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Finals > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Rheumatoid Arthritis

what is it

A

an autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa

it is an inflammatory arthritis

symmetrical polyarthritis

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2
Q

Rheumatoid Arthritis

what does symmetrical polyarthritis mean

A

symmetrical and affects multiple joints

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3
Q

Rheumatoid Arthritis

epidemiology

A

F>M

middle age

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4
Q

Rheumatoid Arthritis

which gene is often present in RF positive patients

A

HLA DR4

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5
Q

Rheumatoid Arthritis

which gene is occasionally present in RA patients

A

HLA DR1

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6
Q

Rheumatoid Arthritis

antibodies

A
  • Rheumatoid Factor (RF)
  • Cyclic citrullinated peptide antibodies (anti-CCP antibodies)
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7
Q

Rheumatoid Arthritis

what is RF

A

an autoantibody that targets the Fc portion of the IgG antibody

which causes activation of the immune system against the patient’s own IgG causing systemic inflammation

RF is most often IgM but can be any class of immunoglobulin

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8
Q

Rheumatoid Arthritis

what are anti-CCP antibodies

A

Cyclic citrullinated peptide antibodies are autoantibodies that are more sensitive and specific to RA than RF

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9
Q

Rheumatoid Arthritis

Key symptoms

A
  • symmetrical distal polyarthropathy
  • joint pain, swelling and stiffness
  • worse after rest but improves with activity
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10
Q

Rheumatoid Arthritis

systemic symptoms

A
  • fatigue
  • weight loss
  • flu like illness
  • muscle aches and weakness
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11
Q

Rheumatoid Arthritis

what is Palindromic Rheumatism

A

self limiting short episodes of inflammatory arthritis with joint pain, stiffness and swelling typically affecting only a few joints

this episode only lasts 1-2d then completely resolves

having positive RF + anti-CCP indicate it will progress to full RA

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12
Q

Rheumatoid Arthritis

which joints are NOT affected

A

distal interphalangeal joints

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13
Q

Rheumatoid Arthritis

common joints affected

A
  • PIP
  • MCP
  • wrist + ankle
  • Metatarsophalangeal joints
  • cervical spine
  • large joints also: knee, hips, shoulders
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14
Q

Rheumatoid Arthritis

what is Atlantoaxial Subluxation

A

occurs in the cervical spine

the axis (C2) and the odontoid peg shift within the atlas (C1)

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15
Q

Rheumatoid Arthritis

what causes Atlantoaxial Subluxation

A

local synovitis and damage to the ligaments and bursa around the odontoid peg of the axis and the atlas

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16
Q

Rheumatoid Arthritis

why is RA relevant in anaesthetics and intubation

A

Subluxation can cause spinal compression

MRI scan can visualise changes in these areas as part of pre-op assessment

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17
Q

Rheumatoid Arthritis

what gives the joints a ‘boggy’ feeling

A

palpation of the synovium in around joints when the disease is active will give this feeling related to inflammation and swelling

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18
Q

Rheumatoid Arthritis

signs in the hands (4)

A
  • Z shaped deformity to the thumb
  • Swan neck deformity
  • Boutonnieres deformity
  • Ulnar deviation of the fingers at the knuckle (MCP joints)
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19
Q

Rheumatoid Arthritis

what is Swan neck deformity

A

hyperextended PIP with flexed DIP

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20
Q

Rheumatoid Arthritis

what is Boutonnieres deformity

A

hyperextended DIP and flexed PIP

due to a tear in the central slip of the extensor component of the finger

the flexor digitorum superficialis tendons (lateral tendons that go around the PIP) pull on the distal phalynx without any other supporting structure

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21
Q

Rheumatoid Arthritis

important extra-articular manifestations (4)

A
  1. pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
  2. bronchiolitis obliterans: inflammation causing small airway destruction
  3. Felty’s syndrome: RA, neutropenia, splenomegaly
  4. Secondary Sjogren’s Syndrome aka sicca syndrome
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22
Q

Rheumatoid Arthritis

other extra-articular manifestations (7)

A
  • anaemia of chronic disease
  • CVS disease
  • episcleritis + scleritis
  • rheumatoid nodules
  • lymphadenopathy
  • carpal tunnel syndrome
  • amyloidosis
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23
Q

Rheumatoid Arthritis

inx

A
  • clinical
  • RF
  • if RF -ve, check anti-CCP antibodies
  • CRP, ESR
  • X-ray of hands and feet
  • USS: synovitis
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24
Q

Rheumatoid Arthritis

x-ray changes

A
  • joint destruction and deformity
  • soft tissue swelling
  • periarticular osteopenia
  • bony erosions
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25
Q

Rheumatoid Arthritis

when to refer

A

any adult with persistent synovitis

urgent: if it involves the small joints of the hands or feet, multiple joints or symptoms present >3m

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26
Q

Rheumatoid Arthritis

diagnostic criteria from ACR/ELAR 2010

A

Patient scored based on:

  1. joints involved (more + smaller joints score higher)
  2. RF + CCP
  3. ESR + CRP
  4. duration of sx (more or less than 6w)

score ≥6 = dx of RA

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27
Q

Rheumatoid Arthritis

what is the DAS28 score

A

Disease Activity Score based on the assessment for 28 joints

useful in monitoring disease activity and response to trx

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28
Q

Rheumatoid Arthritis

what are the points given for on a DAS28 score

A
  • swollen joints
  • tender joints
  • ESR/CRP result
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29
Q

Rheumatoid Arthritis

what is the Health Assessment Questionnaire (HAQ)

A

measures functional ability

NICE recommend using this at diagnosis to check response to trx

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30
Q

Rheumatoid Arthritis

what factors make 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

Rheumatoid Arthritis

what can be used at 1st presentation and during flare ups to quickly settle the disease

A
  • short course of steroids
  • NSAIDs + PPI
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32
Q

Rheumatoid Arthritis

NICE guidelines for DMARDs 1st line

A

monotherapy with:

  • methotrexate
  • leflunomide
  • sulfasalazine
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33
Q

Rheumatoid Arthritis

what DMARD can be considered in mild disease (considered the mildest anti-rheumatic drug)

A

hydroxychloroquine

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34
Q

Rheumatoid Arthritis

NICE guidelines for DMARDs 2nd line

A

2 of either:

  • methotrexate
  • leflunomide
  • sulfasalazine
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35
Q

Rheumatoid Arthritis

NICE guidelines for DMARDs 3rd line

A

Methotrexate
+
biological therapy: usually a TNF inhibitor

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36
Q

Rheumatoid Arthritis

NICE guidelines for DMARDs 4th line

A

Methotrexate
+
rituximab

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37
Q

Rheumatoid Arthritis

why do pregnant women have an improvement in symptoms

A

probs due to the higher natural production of steroid hormones

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38
Q

Rheumatoid Arthritis

what DMARDs can be given in pregnancy

A

Hydroxychloroquine and Sulfasalazine

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39
Q

Rheumatoid Arthritis

what can biological therapies leads to

A

immunosuppression : prone to serious infections

reactivation of dormant infections: TB + Hep B

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40
Q

Rheumatoid Arthritis

Biological therapies: name some Anti-TNFs

A
  • adalimumab
  • infliximab
  • etanercept
  • golimumab
  • certolizumab pegol
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41
Q

Rheumatoid Arthritis

what is rituximab

A

a biological therapy (Anti-CD20)

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42
Q

Rheumatoid Arthritis

how does methotrexate work?

