cytokine involved in inflammation

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46
Q

What are some anti-TNF drugs?

A
  • Adalimumab
  • Infliximab (both monoclonal antibodies)
  • Enteracept (protein that binds TNF to Fc portion of IgG)
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47
Q

What are some side effects of anti-TNF drugs?

A
  • Severe infection and sepsis
  • Reactivation of TB anf Hep B
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48
Q

What is Rituximab?

A

Monoclonal antibody that targets CD20 protein on surface of B cells (used for immunosuppression in auti-immune conditions and cancers related to B cells)

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49
Q

What are the unique side effects of:

Methotrexate

Leflunomide

Sulfasalazine

Hydroxychloroquine

Anti-TNF medications

Rituximab: Night sweats and thrombocytopenia

A

Methotrexate: pulmonary fibrosis

Leflunomide: Hypertension and peripheral neuropathy

Sulfasalazine: Male infertility (reduces sperm count)

Hydroxychloroquine: Nightmares and reduced visual acuity

Anti-TNF medications: Reactivation of TB or hepatitis B

Rituximab: Night sweats and thrombocytopenia

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50
Q

What hand joints are typically affected in psoriatic arthritis (inflammatory arthritis)?

A

Wrists, DIPs (MCP NOT AFFECTED UNLIKE RA)

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51
Q

What are some recognised patterns of rheumatoid arthritis?

A

Symmetrical polyarthritis = similarly to rheumatoid arthritis, more common in women. The hands, wrists, ankles and DIP joints are affected. The MCP joints are less commonly affected (unlike rheumatoid).

Asymmetrical pauciarthritis affecting mainly the digits (fingers and toes) and feet. Pauciarthritis describes when the arthritis only affects a few joints.

Spondylitic pattern is more common in men. It presents with:

  • Back stiffness
  • Sacroiliitis
  • Atlanto-axial joint involvement

Other areas can be affected:

  • Spine
  • Achilles tendon

Plantar fascia

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52
Q

How does psoriatic arthritis present?

A

Plaques on the skin

Pitting of the nails

Onycholysis (separation of nail from nail bed)

Dactylitis (inflammation of full finger)

Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)

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53
Q

What are some other associations of psoriatic arthritis?

A

Conjunctivitis / anteior uveitis

Aortitis

Amyloidosis

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54
Q

What are the xray changes for psoriatic arthritis?

A

Periostitis = inflammation of the periosteum causing a thickened and irregular outline of the bone

Ankylosis = bones joining together causing joint stiffening

Osteolysis = destruction of bone

Dactylitis = inflammation of the whole digit and appears on the xray as soft tissue swelling

Pencil-in-cup appearance

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55
Q

What is arthritis mutilans?

A

Severe form of psoriatic arthrits in phalanxes

Osterlysis of the bone around the joint causing progressive shortening of digit = telescopic finger

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56
Q

What are the medication options for psoriatic arthritis?

A

NSAIDs for pain

DMARDs (methotrexate, leflunomide or sulfasalazine)

Anti-TNF medication (entanercept, infliximab or adalimumab)

Ustekinumab is last line (after anti-TNF medications) = monoclonal antibody targetting IL 12 and 23

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57
Q

Reactive arthritis causes what ?

What gene is it linked to?

A

Used to be known as Reiter’s syndrome - synovitis occurs in joint

Acute monoarthritis (usually lower limb = leg)

No infection in the joint (unlike sepsis)

Linked to HLA B27 gene (part of seronegative spongyloarthropathies)

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58
Q

What are the most common causes of reactive arthritis?

A

Gastroenteritis

STIs

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59
Q

What are the symptoms of reactive arthritis?

A

Balanitis (dermatitis of head of penis)

Anterior uveititis

Bilateral conjunctivitis

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60
Q

What is the management for reactive arthritis?

A

Give abx until septic arthritis is ruled out

Aspirate joint and send for gram staining, cultures, sensitity and crystal examination

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61
Q

What is the management of reactive arthritis?

A

NSAIDs

Steroid injections

Systemic steroids may be required

Recurrent cases = DMARDs or anti-TNF medications

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62
Q

What are the seronegative spondyloarthropathies?

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis

All related to HLA B27

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63
Q

What joints are affected in Ankylosing Spondylitis?