A

by interfering with the metabolism of folate and suppressing certain components of the immune system

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43
Q

Rheumatoid Arthritis

how often is methotrexate taken and by which route

A

injection or tablet

once a week

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44
Q

Rheumatoid Arthritis

what is prescribed alongside methotrexate and when should it be taken

A

Folic acid 5mg

once a week

taken on a different day to methotrexate

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45
Q

Rheumatoid Arthritis

notable SEs of methotrexate (5)

A
  • pulmonary fibrosis
  • Teratogenic: avoid prior to conception in mothers and fathers
  • mouth ulcers and mucositis
  • liver toxicity
  • bone marrow suppression + leukopenia (low WCC)
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46
Q

Rheumatoid Arthritis

how does Leflunomide work

A

an immunosuppressant medication

interferes with the production of pyrimidine (an important component of RNA + DNA)

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47
Q

Rheumatoid Arthritis

side effects of Leflunomide (2)

A
  • Peripheral neuropathy
  • increased BP
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48
Q

Rheumatoid Arthritis

how does Sulfasalzine work

A

immunosuppressive + anti-inflammatory medication

mechanism not clear but may be related to folate metabolism

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49
Q

Rheumatoid Arthritis

what needs to be prescribed alongside Sulfasalzine

A

folic acid

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50
Q

Rheumatoid Arthritis

SEs of Sulfasalzine (2)

A
  • temporary male infertility (reduced sperm count)
  • bone marrow suppression
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51
Q

Rheumatoid Arthritis

how does hydroxychloroquine work

A

traditionally an anti-malarial med

acts as an immunosuppressive medication by interfering with Toll-like receptors

disrupting antigen presentation and increasing the pH in the lysosomes of immune cells

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52
Q

Rheumatoid Arthritis

SEs of hydroxychloroquine (4)

A
  • nightmares
  • reduced visual acuity (macular toxicity)
  • liver toxicity
  • skin pigmentation
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53
Q

Rheumatoid Arthritis

how do anti-TNF drugs work

A

tumour necrosis factor is a cytokine involved in stimulating inflammation

blocking TNF reduces inflammation

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54
Q

Rheumatoid Arthritis

what is the difference between Adalimumab, infliximab, golimumab and certolizumab pegol

and Etanercept

A

the first 4 are monoclonal antibodies to TNF

Etanercept is a protein that binds TNF to the Fc portion of IgG and thereby reduces its activity

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55
Q

Rheumatoid Arthritis

SEs of Anti-TNF drugs

A
  • Vulnerability to severe infections and sepsis
  • Reactivation of TB and hepatitis B
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56
Q

Rheumatoid Arthritis

how does Rituximab work

A

a monoclonal antibody that targets the CD20 protein on the surface of B cells

This causes destruction of B cells

used for immunosuppression for autoimmune conditions

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57
Q

Rheumatoid Arthritis

SEs for Rituximab

A
  • Night sweats
  • thrombocytopenia
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58
Q

Myositis

what is Polymyositis

A

autoimmune condition of chronic inflammation of muscles

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59
Q

Myositis

what is dermatomyositis

A

an autoimmune connective tissue disorder where there is chronic inflammation of the skin and muscles

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60
Q

Myositis

what is the key inx to diagnose it

A

creatine kinase blood test

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61
Q

Myositis

what is a normal CK

A

<300 U/L

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62
Q

Myositis

what is the CK in polymyositis and dermatomyositis

A

usually >1000

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63
Q

Myositis

what are other causes of raised CK levels

A
  • rhabdomyolysis
  • AKI
  • MI
  • statins
  • strenuous exercise
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64
Q

Myositis

what causes a raised CK

A

inflammation in the muscles cells leads to the release of CK (an enzyme found in muscle cells)

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65
Q

Myositis

what makes Polymyositis or dermatomyositis a paraneoplastic syndrome

A

they can be caused by an underlying malignancy:

  • lung
  • breast
  • ovarian
  • gastric
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66
Q

Myositis

presentation (4)

A
  • muscle pain, fatigue, weakness
  • bilateral and typically proximal muscles
  • mostly shoulder and pelvic girdle affected
  • develops over weeks
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67
Q

Myositis

difference in presentation between Polymyositis or dermatomyositis

A

Polymyositis occurs without any skin features

Dermatomyositis has skin features

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68
Q

dermatomyositis skin features

A
  • Gottron lesions on the knuckles, elbows and knees
  • photosensitive erythematous rash on the back shoulders and neck
  • purple rash on the face and eyelids
  • periorbital oedema (swelling around the eyes)
  • subcutaneous calcinosis (Ca deposits in the subcut tissue)
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69
Q

Dermatomyositis

what are Gottron lesions

A

scaly erythematous patches found on the knuckles elbows and knees

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70
Q

Polymyositis autoantibodies

A

Anti-Jo-1 antibodies

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71
Q

dermatomyositis autoantibodies

A

Anti-Mi-2 antibodies

Anti-nuclear antibodies

Anti-Jo-1 antibodies (also in polymyositis)

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72
Q

Myositis

dx

A
  • definitive: muscle biopsy
  • clinical presentation
  • elevated CK
  • autoantibodies
  • electromyography (EMG)
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73
Q

Myositis

mnx

A

refer to rheumatologist
- physio, occupational therapy

1st line: corticosteroids

  • immunosuppressants (azithioprine)
  • IV immunoglobulins
  • Biological therapy (infliximab or etanercept)
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74
Q

Osteomalacia

what is it

A

osteo: bone
malacia: soft

condition where there is defective bone mineralisation causing soft bones

results from insufficient vit D

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75
Q

Osteomalacia

what is rickets

A

osteomalacia in children prior to their growth plates closing

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76
Q

Osteomalacia

why is vit D deficiency common in CKD

A

the kidneys are essential in metabolising vit D to its active form

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77
Q

Osteomalacia

what is vit D essential for

A
  • calcium and phosphate absorption from the intestines and kidneys
  • bone turnover
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78
Q

Osteomalacia

what causes defective bone mineralisation

A

inadequate levels of vit D –> low ca and phosphate in blood

ca and phosphate are required for construction of bone

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79
Q

Osteomalacia

why does low calcium cause secondary hyperparathyroidism

A

parathyroid gland tries to raise ca levels by secreting parathyroid hormone

which increases reabsorption of ca from the bones

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80
Q

Osteomalacia

symptoms

A

may not have any

  • fatigue
  • bone pain
  • muscle weakness
  • muscle aches
  • pathological or abnormal fractures
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81
Q

Osteomalacia

what are looser zones

A

fragility fractures that go partially through the bone

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82
Q

Osteomalacia

RFs

A

RFs for Vit D deficiency

  • darker skin
  • low exposure to sunlight
  • live in colder climates
  • spend majority of time indoors
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83
Q

Osteomalacia

what is the lab inx for vit D

A

serum 25-hydroxyvitamin D

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84
Q

Osteomalacia

interpretation of Serum 25-hydroxyvitamin D <25 nmol/L

A

vitamin D deficiency

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85
Q

Osteomalacia

interpretation of Serum 25-hydroxyvitamin D 25 – 50 nmol/L

A

vitamin D insufficiency

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86
Q

Osteomalacia

interpretation of Serum 25-hydroxyvitamin D 75 nmol/L or above

A

optimal

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87
Q

Osteomalacia

inx results

A
  • low serum ca
  • low serum phosphate
  • Serum alkaline phosphatase may be high
  • PTH may be high
  • X-Ray: may show osteopenia (more radiolucent bones)
  • DEXA scan shows low bone mineral density
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88
Q

Osteomalacia

trx

A

Colecalciferol with one of the following regimes:

  • 50,000 IU once weekly for 6 weeks
  • 20,000 IU twice weekly for 7 weeks
  • 4000 IU daily for 10 weeks

A maintenance supplementary dose of 800 IU or more per day should be continued for life after the initial treatment.

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89
Q

Osteomalacia

trx for pts with only vitamin D insufficiency

A

started on the maintenance dose without the initial treatment regime

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90
Q

SLE

what is it

A

Systemic Lupus Erythematosus

an inflammatory autoimmune connective tissue disease

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91
Q

SLE

whom is it more common in

A

women and Asians

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92
Q

SLE

when does it present

A

in young to middle aged adults

but can present later in life

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93
Q

SLE

what are the leading causes of death

A

CVD and infection

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94
Q

SLE

pathophysiology

A

inflammatory response to anti-nuclear antibodies

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95
Q

SLE

symptoms

A
  • photosensitive malar rash. Butterfly shaped rash across nose and cheek bones that gets worse with sunlight
  • hair loss
  • SOB
  • splenomegaly
  • joint pain
  • lymphadenopathy
  • myalgia
  • fatigue
  • weight loss
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96
Q

SLE

which antibodies are associated with it

A

anti-nuclear antibodies (ANA)

anti-double stranded DNA (anti-dsDNA)

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97
Q

SLE

inx

A
  • autoantibodies (ANA, anti-dsDNA)
  • FBC: normocytic anaemia
  • C3+4: low
  • CRP+ESR: high
  • Immunoglobulins: raised
  • Urinalysis: proteinuria in lupus nephritis
  • renal biopsy: lupus nephritis
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98
Q

SLE

what are ANA

A

anti-nuclear antibodies

antibodies against normal proteins in the cell nucleus

not specific

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99
Q

SLE

what are anti-dsDNA

A

specific to SLE. Useful for monitoring disease activity

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100
Q

SLE

which type of ANA is highly specific to SLE but not very sensitive

A

Anti-Smith

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101
Q

which type of ANA is associated with systemic sclerosis

A

Anti-Scl-70

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102
Q

which type of ANA is associated with Sjogren’s syndrome

A

Anti-Ro and Anti-La

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103
Q

which type of ANA is associated with limited cutaneous systemic sclerosis

A

Anti-centromere antibodies

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104
Q

SLE

what can occur secondary to SLE

A

Antiphospholipid antibodies and antiphospholipid syndrome

associated with an increased risk of VTE

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105
Q

SLE

what do you use to establish a diagnosis

A

the SLICC Criteria or the ACR Criteria

involves confirming the presence of ANA and establishing a certain number of clinical features

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106
Q

SLE

complications: why does it cause CVD

A

chronic inflammation in the blood vessels –> HTN + coronary artery disease

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107
Q

SLE

complications: why is infection more common

A

part of the disease process and secondary to immunosuppressants.

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108
Q

SLE

complications: why is anaemia of chronic disease more common

A

It affects the bone marrow causing a chronic normocytic anaemia

can also get low WCC, neutrophils and platelets

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109
Q

SLE

complications: why does lupus nephritis occur

A

inflammation in the kidney. it can progress to end-stage renal failure

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110
Q

SLE

1st line trx

A

anti-inflammatory and immunosuppression

  • NSAIDs
  • steroids (prednisolone)
  • ## hydroxychloroquine
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111
Q

SLE

what is 1st line trx for mild SLE

A

hydroxychloroquine

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112
Q

SLE

other commonly used immunosuppressants in resistant or more severe lupus

A

Methotrexate
Mycophenolate mofetil
Azathioprine
Tacrolimus
Leflunomide
Ciclosporin

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113
Q

SLE

what is considered for patients with severe disease or where patients have not responded to other treatments.

A

Biological therapies:

  • Rituximab
  • Belimumab
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114
Q

SLE

how does Belimumab work

A

monoclonal antibody that targets B-cell activating factor

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115
Q

what needs to be tested before giving azathioprine

A

Thiopurine methyltransferase enzyme activity

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116
Q

why does the activity of thiopurine methyltransferase need to be tested before starting azathioprine

A

metabolism + elimination of azathioprine and its metabolites involve xanthine oxidase and thiopurine methyltransferase (TPMT) ​

azathioprine should not be prescribed to patients with absent TPMT activity ​

​

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117
Q

Psoriatic Arthritis

what is it

A

an inflammatory arthritis associated with psoriasis

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118
Q

Psoriatic Arthritis

what is arthritis mutilans

A

most severe form of psoriatic arthritis

osteolysis (destruction) of the bones around the joints in the digits.

This leads to progressive shortening of the digit.

The skin then folds as the digit shortens giving an appearance that is often called a “telescopic finger”.