A

Sacroiliac joints

Vertebral column

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64
Q

What is the classic finding on X-Ray for Ank Spondylitis?

A

Bamboo spine (due to fusion of spine)

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65
Q

What is the presenting feature of Ankylosing Spondylitis?

A

Lower back pain and stiffness

Sacroiliac pain

In 20s usually and affects men: women equally

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66
Q

When is the pain from Ankylosing spondylitis worse?

What is a key complication of AS?

A

Night and in morning (worse with rest)

Vertebral fractures

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67
Q

What are some associations of anylosing spondylitis?

A

Systemic symptoms = weight loss, fatigue

Chest pain = involvement of costovertebral and costosternal joints

Enthesitis (causing plantar fasciitis and achilles tendonitis)

Dactylitis

Anterior Uveitis

Aoritits

Heart block (fibrosis of heart’s conductive system)

Pulmonary fibrosis

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68
Q

How is Schober’s test performed?

What indicates a normal ROM?

A

Patient stand straight - find L5 vertebrae - mark 10cm above and 5cm below (15cm apart - pt bends forwards and assess distance)

>20cm between points on back

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69
Q

What investigations are there for Ank Spond?

A

Inflammatory markers (CRP and ESR) raised

HLA B27 genetic testing

X ray of the spine

MRI of spine can show bone marrow oedema early in disease before any X-ray changes

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70
Q

What are the x-ray changes for Ank Spond?

A
  • Bamboo spine
  • Squaring of the vertebral bodies
  • Subchondral sclerosis and erosions
  • Syndesmophytes = areas of bone growth where the ligaments insert into the bone
  • Ossification of the ligaments, discs and joints. This is where these structures turn to bone.
  • Fusion of the facet, sacroiliac and costovertebral joints
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71
Q

What is the management of Ank Spond?

A

NSAIDs to help with pain (if not adequately treated afrer 2-4 weeks of max dose then switch to another NSAID)

Steroids (oral / IM / joint injections)

Anti-TNF (e.g. etanercept or monoclonal antibody against TNF e.g. infliximab, adalimumab or certolizumab pegol)

Secukinumab is a monoclonal antibody against IL-17 (recommended if response to NSAIDs and TNF inhibitors is inadequate)

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72
Q

What are some additional management steps for patients with ANK SPOND?

A
  • Physio
  • Exercise
  • Avoid smoking
  • Bisphosponates for osteoporosis
  • Treat complications
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73
Q

What is systemic lupus erythematosus?

A

Inflammatory autoimmune connective tissue disorder

(erythematosus refers to typical red malar rash across face)

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74
Q

What is the disease course of SLE?

A

Relapsing-remitting

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75
Q

What are the leading causes of death in SLE?

A

Cardiovascular disease

Infection

(chronic inflammation cause shortened life expectancy)

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76
Q

What antibodies are present in SLE?

A

Anti-nuclear antibodies (antibodies to proteins within persons own cell nucleus)

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77
Q

How does SLE present?

A
  • Fatigue
  • Weight loss
  • Arthralgia
  • Myalgia
  • Fever
  • Photosensitive malar rash
  • Lymphadenopathy
  • SOB
  • Pleuritic chest pain
  • Mouth ulcers
  • Hair loss
  • Raynauds
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78
Q

What investigations are there for SLE?

A

- Autoantibodies

- FBC (anaemia of chronic disease)

- C3 and C4 levels (decreased in active disease)

- CRP and ESR (raised with active inflammation)

- Immunoglobulins (raised due to activation of B cells with inflammation)

- Urine protein: creatinine ratio for proteinuria

- Renal biopsy for lupus nephritis

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79
Q

What autoantibody is SLE associated with?

A

Anit-nuclear antibodies ANA = 85% (also autoimmune hepatitits)

anti-dsDNA (very specific to SLE and vary with disease activity)

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80
Q

How is SLE diagnosed?

What can occur secondary to SLE

A

Confirm presence of Antinuclear anitbodies and clinical features suggestive of SLE

Secondary = antiphospholipid antibodies and antiphospholipid syndrome

81
Q

What are some complciations of SLE?