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119
Q

Psoriatic Arthritis

what group of conditions is it part of

A

seronegative spondyloarthroapathy

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120
Q

Psoriatic Arthritis

name 3 patterns of it

A
  1. Symmetrical polyarthritis
  2. Asymmetrical pauciarthritis
  3. Spondylitic pattern
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121
Q

Psoriatic Arthritis

describe the symmetrical polyarthritis pattern

A
  • similar to RA presentation
  • more common in women
  • hands, wrists, ankles, DIP joints are affected
  • MCP joints are less commonly affected (unlike rheumatoid)
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122
Q

Psoriatic Arthritis

describe the asymmetrical pauciarthritis pattern

A
  • affects mainly digits and feet
  • pauciarthritis: only affects a few joints
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123
Q

Psoriatic Arthritis

describe the spondylitic pattern

A
  • more common in men
  • back stiffness
  • sacroilitis
  • atlanto-axial joint involvement
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124
Q

Psoriatic Arthritis

what other areas can be affected (not the patterns)

A
  • spine
  • achilles tendon
  • plantar fascia
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125
Q

Psoriatic Arthritis

signs (5)

A
  1. plaques of psoriasis on skin
  2. pitting of the nails
  3. onycholysis
  4. dactylitis
  5. enthesitis
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126
Q

Psoriatic Arthritis

what is onycholysis

A

separation of the nail from the nail bed

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127
Q

Psoriatic Arthritis

what is dactylitis

A

inflammation of the full finger

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128
Q

Psoriatic Arthritis

what is enthesitis

A

inflammation of the entheses (points of insertion of tendons into bone)

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129
Q

Psoriatic Arthritis

other associations (3)

A
  • eye disease: conjunctivtiis + anterior uveitis)
  • aortitis (inflammation of the aorta)
  • amyloidosis
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130
Q

Psoriatic Arthritis

what screening tool is recommended by NICE to use in patients with psoriasis

A

Psoriasis Epidemiological Screening Tool (PEST)

to screen for psoriatic arthritis

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131
Q

Psoriatic Arthritis

what does the Psoriasis Epidemiological Screening Tool (PEST) involve

A

questions asking about joint pain, swelling, a history of arthritis and nail pitting.

A high score triggers a referral to a rheumatologist.

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132
Q

Psoriatic Arthritis

x-ray changes (6)

A

1) pencil in cup appearance
2) periostitis
3) ankylosis
4) osteolysis
5) dactylitis

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133
Q

Psoriatic Arthritis

x-ray changes: what is pencil in cup

A

central erosions of the bone beside the joints

this causes the appearance of one bone in the joint being hollow and looking like a cup

whilst the other is narrow and sits in the cup.

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134
Q

Psoriatic Arthritis

x-ray changes: what is periostitis

A

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

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135
Q

Psoriatic Arthritis

x-ray changes: what is ankylosis

A

bones joining together causing joint stiffening

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136
Q

Psoriatic Arthritis

x-ray changes: what is osteolysis

A

destruction of bone

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137
Q

Psoriatic Arthritis

x-ray changes: what is dactylitis

A

inflammation of the whole digit

appears on the xray as soft tissue swelling

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138
Q

Psoriatic Arthritis

mnx

A
  • NSAIDs for pain
  • DMARDS (methotrexate, leflunomide or sulfasalazine)
  • Anti-TNF medications (etanercept, infliximab or adalimumab)
  • Ustekinumab (last line)
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139
Q

Psoriatic Arthritis

what is last line mnx and what is it

A

Ustekinumab: a monoclonal antibody that targets interleukin 12 and 23

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140
Q

Gout

what are gouty tophi

A

subcutaneous deposits of uric acid typically effecting the small joints and connective tissues of the hands, elbows and ears

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141
Q

Gout

which joint in the hands is most effected by gouty tophi

A

the DIP joints

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142
Q

Gout

presentation

A

single acute hot swollen and painful joint

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143
Q

Gout

RFs (7)

A
  • male
  • obese
  • high purine diet (meat+seafood)
  • alcohol
  • diuretics
  • existing CVD or kidney disease
  • FH
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144
Q

Gout

which typical joints are affected

A
  • Base of the big toe (metatarsophalangeal joint)
  • Wrists
  • Base of thumb (carpometacarpal joints)
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145
Q

Gout

Dx

A

clinically or by aspiration of fluid from the joint

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146
Q

Gout

what will aspirated fluid show

A
  • no bacterial growth
  • needle shaped crystals
  • negatively birefringent of polarised light
  • monosodium urate crystals
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147
Q

Gout

what will x-ray show

A
  • joint space maintained
  • lytic lesions
  • punched out erosions:
    sclerotic borders
    overhanging edges
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148
Q

Gout

acute flare mnx

A

1st line: NSAIDs
2nd line: colchicine
3rd line: steroids

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149
Q

Gout

when is colchicine used

A

during an acute flare when NSAIDs are inappropriate: renal impairment or significant heart disease

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150
Q

Gout

common SE of colchicine

A

diarrhoea (dose dependent)

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151
Q

Gout

prophylaxis mnx

A

allopurinol

lifestyle changes

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152
Q

Gout

what is allopurinol

A

a xanthine oxidase inhibitor used for the prophylaxis of gout: it reduces uric acid levels

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153
Q

Antiphospholipid Syndrome

what is it

A

a disorder associated with antiphospholipid antibodies where the blood becomes prone to clotting. The patient is in a hyper-coagulable state.

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154
Q

Antiphospholipid Syndrome

main associations

A
  • thrombosis
  • recurrent miscarriages
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155
Q

Antiphospholipid Syndrome

can occur secondary to which condition

A

SLE

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156
Q

Antiphospholipid Syndrome

which antiphospholipid antibodies is it associated with

A
  • lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein I antibodies
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157
Q

Antiphospholipid Syndrome

what do the antiphospholipid antibodies do

A

interfere with coagulation and create a hypercoagulable state where the blood is more prone to clotting.

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158
Q

Antiphospholipid Syndrome

what is the rash that you get called

A

livedo reticularis

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159
Q

Antiphospholipid Syndrome

what is livedo reticularis

A

a purple lace like rash that gives a mottled appearance to the skin

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160
Q

Antiphospholipid Syndrome

what is Libmann-Sacks endocarditis

A

a type of non-bacterial endocarditis where there are growths (vegetations) on the valves of the heart

mitral valve is most commonly affected

associated with SLE and antiphospholipid syndrome.

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161
Q

Antiphospholipid Syndrome

blood results

A

thombocytopenia (low platelets)

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162
Q

Antiphospholipid Syndrome

dx

A

hx of thrombosis or pregnancy complication
AND persistent antibodies:
- lupus anticoagulant
- anticardiolipin antibodies
- anti-beta-2 glycoprotein I antibodies

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163
Q

Antiphospholipid Syndrome

mnx if not pregnant

A
  • long term warfarin (INR 2-3)
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164
Q

Antiphospholipid Syndrome

mnx if pregnant

A

LMWH (enoxaparin) + Aspirin

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165
Q

Pseudogout

which crystals are present

A

calcium pyrophosphate crystals

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166
Q

Pseudogout

common joint affected

A

knee, shoulders, wrists and hips

167
Q

Pseudogout

Typical presentation

A

an older adult with a hot, swollen, stiff, painful knee.

168
Q

Pseudogout

Definitive diagnostic inx

A

joint aspiration for synovial fluid

169
Q

Pseudogout

what will aspiration fluid show

A
  • no bacterial growth
  • calcium pyrophosphate crystals
  • rhomboid shaped crystals
  • positive birefringent of polarised light
170
Q

Pseudogout

what is the classic xray change in pseudogout (pathognomonic)

A

chondrocalcinosis

171
Q

Pseudogout

what is chondrocalcinosis

A

x-ray finding: thin white line in the middle of the joint space caused by the calcium deposition.

172
Q

Pseudogout

x-ray changes

A

chondrocalcinosis

similar to osteoarthritis:
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

173
Q

Pseudogout

symptomatic mnx

A

NSAIDs
Colchicine
Joint aspiration
Steroid injections
Oral steroids

usually resolves over several weeks

174
Q

Pseudogout

mnx in severe cases

A

Joint washout (arthrocentesis)

175
Q

Ankylosing Spondylitis

what group of conditions is it in

A

seronegative spondyloarthropathy group of conditions relating to the HLA B27 gene.

176
Q

Ankylosing Spondylitis

what key joints are affected

A

sacroiliac joints

joints of the vertebral column

177
Q

Ankylosing Spondylitis

what causes the classical ‘bamboo spine’

A

fusion of the spine

178
Q

Ankylosing Spondylitis

which gene is it strongly associated with

A

HLA B27 gene

179
Q

Ankylosing Spondylitis

main presenting features

A

lower back pain and stiffness

sacroiliac pain in the buttock region.

worse with rest and improves with movement

180
Q

Ankylosing Spondylitis

at least how long does it take for stiffness to improve in the morning

181
Q

Ankylosing Spondylitis

typical exam presentation

A

young adult male with lower back pain

slow onset >3m

182
Q

Ankylosing Spondylitis

key complication

A

vertebral fractures

183
Q

Ankylosing Spondylitis

what tests how much mobility there is in the spine

A

Schober’s Test

184
Q

Ankylosing Spondylitis

what result in the Schober test helps diagnosis Ankylosing Spondylitis

A

If the distance with them bending forwards is less than 20cm

185
Q

Ankylosing Spondylitis

what does the Schober’s test involve

A

mark a point 10cm above and 5cm below the L5 vertebrae

pt bends down as far as they can and measure the distance between the points

186
Q

Ankylosing Spondylitis

inx

A
  • CRP and ESR may be raised
  • HLA B27 genetic test
  • X-ray spine and sacrum
  • MRI: bone marrow oedema
187
Q

Ankylosing Spondylitis

x ray changes (6)

A
  1. bamboo spine
  2. squaring of vertebral bodies
  3. Subchondral sclerosis and erosions
  4. Syndesmophytes
  5. Ossification
  6. fusion of the facet, sacroiliac and costovertebral joints
188
Q

Ankylosing Spondylitis

xray: what is Syndesmophytes

A

areas of bone growth where the ligaments insert into the bone

189
Q

Ankylosing Spondylitis

medical mnx

A
  • NSAIDs
  • Steroids
  • Anti-TNF (etanercept) or inflixamb

final line: Secukinumab (monoclonal antibody against interleukin-17)

190
Q

Ankylosing Spondylitis

additional mnx

A
  • Physiotherapy
  • Exercise and mobilisation
  • Avoid smoking
  • Bisphosphonates to treat osteoporosis
  • Treatment of complications
  • Surgery is occasionally required for deformities to the spine or other joints
191
Q

Reactive Arthritis

what is it

A

synovitis occurs in the joints as a reaction to a recent infective trigger

192
Q

Reactive Arthritis

what did it used to be known as

A

Reiter Syndrome

193
Q

Reactive Arthritis

difference between septic and reactive arthritis

A

reactive: no infection in joint

194
Q

Reactive Arthritis

what are the most common infections that trigger it

A
  • gastroenteritis
  • Chlamydia
195
Q

what do gonorrhoea commonly cause

A

gonococcal septic arthritis

196
Q

Reactive Arthritis

what group of conditions is it part of

A

seronegative spondyloarthropathy group of conditions

197
Q

Reactive Arthritis

what gene is it linked to

198
Q

Reactive Arthritis

associations

A
  • bilateral conjunctivitis
  • anterior uveitis
  • circinate balanitis
199
Q

Reactive Arthritis

what is the common saying used to remember the features of reactive arthritis

A

can’t see
can’t pee
or climb a tree

200
Q

Reactive Arthritis

presentation of joint

A

acute monoarthritis,

most often the knee

warm, swollen and painful joint.

201
Q

Reactive Arthritis

what is circinate balanitis

A

dermatitis of the head of the penis

202
Q

Reactive Arthritis

mnx to exclude septic arthritis

A
  • abx
  • aspirate for C+S and send for crystal examination
203
Q

Reactive Arthritis

mnx when septic arthritis is excluded

A
  • NSAIDs
  • steroid injections into the affected joints
  • systemic steroids may be needed
204
Q

Reactive Arthritis

prognosis

A

most resolve within 6m and don’t recur

Recurrent cases may require DMARDs or anti-TNF medications.

205
Q

Vasculitis

Types of Vasculitis Affecting The Small Vessels (4)

A
  • Henoch-Schonlein purpura
  • Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)
  • Microscopic polyangiitis
  • Granulomatosis with polyangiitis (Wegener’s granulomatosis)
206
Q

Vasculitis

Types of Vasculitis Affecting The Medium Sized Vessels (3)

A
  • Polyarteritis nodosa
  • Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)
  • Kawasaki Disease
207
Q

Vasculitis

Types of Vasculitis Affecting The Large Vessels (2)

A
  • Giant cell arteritis
  • Takayasu’s arteritis
208
Q

Vasculitis

what is the blood test to remember for vasculitis

A

Anti neutrophil cytoplasmic antibodies (ANCA)

209
Q

Vasculitis

what are the 2 types of ANCA blood tests

A

p-ANCA aka anti-MPO antibodies

c-ANCA aka anti-PR3 antibodies

210
Q

Vasculitis

which vasculitis is p-ANCA (MPO antibodies) associated with

A

Microscopic polyangiitis and

Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)

211
Q

Vasculitis

which vasculitis is c-ANCA (PR3 antibodies) associated with

A

Granulomatosis with polyangiitis (Wegener’s granulomatosis)

212
Q

Vasculitis

usual mnx

A

steroids + immunosuppressants

213
Q

Vasculitis

what steroids may be used for mnx

A
  • Oral (i.e. prednisolone)
  • Intravenous (i.e. hydrocortisone)
  • Nasal sprays for nasal symptoms
  • Inhaled for lung involves (e.g. Churg-Strauss syndrome)
214
Q

Vasculitis

what immunosuppressants may be used for mnx

A
  • Cyclophosphamide
  • Methotrexate
  • Azathioprine
  • Rituximab and other monoclonal antibodies
215
Q

Vasculitis

how does Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome) present

A
  • severe asthma in late teenage years or adulthood
  • elevated eosinophil levels
216
Q

Vasculitis

what organs does Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome) mainly effect

A

lung and skin

217
Q

Vasculitis

what sized vessels does Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome) affect

A

small and medium vessel vasculitis

218
Q

Vasculitis

what sized vessels does Microscopic polyangiitis affect

A

small vessel vasculitis

219
Q

Vasculitis

main features of Microscopic polyangiitis

A
  • RENAL FAILURE
  • SOB
  • haemoptysis
220
Q

Vasculitis

what sized vessels does Granulomatosis with polyangiitis (Wegener’s granulomatosis) affect