A
  • CVD: hypertension from inflammation of vessels
  • Infection: secondary to immunosuppressants
  • Anaemia of chronic disease (affecting bone barrow causing normocytic anaemia) - leukopenia, neutropenia, thrombocytopenia
  • Pericarditis
  • Pleuritis

- Interstitial lung disease

  • Lupus nephritis
  • Neuropsychiatry SLE (due to inflammation of CNS - presents with optic neuritis, transverse myelitis - inflammation of spinal cord or psychosis)

Reccurent miscarriage (and intrauterine growth restrictiom, pre-eclampsia and pre-term labour)

VTE associated with antiphospholipid syndrome secondary to SLE

82
Q

What are the treatment options for SLE?

A

Autoimmune condition so anti-inflammatories and immunosuppression

  • NSAIDs
  • Steroids
  • Hydroxychloroquine
  • Suncream and sun avoidance for the rash
83
Q

What are some other commonly used immunosuppressants in SLE?

A
  • Methotrexate
  • Mycophenolate mofetil
  • Azathioprine
  • Tacrolimus
  • Leflunomide
  • Ciclosporin
84
Q

What biologic therapy can be used for SLE?

A

Rituximab - monoclonal antibody targetting CD20 protein on surface of B cells

Belimumab - monoclonal antibody targetting B-cell activating factor

85
Q

What is discoid lupus erythmatosus?

A

Non-cancerous chronic skin condition - more common in women - increased risk of developing SLE

86
Q

How does discoid lupus erythromatosus present?

A

Photosensitive lesions

Scarring alopecia

Lesions = inflammed, erythmatous, patchy, crusty

87
Q

What is the management of discoid lupus erythromatosus?

A
  • Sun protect
  • Topical steroids
  • Intralesional steroid injection
  • Hydroxychloroquine
88
Q

What is the difference between systemic sclerosis and scleroderma?

A

They can be used interchangably but there is a local version of sclerodoma which only affect the skin

89
Q

What causes systemic sclerosis?

What type of disease is systemic sclerosis?

A

Unsure

Autoimmune inflammatory and fibrotic connective tissue disorder

90
Q

What is the mneumonic for limited cutaneous systemic sclerosis (as opposed to diffuse cutanrous systemic sclerosis)?

A

CREST

Calcinosis

Raynaud’s phenomenon

oEsophageal dysmotility

Sclerodactyly

Telangiectasia

91
Q

What does diffuse cutaneous systemic sclerosis affect?

A

All features of CREST including

Cardiovascular problems HTN and coronary artery disease

Lung problems: pulmonacy HTN, pulmonary fibrosis

Kidney problems: glomerulonephritis

92
Q

What are the physical manifestations of systemic sclerosis?

A

Scleroderma (hardening of the skin)

Scterodactyly (hardening of the hands - tight skin restricts range of motion, can break and ulcerate)

Telangiectasia (dilated blood vessels of the skin)

Calcinosis (calcium deposits under the skin, most commonly on fingertips)

Raynaud’s phenomenon

Oesophageal dysmotility (connective tissue dysfunction in oesophagus associated with swallowing difficulties)

Systemic hypertension (connective tissue dysfunction in systemic and pulmonary arterial systems)

Pulmonary fibrosis (presents as gradual dry cough and SoB)

93
Q

What are the autoantibodies associated with systemic sclerosis?

A

Antinuclear antibodies (not specific to SS)

Anti-centromere antibodies (associated with limited cutaneous systemic sclerosis)

Acti-Scl-70 antibodies (associated with diffuse cutaneous systemic sclerosis)

94
Q

How is a diagnosis of systemic sclerosis made?

A

- Clinical features

- Antibodies

- Nailfold capillaroscopy (avascular areas and micro-haemorrhages indicate SS)

95
Q

What are some non-medical management options for systemic slerosis?

A

Avoid smoking

Skin stretching to maintain range of motion

Regular emollients

Avoid cold triggers for Raynaud’s

Physio

OT for adaptations to daily living

96
Q

What medication can be used for systemic sclerosis?

A

Steriods and immunosuppressants (no standardised and proven treatment)

Nifedipine (for Raynaud’s)

Analgesia for joint pain

Pro-motility medications (e.g. metoclopramide) for GI symptoms

Antibiotics for skin infections

Antihypertensives for hypertension (ACEi)

Treat pulmonary artery hypertension

97
Q

What is polymyalgia rheumatica?