A

small vessel vasculitis

221
Q

Vasculitis

what organs does Granulomatosis with polyangiitis (Wegener’s granulomatosis) affect

A

respiratory tract and kidneys

222
Q

Vasculitis

resp tract presentation of Granulomatosis with polyangiitis (Wegener’s granulomatosis)

A
  • epistaxis
  • crustal nasal secretions
  • hearing loss
  • sinusitis
  • saddle shaped nose due to perforated nasal septum
  • cough, wheeze, haemoptysis
223
Q

Vasculitis

what may the CXR show in Granulomatosis with polyangiitis (Wegener’s granulomatosis)

A

consolidation and it may be misdiagnosed as pneumonia

224
Q

Vasculitis

renal presentation in Granulomatosis with polyangiitis (Wegener’s granulomatosis)

A

rapidly progressing glomerulonephritis

225
Q

Vasculitis

what sized vessels does Polyarteritis Nodosa affect

A

medium vessel vasculitis.

226
Q

Vasculitis

what is Polyarteritis Nodosa most associated with

A

Hep B

also hep c and HIV

227
Q

Vasculitis

Polyarteritis Nodosa presentation

A
  • livedo reticularis
  • renal impairment
  • strokes
  • MI
228
Q

Vasculitis

what sized vessels does Takayasu’s arteritis affect

A

large vessel vasculitis.

229
Q

Vasculitis

which part of the body does Takayasu’s arteritis mainly affect

A

the aorta and its branches

also the pulmonary arteries

230
Q

Vasculitis

why is Takayasu’s arteritis aka ‘pulseless disease’

A

large vessels and their branches can swell and form aneurysms or become narrowed and blocked.

231
Q

Vasculitis

Takayasu’s arteritis presentation

A
  • before 40y
  • fever, malaise, muscle aches
  • arm claudication, syncope
232
Q

Vasculitis

Takayasu’s arteritis diagnostic inx

A

CT or MRI angiography

233
Q

Sjogren’s Syndrome

what is it

A

autoimmune conditions that affects the exocrine glands

234
Q

Sjogren’s Syndrome

presentation

A

dry mucous membranes:

  • dry mouth
  • dry eyes
  • dry vagina
235
Q

Sjogren’s Syndrome

what is Primary Sjogren’s

A

the condition occurs in isolation

236
Q

Sjogren’s Syndrome

what is Secondary Sjogren’s

A

the condition occurs related to SLE or rheumatoid arthritis.

237
Q

Sjogren’s Syndrome

what antibodies is it associated with

A

anti-Ro
anti-La

238
Q

Sjogren’s Syndrome

what is the Schirmer Test

A

inserting a folded piece of filter paper under the lower eyelid with a strip hanging out over the eyelid

leave for 5min

distance along the strip hanging out that becomes moist is measured

239
Q

Sjogren’s Syndrome

Schirmer Test results if the pt has Sjogren’s Syndrome

A

The tears should travel 15mm in a healthy young adult.

< 10mm is significant.

240
Q

Sjogren’s Syndrome

mnx

A
  • Artificial tears
  • Artificial saliva
  • Vaginal lubricants
  • Hydroxychloroquine: to halt the progression of the disease.
241
Q

Sjogren’s Syndrome

complications of the eye

A

conjunctivitis and corneal ulcers

242
Q

Sjogren’s Syndrome

complications of the mouth

A

dental cavities and candida infections

243
Q

Sjogren’s Syndrome

complications of the vagina

A

candidiasis and sexual dysfunction

244
Q

Sjogren’s Syndrome

rare complications

A
  • Pneumonia and bronciectasis
  • Non-Hodgkins lymphoma
  • Peripheral neuropathy
  • Vasculitis
  • Renal impairment
245
Q

Behçet’s Disease

what is it

A

a complex inflammatory condition. It characteristically presents with recurrent oral and genital ulcers.

246
Q

Behçet’s Disease

what gene is it linked to

A

HLA B51 gene. This is a prognostic indicator of severe disease.

247
Q

Behçet’s Disease

Ddx

A
  • Simple aphthous ulcers are very common
  • IBD (esp Crohn’s)
  • Coeliac disease
  • Vit deficiency (B12, folate or iron)
  • Herpes simplex ulcers
  • Hand, foot and mouth disease (coxsackie A virus)
  • Squamous cell carcinoma
248
Q

Behçet’s Disease

presentation of mouth ulcers

A
  • at least 3 episodes of oral ulcers/year
  • painful, sharply circumscribed erosions with a red halo
  • occur on the oral mucosa
  • heals over 2-4 weeks
249
Q

Behçet’s Disease

presentation of genital ulcers

A

“Kissing ulcers”
ulcer develops on two opposing surfaces so that they are facing each other.

250
Q

Behçet’s Disease

skin findings (3)

A
  1. Erythema nodosum
  2. Papules and pustules (similar to acne)
  3. Vasculitic type rashes
251
Q

Behçet’s Disease

eye manifestations

A
  • Anterior or posterior uveitis
  • Retinal vasculitis
  • Retinal haemorrhage
252
Q

Behçet’s Disease

MSK presentation

A
  • Morning stiffness
  • Arthralgia
  • Oligoarthritis often affecting the knee or ankle. This causes swelling without joint destruction.
253
Q

Behçet’s Disease

inflammation and ulceration can occur through which part of the GI tract

A
  • ileum
  • caecum
  • ascending colon
254
Q

Behçet’s Disease

how does it affect the veins

A

veins can become inflamed and this can lead to vein thrombosis. Eg:

  • Budd Chiari syndrome
  • DVT
  • thrombus in pulmonary veins
  • cerebral venous sinus thrombosis
255
Q

Behçet’s Disease

how may the lungs be affected

A

Pulmonary artery aneurysms can develop

256
Q

Behçet’s Disease

which particular inx is used

A

the pathergy test

257
Q

Behçet’s Disease

what is the pathergy test

A
  • tests for non-specific hypersensitivity in the skin
  • needle creates a SC abrasion on forearm
  • reviewed 24-48h later to look for a weal ≥5mm
258
Q

Behçet’s Disease

which conditions it the pathergy test positive in

A
  • Behçet’s disease
  • Sweet’s syndrome
  • pyoderma gangrenosum
259
Q

Behçet’s Disease

mnx

A
  • Topical steroids to mouth ulcers (e.g. soluble betamethasone tablets)
  • Systemic steroids (i.e. oral prednisolone)
  • Colchicine: anti-inflammatory to treat symptoms
  • Topical anaesthetics for genital ulcers (e.g. lidocaine ointment)
  • Immunosuppressants e.g. azathioprine
  • Biologic therapy e.g. infliximab
260
Q