A

Inflammatory condition causing pain and stiffness in the shoulders, pelvis and neck.

Strongly linked to GCA, both respond well to steroids

98
Q

Who does polymyalgia rheumatic normally affect?

A

>50 y/o caucasian women

99
Q

What are the core features of polymyalgia rheumatica?

A

Bilateral shoulder pain, radiating to elbow

Pelvic girdle pain

Interferes with sleep

Worse with movement

At least 45 min morning stiffness

100
Q

What are some other features of polymyalgia rheumatica?

A

Systemic symptoms = weight loss, fatigue, low grade fever and low mood

Upper arm tenderness

Carpel tunnel syndrome

Pitting oedema

101
Q

What are some differentials for shoulder, neck and oelvis stiffness and inflammation?

A
  • OA
  • RA
  • SLE
  • Myositis (from conditions like polymyositis or medications like statins)
  • Cervical spondylosis
  • Adhesive capsulitis
  • Hyper / hypothyroidism
  • Osteomalacia
  • Fibromyalgia
102
Q

How is polymyalgia rheumatica typically diagnosed?

A

Clinical presentation and response to steroids (ESR, plasma viscosity and CRP)

103
Q

What additional investigations for polymyalgia rheumatica before starting steroids to rule out other conditions?

A

FBC

U&Es

LFTs

Calcium raised in hyperparathyroidims / cancer and low in osteomalacia

Serum protein electrophoresis for myeloma and other protein disorders

TSH

CK for myositis

Rheumatoid factor for RA

Urine dipstick

ANA for SLE

anti-CCP for RA

Urine Bence Jones protein for myeloma

CXR for lung and mediastinal abnormalities

104
Q

What is the treatment for PMR?

A

Steroids (expecting an improvement in symptoms)

Assess 1 week = if poor response then probably not PMR and stop, look for other diagnosis

Assess 3-4 weeks = 70% improvement expected, inflammatory markers normal = PMR (if no improvement then start reducing regime of steroids)

105
Q

What is the osteoporosis protection / gastric protection when on steroids?

A

Bisphosphonates

Calcium

Vitamin D

PPI

106
Q

What is GCA?

A

Systemic vasculitis of the medium and large arteries (usually affects temporal arteries)

107
Q

What are the symptoms of GCA?

A
  • Severe unilateral headache
  • Scalp tenderness
  • Jaw claudication
  • Blurred vision
  • Irreversible painless complete sight loss
108
Q

What are the associated symtoms of GCA?

A

Fever

Muscle aches

Fatigue

Weight loss

Loss of appetite

Peripheral oedema

109
Q

How is a definitive diagnosis of GCA made?

A
  • Clinical presentation
  • Raised ESR
  • Temporal artery biopsy findings
110
Q

What is found on the biopsy for GCA?

A

Multinucleated giant cells

111
Q

What do the blood tests show for GCA?

What imaging for GCA?

A
  • Normocytic anaemia and thrombocytosis
  • LFTs raised ALP
  • C reactive protein is usually raised

Duplex ultrasound of temporal artery shows hypoechoic halo sign

112
Q

What is the initial management for GCA?

A

Steroids - reduce risk of permanent sight loss (and PPI) - review after 48 hrs

Aspirin

113
Q

Who to refer a patient with GCA to?

A

Vascular surgeons (temporal artery biopsy)

Rheumatology for diagnosis

Opthamology if visual symotoms

114
Q

What are the sick day rules and treatment card for patients on steroids?

A

Increase dose when sick and take at treatment card with you

115
Q

What are some complications of GCA?

A
  • Vision loss
  • Stroke
  • Relapse
  • Steroid side effects
  • Aortitis leading to aortic aneurysm and aortic dissection
116
Q

What are polymyositis and dermatomyositis?

A

Autoimmune disorders where there is inflammation of the muscles (myositis) and or skin (in dermatomyositis)

117
Q

What is the key investigation for polymyositis and dermatomyositis?

A

Creakine Kinase > 1000 (caused by myositis)

118
Q

What are some other causes of a raised CK?

A

Rhabdomyolysis

AKI

MI

Statins

Strenuous exercise

119
Q

What can polymyositis / dermatomyositis be caused by?

A

Paraneoplastic syndrome from malignancy (lung, breast, ovarian, gastric)

120
Q

What is the presentation of polymyositis?

A
  • Muscle pain, fatigue and weakness
  • Proximal muscles normally affects
  • Shoulder and pelvic girdle
  • Develops over weeks

Polymyositis occurs without any skin features whereas dermatomyositis is associated with involvement of skin

121
Q

What are the skin features of dermatomyositis?

A
  • Gotton lesions (scaly erythomatous patches) on the knuckles, elbows and knees
  • Photosensitive erythmatous rash on back, shoulders and neck
  • Purple rash on face and eyelids
  • Periorbital oedema (swelling around eyes)
  • Subcutaneous calcinosis (calcium deposits in subcut tissue)
122
Q

What antibodies are seen in polymyositis and dermatomyositis respectively?

A

Polymyositis = anti Jo-1 antibodies

Dermatomyositis = anti-Mi-2 antibodies and anti-nuclear antibodies

123
Q

What is the diagnosis of polymyositis basedon ?

A
  • Clinical presentation
  • Elevated CK
  • Autoantibodies
  • Electromyography (EMG)
  • Muscle biopsy
124
Q

What is the first line medication for polymyositis/dermatomyositis?

A

Corticosteroids

  • Immunosuppressants (e.g. azathioprine)
  • IV immunoglobulins
  • Biological therapy (e.g. infliximab or etanercept)
125
Q

What is antiphospholipid syndrome?

A

Problem with antiphospholipid antibodies where the blood becomes prone to clotting

126
Q

When does antiphospholipid syndrome commonly occur?

A

Secondary to SLE

127
Q

What are the main associations of antiphospholipid syndrome?

A

Thromobosis

Pregnancy complications e.g. recurrent miscarriage

128
Q

Which antibodies as associated with antiphospholipid syndrome?

A

Lupus anticoagulant

Anticardiolipin antibodies

Anti-beta-2 glycoprotein I antibodies

129
Q

What are some associations of antiphospholipid syndrome?

A

DVT

PE

Stroke

MI

Renal thrombosis

Recurrent miscarriage, stillbirth, preeclampsia

Livedo reticularis (purple rash)

Libmann-Sacks endocarditis (type of non-bacterial endocarditis causing vegetation on the valves of the heart - mitral is commonly affected)

Thrombocytopenia (low platelets)

130
Q

How is the diagnosis of antiphospholipid syndrome made?

A

Lupus anticoagulant

Anticardiolipin antibodies

Anti-beta-2 glycoprotein I antibodies

131
Q

What is the management of antiphospholipid syndrome?

A
  • Long term warfarin aiming for 2-3 (LMWH if pregnant e.g. enoxaparin plus aspirin)
132
Q

What is Sjogren’s syndrome?

A

Autoimmune condition affecting the exocrine glands leading to dry mucous membranes e.g. dry mouth, eyes, vagina

133
Q

What is primary sjogren’s?

A

Disease occurs in isolation

134
Q

What is secondary Sjogren’s ?

A

Occurs related to SLE or RA

135
Q

What antibodies is Sjogren’s associated with?

A

Anti-Ro

Anti-La

136
Q

What is the Schimer’s test for Sjogren’s?

A

Filter paper under eyelid (but in eye), leave for 5 mins and see how far tear travels - should be 15mm in healthy young adult (less than 10mm is significant)

137
Q

What is the management of Sjogren’s ?

A

Artificial tears

Artifical saliva

Vaginal lubricants

Hydroxychloroquine to halt disease progression

138
Q

What are some complications of Sjogren’s?

A

Eye infections = conjunctivits / corneal ulcers

Oral problems = dental cavities and candida infections

Vaginal problems = candidiasis and sexual dysfunction

Along with:

  • Pneumonia and bronciectasis
  • NHL
  • Peripheral neuropathy
  • Vasculitis
  • Renal impairment
139
Q

What vasculitis affects the small vessels?

A

Henoch-Schonlein purpura

Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)

Microscopic polyangiitis

Granulomatosis with polyangiitis (Wegener’s granulomatosis)

140
Q

What vasculitis affect the medium sized vessels?