Behçet’s Disease

prognosis

A
  • relapsing remitting condition
  • normal life expectancy
  • increased mortality with haemoptysis, neuro involvement and other major complications
261
Q

Osteoarthritis

RFs

A
  • obesity
  • age
  • occupation
  • trauma
  • female
  • FH
262
Q

Osteoarthritis

pathophysiology

A

an imbalance between the cartilage being worn down and the chondrocytes repairing it

leading to structural issues in the joint

263
Q

Osteoarthritis

what are the 4 key xray changes

A

LOSS

Loss of joint space

Osteophytes

Subchondral sclerosis

Subchondral cysts

264
Q

Osteoarthritis

what is subchondral sclerosis

A

increased density of the bone along the joint line

265
Q

Osteoarthritis

what is subchondral cysts

A

fluid-filled holes in the bone, aka geodes

266
Q

Osteoarthritis

presentation

A
  • joint pain + stiffness
  • worsened by activity
  • deformity, instability + reduced function in the joint
267
Q

Osteoarthritis

commonly affected joint s

A
  • Hips
  • Knees
  • Sacro-iliac joints
  • Distal-interphalangeal joints in the hands (DIPs)
  • The CMC joint at the base of the thumb
  • Wrist
  • Cervical spine
268
Q

Osteoarthritis

signs in the hand

A
  • Heberden’s nodes
  • Bouchard’s nodes
  • Squaring at the base of the thumb at the carpo-metacarpal joint
  • Weak grip
  • Reduced range of motion
269
Q

Osteoarthritis

which joints do Heberden’s nodes affect

270
Q

Osteoarthritis

which joints do Bouchard’s nodes affect

271
Q

Osteoarthritis

what kind of joint is the carpo-metacarpal joint at the base of the thumb

A

a saddle joint

272
Q

Osteoarthritis

diagnosis

A

NICE: no inx if:

  • pt>45y
  • has typical activity related pain
  • has no morning stiffness or stiffness lasting <30min
273
Q

Osteoarthritis

conservative mnx

A
  • weight loss
  • physio
  • occupational therapy + orthotics
274
Q

Osteoarthritis

stepwise analgesia

A
  1. PO paracetamol + top NSAIDs or top capsaicin (chilli pepper extract)
  2. add PO NSAIDs (+PPI)
  3. consider opiates: codeine + moprhine
275
Q

Osteoarthritis

what mnx provides a temporary reduction in inflammation and improve symptoms.

A

Intra-articular steroid injections

276
Q

Osteoarthritis

what can be used in severe cases

A

joint replacement

277
Q

Osteoporosis

what is it

A

a reduction in the density of the bones

278
Q

Osteoporosis

what is osteopenia

A

a less severe reduction in bone density than osteoporosis

279
Q

Osteoporosis

RFs

A
  • Older age
  • Female
  • Reduced mobility and activity
  • Low BMI (<18.5 kg/m2)
  • Rheumatoid arthritis
  • Alcohol and smoking
  • Long term corticosteroids.
  • SSRIs, PPIs, anti-epileptics and anti-oestrogens
280
Q

Osteoporosis

what dose of long term corticosteroids increase the risk significantly

A

>7.5mg prednisolone/day for >3m

281
Q

Osteoporosis

why are post-menopausal women at risk

A

Oestrogen is protective against osteoporosis

postmenopausal women have less oestrogen

and older and often have other risk factors

282
Q

Osteoporosis

what is the FRAX tool

A

gives a prediction of the risk of a fragility fracture over the next 10 years

283
Q

Osteoporosis

what is the 1st step in assessing someone’s risk of osteoporosis

284
Q

Osteoporosis

what information is inputted in the FRAX tool

A
  • age
  • BMI
  • co-morbidities
  • smoking
  • alcohol
  • family history
  • bone mineral density (from DEXA scan)
285
Q

Osteoporosis

the FRAX tool gives results as a % 10 year probability of?

A
  • major osteoporotic fracture
  • hip fracture
286
Q

Osteoporosis

how is the bone mineral density calculated

A

using dual-energy xray absorptiometry (DEXA scan)

they measure how much radiation is absorbed by the bones, indicating how dense the bone is.

287
Q

Osteoporosis

where is the DEXA scan reading done on the skeleton

288
Q

Osteoporosis

DEXA scan: what is the Z score

A

the number of standard deviations the patients bone density falls below the mean for their age

289
Q

Osteoporosis

DEXA scan: what is the T score

A

the number of standard deviations the patients bone density falls below the mean for a healthy young adult

290
Q

Osteoporosis

DEXA scan: which is the most clinically important outcome, the T or Z score

A

T score at the person’s hip

291
Q

Osteoporosis

what is the bone mineral density if T score at the hip is > -1

292
Q

Osteoporosis

what is the bone mineral density if T score at the hip is -1 to -2.5

293
Q

Osteoporosis

what is the bone mineral density if T score at the hip is

A

osteoporosis

294
Q

Osteoporosis

what is the bone mineral density if T score at the hip is

A

severe osteoporosis

295
Q

Osteoporosis

who do you perform a FRAX assessment on

A

patients at risk of osteoporosis:

  • F>65
  • M>75
  • younger pts with RFs: previous fragility fracture, hx of falls, low BMI, long term steroids, endocrine disorders, RA
296
Q

Osteoporosis

FRAX outcome without a BMD result will suggest one of three outcomes:

A

Low risk – reassure

Intermediate risk – offer DEXA scan and recalculate the risk with the results

High risk – offer treatment

297
Q

Osteoporosis

FRAX outcome with a BMD result will suggest one of two outcomes:

A
  • Treat
  • Lifestyle advice and reassure
298
Q

Osteoporosis

mnx

A
  • lifestyle changes
  • vit D + calcium
  • bisphosphonates
299
Q

Osteoporosis

what lifestyle changes can be made

A
  • Activity and exercise
  • Maintain a healthy weight
  • Adequate calcium intake
  • Adequate vitamin D
  • Avoiding falls
  • Stop smoking
  • Reduce alcohol consumption
300
Q

Osteoporosis

who does NICE recommend calcium + vit D to

A

in patients at risk of fragility fractures with an inadequate intake of calcium

301
Q

Osteoporosis

what does Calcichew-D3 contain

A
  • 1000mg of calcium
  • 800 units of vit D (colecalciferol).
302
Q

Osteoporosis

what should pts with adequate Ca intake but lack of sun exposure take

303
Q

Osteoporosis

what is the 1st line trx

A

bisphosphonates

304
Q

Osteoporosis

how do bisphosphonates work

A

interfering with osteoclasts and reducing their activity, preventing the reabsorption of bone

305
Q

Osteoporosis

SE’s of bisphosphonates

A
  • Reflux and oesophageal erosions
  • Atypical fractures (e.g. atypical femoral fractures)
  • Osteonecrosis of the jaw
  • Osteonecrosis of the external auditory canal
306
Q

Osteoporosis

example of bisphosphonates

A
  • Alendronate 70mg once weekly (oral)
  • Risedronate 35 mg once weekly (oral)
  • Zoledronic acid 5 mg once yearly (intravenous)
307
Q

Osteoporosis

other options if bisphosphonates are CId, not tolerated or not effective

A
  • Denosumab
  • Strontium ranelate
  • Raloxifene
  • HRT
308
Q

Osteoporosis

what is denosumab

A

a monoclonal antibody that works by blocking the activity of osteoclasts.