A

Polyarteritis nodosa

Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)

Kawasaki disease

141
Q

Which vasculitis affect the large vessels?

A

Giant cell arteritis

Takayasu’s arteritis

142
Q

What symptoms are shared amongst most types of vasculitis?

A

Purpura. These are purple-coloured non-blanching spots caused by blood leaking from the vessels under the skin.

Joint and muscle pain

Peripheral neuropathy

Gastrointestinal disturbance (diarrhoea, abdominal pain and bleeding)

Renal impairment

Anterior uveitis and scleritis

Hypertension

143
Q

What are some systemic manifestations of vasculitis?

A

Fatigue

Fever

Weight loss

Anorexia (loss of appetite)

Anaemia

144
Q

What are the tests for Vasculitis?

A

Inflammatory markers: CRP and ESR

Anti-neutrophil cytoplasmic antibodies (ANCA)

145
Q

What is p-ANCA (anti-MPO) associated with?

A

Microscopic polyangiitis and Churg-Strauss syndrome

146
Q

What is c-ANCA associated with?

A

Wegener’s granulomatosis

147
Q

What is the treatment of vasculitis?

A

Steroids (oral e.g. prednisolone, hydrocortisone, nasal spray, inhaled for lung e.g. Churg-Strauss)

Immunosuppressants: cyclophosphamide, methotrexate, azathioprine, rituximab

148
Q

What is Henoch-Schonlein purpura?

Why does the rash occur?

What is it triggered by?

What are the classic 4 features?

What is the management?

A

IgA vasculitis presenting with purpuric rash on lower limbs

Rash due to IgA deposits in blood vessels of affected organs e.g. skin, kidbeys, and GI tract

Triggered by upper airway infection (e.g. tonsilitis)/ GI

Most common in children under 10 y/o

Features = purpura, joint pain, abdo pain, renal involvement

Management = simple analgesia, rest and proper hydration (benefits of steroids = unclear)

149
Q

How does Eosinophilic Granulomatosis with Polyangiitis present (aka Churg-Strauss syndrome)?

How does it present?

What is a characteristic finding?

A

Small and medium sized vasculitis affecting lungs and skin

Presents with severe asthma in late teenage ears

Characteristic finding = elevate eosinophil levels

150
Q

How does microscopic polyangiitis present?

A

Small vessel vasculitis causing renal failure also affecting lungs causing SoB and haemoptysis

151
Q

How does granulomatosis with polyangiitis (Wegener’s granulomatosis) present?

A

Small vessel vasculits affecting resp tract and kidneys

Epistaxis, hearing loss, saddle shaped nose (due to perforated nasal septum),

Cough, wheeze, haemoptysis

Glomerulonephritis

152
Q

How does Polyarteritis Nodosa present?

What is it associated with?

A

Medium sized vasculitis associated with hep B/C and HIV

Affects skin, GI, kidneys and heart causing renal impairment, strokes and MI

Causes livedo reticularis (mottled, purple, lace rash)

153
Q

Where does Kawasaki disease affect?

What are the clinical features?

What is a key complication?

A

A medium vessel vasculitis affecting young children < 5 years old

Features = persistent high fever > 5 days, erythematous rash, bilateral conjunctivitis, erythema and desquamation (skin peeling) of palms and soles

Strawberry tongue (red tongue with prominent papillae)

Complication = coronary artery aneurysms

Treatment = aspirin and IV immunoglobulins

154
Q

How does Takayasu’s arteritis present?

How is it diagnosed?

A

Large vessel vasculitis mainly affecting the aorta and pulmonary arteries (also called pulseless disease)

Presents before 40 years with non-specific symptoms e.g. fever, malaise and muscle aches

Diagnosis = CT or MRI angiography

Doppler ultrasound of carotids can detect carotid disease

155
Q

How does Behçet’s disease present?

A

Oral and genital ulcers (also cayses inflammation in skin, GI tract, lungs, blood vessels, MSK, CNS)

156
Q

What gene is linked to Behçet’s disease?

A

HLA B51

157
Q

What are the differentials to mouth ulcers?

A

Simple aphthous ulcers

Inflammatory bowel disease

Coeliac disease

Vitamin deficiency (B12, folate, or iron)

Herpes simplex ulcers

Hands, foot and mouth disease (coxsackie A virus)

Squmaous cell carcinoma

158
Q

What are the features of Behçet’s disease?

A

Mouth ulcers

Genital ulcers (kissing ulcers on two opposing surfaces)

Skin inflammation - erythema nodosum, papules and pustules, vasculitic type rashes

Eyes - uveitis, retinal vasculitis, retinal haemorrhages

MSK system - morning stiffness, arthralgia, oligoarthritis

GI system - inflammation and ulceration affecting ileum, caecum, ascending colon

Central nervous system - memory impairment, headaches and migraines, aseptic meningitis, meningoencephalitis

Veins - inflammation and vein thrombosis (e.g. Budd Chiari syndrome, DVT, thrombus in pulmonary veins, cerebral venous sinus thrombosis

Lungs - pulmonary artery aneurysms can rupture (and be fatal)

159
Q

How is Behçet’s disease diagnosed?

A

Clinical diagnosis

Pathergy test - subcut abrasion is made on arm and examined after for reaction (weal for 5mm or more - testing for non-specific hypersensitivity in skin, positive in Behcet’s disease, Sweet’s syndrome and pyoderma gangrenosum)

160
Q

What is the management of Behçet’s disease?

What is the prognosis?

A

Topical steroids for mouth ulcers (e.g. soluble betamethasone)

Systemic steroids (i.e. oral prednisolone)

Colchicine usually effective as anti-inflammatory to treat symptoms

Topical anaesthetics for genital ulcers (e.g. lidocaine ointment)

Immunosuppressants - azathioprine

Biologics e.g. infliximab

Prognosis = relapsing-remitting with normal life expectancy

161
Q

What are the most commonly affected joints in the hand by gout?

What causes it?

What are gouty tophi?

How does gout present?

A

DIP joints

Chronically high uric acid (urate crystals are deposited in the joint)

Gouty tophi are subcut deposits of uric acid

Presents = single acute, hot, swollen and painful joint (differential = septic arthritis)

162
Q

What are some risk factors for gout?

A
  • Male
  • Obesity
  • High purine diet (e.g. meat and seafood)
  • Alcohol
  • Diuretics
  • FH
163
Q

Which joints are affected by gout?

A

1st metatarsalphalangeal joint (base of big toe)

Wrists

1st carpometacarpal joint (base of thumb)

Can affect large joints

164
Q

How is gout diagnosed?

A

Aspiration of fluid from joint

165
Q

What will aspirated fluid from gout show?

A
  • No bacterial growth
  • Needle shaped crystals
  • Negative birefringent of polarised light
  • Monosodium urate crystals
166
Q

What does a joint Xray show for gout?

A

Maintained joint space

Lytic lesions in the bone

Punched out erosions with sclerotic borders

167
Q

What is used to treat gout?

When is colchicine used? Whats a side effect of this?

A

Acute = NSAIDs, Colchicine, steroids

Used when NSAIDs not appropriate e.g. renal impairment / significant heart disease

Side effect = diarrhoea

168
Q

What is used as prophylaxis against gout?

A

Allopurinol (xanthine oxidase inhibitor)

169
Q

What lifestyle changes are there to reduce risk of gout?

A

Losing weight, staying hydrated, less alcohol

Less purine based foods (meat and seafoods)

170
Q

What joint is commonly affected in pseudogout?

What is it?

A

Knee

Crystal arthropathy caused by calcium pyrophosphate crystals aka chondrocalcinosis

171
Q

What will aspirated fliud show from pseudogout?

A
  • No bacterial
  • Calcium pyrophosphate crystals
  • Rhomboid shaped
  • Postivie birefringent of polarised light
172
Q

What is the classic xray change in pseudogout?

A

Chondrocalcinosis - thin white line in middle of joint space (pathognomonic)

173
Q

What is the treatment of pseudogout?

A

NSAIDs, colchicine, joint aspiration, steroid injections, joint washout (if severe)

174
Q

What are some risk factors for osteoporosis?

A
  • Older age
  • Female
  • Reduced mobility and activity
  • Low BMI
  • Rheumatoid arthritis
  • Alcohol and smoking
  • Long term corticosteroids
175
Q

Why does osteoporosis occur in post menopausal women?

A

Oestrogen is protective against osteoporosis

176
Q

What tool gives the risk of a fragility fracture over the next 10 years in osteoporosis?

A

FRAX tool (using age, BMI, smoking, alcohol, FH)

177
Q

What is bone mineral density measured using?

What score indicates bone density?

A

DEXA scan (xrays)

T score at hip is the most important (density compared to a healthy young adult)

Z score (compare to mean for age) or T score (compared to mean for healthy young adult - this is most clinically important outcome)

178
Q

What are the lifestyle changes that a patient with osteoporosis can do?

A

Activity and exercise

Maintain a health weight

Adequate calcium intake

Adequate vitamin D

Avoiding falls

Stop smoking

Reduce alcohol consumption

179
Q

What are some medical options for osteoporosis?

A

Calcium and vitamin D (colecalciferol)

Bisphosphonates (reduce activity of osteoclasts)

180
Q

What are the key side effects to bisphosphonates?

A

Reflux and oesophagel erosions (take on empty stomach, sitting up 30 mins before any food)

Osteonecrosis of the jaw

Osteonecrosis of the external auditory canal

181
Q

What are some example of some bisphosphonates?

A

Alendronate

Risedronate

Zoledronic acid

182
Q

What are some other medical options for osteoporosis?

A

Denosumab = monoclonal antibody that blocks osteoclasts

Strontium ranelate = similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases risk of DVT, PE and MI

Raloxifene

HRT if menopause early

183
Q

What is osteomalacia? Why does it happen?

What does it cause? What is it called in children?

A

Soft bone due to defective bone mineralisation as a result of low Vit D

Weak bone, bone pain, muscle weakness and fractures

Causes rickets

184
Q

What is vitamin D?

A

A hormone created from cholesterol by the skin in response to UV radiation

185
Q

Which patients are more likely to have vitamin D deficiency?

A

Patients with malabsorption conditions IBD

Kidneys are needed to make active form therefore vit D deficinency is common in CKD

186
Q

What is vitamin D needed for?

A

Calcium and phosphate absorption from the intestines and kidneys, also for regulating bone turnover

187
Q

How does parathyroid hormone interfere with problems due to low vitamin D?

A

Low calcium causes more PTH released which stimulates more resporption from the bones causing further mineralisation problems

188
Q

What is the typical presentation of a patient with osteomalacia?

A
  • Fatigue
  • Bone pain
  • Muscle weakness
  • Muscle aches
  • Pathological fractures
189
Q

What is the investigation for osteomalacia?

A

Serum-25-hydroxyvitamin D

190
Q

What are the other findings for osteomalacia?

A

Low serum calcium

Low serum phosphate

High ALP

High PTH

Xray may show osteopenia (more radiolucent bones)

DEXA show low bone mineral density

191
Q

What is the treatment of osteomalacia?

A

Colecalciferol

192
Q

What is Paget’s disease?

A

Disorder of bone turnover - excessive - due to overactive osteoblasts and osteoclasts

Causing enlarged and misshapen bones with increased risk of pathological fractures

193
Q

How does Paget’s disease present?

A

Bone pain

Bone deformity

Fractures

Hearing loss if affecting bones of ears

194
Q

What are the xray findings for Paget’s disease?

A

Bone enlargement and deformity

Osteoporosis circumscripta = well defined osteolytic lesions that appear less dense with normal bone

Cotton wool appearance of the skull describes patchy areas of increased density and decreased density

V-shaped defects in long bones

195
Q

What is the only lab abnormality in Pagets?

A

Raised ALP (normal calcium and phosphate)

196
Q

What is the management for Paget’s disease?

A

Bisphosphonates

NSAIDs for bone pain

(Calcium and Vit D supplementation particularily for bisphosphonates)

Monitor serum ALP

197
Q

What are two complications of Paget’s disease?

A

Osteosarcoma - bone cancer - presents with focal bones pain and swelling

Spinal stenosis - deformity causes spinal canal narrowing - diagnosed with MRI treated with bisphosphonates

198
Q
A

Medicine (12 decks)

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