309
Q

Osteoporosis

what is Strontium ranelate

A

a similar element to calcium that stimulates osteoblasts and blocks osteoclasts

but increases the risk of DVT, PE and myocardial infarction.

310
Q

Osteoporosis

what is Raloxifene

A

used as secondary prevention only.

a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus

311
Q

Osteoporosis

what should low risk pts not on trx be given

A

lifestyle advice and followed up within 5 years for a repeat assessment.

312
Q

Osteoporosis

when should pts on biphosphonates have a repeat FRAX and DEXA scan

A

3-5 years

treatment holiday should be considered if their BMD has improved and they have not suffered any fragility fractures

313
Q

Osteoporosis

what is a treatment holiday

A

a break from treatment of 18 months to 3 years before repeating the assessment.

314
Q

Paget’s Disease of Bone

pathophysiology

A

excessive bone turnover due to excessive activity of osteoblasts and osteoclasts

not coordinated, leading to patchy areas of high density (sclerosis) and low density (lysis).

315
Q

Paget’s Disease of Bone

presentation

A

older adults:

  • bone pain
  • bone deformity
  • fractures
  • hearing loss
316
Q

Paget’s Disease of Bone

key inx

A
  • x ray
  • LFTs, ca, phosphate
317
Q

Paget’s Disease of Bone

xray findings

A
  • Bone enlargement and deformity
  • “Osteoporosis circumscripta”
  • “Cotton wool appearance” of the skull
  • “V-shaped defects” in the long bones
318
Q

Paget’s Disease of Bone

xray: what is Osteoporosis circumscripta

A

well defined osteolytic lesions that appear less dense compared with normal bone

319
Q

Paget’s Disease of Bone

xray: what is “Cotton wool appearance” of the skull

A

patchy areas of increased density (sclerosis) and decreased density (lysis)

320
Q

Paget’s Disease of Bone

xray: what is “V-shaped defects” in the long bones

A

V shaped osteolytic bone lesions within the healthy bone

321
Q

Paget’s Disease of Bone

what will biochemistry show

A
  • raised ALP (other LFTs normal)
  • normal calcium
  • normal phosphate
322
Q

Paget’s Disease of Bone

what is the main trx

A

bisphosphonates

323
Q

Paget’s Disease of Bone

other mnx apart from biphosphonates

A
  • NSAIDs for bone pain
  • Ca + Vit D
  • surgery for fractures, deformity or arthritis
324
Q

Paget’s Disease of Bone

what does monitoring involve

A

ALP and review sx

.Effective treatment should normalise the ALP and eliminate symptoms.

325
Q

Paget’s Disease of Bone

2 key complications

A

Osteogenic sarcoma (osteosarcoma)

Spinal stenosis and spinal cord compression

326
Q

Paget’s Disease of Bone

what is osteosarcoma

A

a type of bone cancer with a very poor prognosis

327
Q

Paget’s Disease of Bone

how does osteosarcoma present

A

increased focal bone pain, bone swelling or pathological fractures

328
Q

Paget’s Disease of Bone

how is spinal stenosis diagnosed

A

with an MRI scan

329
Q

Paget’s Disease of Bone

how is spinal stenosis usually treated

A

bisphosphonates

330
Q

Discoid Lupus Erythematosus

what is it

A

a non-cancerous chronic skin condition.

331
Q

Discoid Lupus Erythematosus

who is it more common in

A
  • women
  • aged 20-40
  • darker-skinned pts
  • smokers
332
Q

Discoid Lupus Erythematosus

what is there an increased risk of developing

A

SLE (<5%)

rarely, lesions can progress to SCC of the skin

333
Q

Discoid Lupus Erythematosus

where do lesions typically present

A

on the face, ears and scalp

334
Q

Discoid Lupus Erythematosus

appearance of lesions

A
  • Inflamed
  • Dry
  • Erythematous
  • Patchy
  • Crusty and scaling
  • hyper or hypo-pigmented scars.
335
Q

Discoid Lupus Erythematosus

are the lesions photosensitive

336
Q

Discoid Lupus Erythematosus

what is scarring alopecia

A

hair loss in affected areas that does not grow back

337
Q

Discoid Lupus Erythematosus

diagnostic inx

A

skin biopsy

338
Q

Discoid Lupus Erythematosus

trx

A
  • Sun protection
  • Topical steroids
  • Intralesional steroid injections
  • Hydroxychloroquine
339
Q

Systemic Sclerosis

what is it

A

an autoimmune inflammatory and fibrotic connective tissue disease

340
Q

Systemic Sclerosis

what is scleroderma

A

hardening of the skin.

most patients with scleroderma have systemic sclerosis

341
Q

Systemic Sclerosis

what are the 2 main patterns of disease

A
  • Limited cutaneous systemic sclerosis
  • Diffuse cutaneous systemic sclerosis
342
Q

Systemic Sclerosis

what did Limited cutaneous systemic sclerosis used to be called

A

CREST syndrome

343
Q

Systemic Sclerosis

features of limited cutaneous systemic sclerosis

A

Calcinosis

Raynaud’s phenomenon

Esophageal dysmotility

Sclerodactyly

Telangiectasis

344
Q

Systemic Sclerosis

what is Diffuse cutaneous systemic sclerosis

A

includes the features of CREST syndrome plus:

  • CVD problems
  • lung problems
  • kidney problems
345
Q

Systemic Sclerosis

Diffuse cutaneous systemic sclerosis: what CVD problems are there

A

HTN + coronary artery disease

346
Q

Systemic Sclerosis

Diffuse cutaneous systemic sclerosis: what lung problems are there

A

pulmonary hypertension and pulmonary fibrosis

347
Q

Systemic Sclerosis

Diffuse cutaneous systemic sclerosis: what kidney problems are there

A

glomerulonephritis

scleroderma renal crisis

348
Q

Systemic Sclerosis

what is the appearance of scleroderma

A

hardening of the skin

shiny, tight skin without the normal folds in the skin.

most notable on the hands and face.

349
Q

Systemic Sclerosis

what is sclerodactyly

A

the skin tightens around joints

it restricts the range of motion in the joint and reduces the function of the joints.

fat pads on the fingers are lost. Skin can break + ulcerate

350
Q

Systemic Sclerosis

what is calcinosis and where is it commonly found

A

calcium deposits build up under the skin

fingertips

351
Q

Systemic Sclerosis

what is Raynaud’s phenomenon

A

fingertips go completely white and then blue in response to even mild cold.

352
Q

Systemic Sclerosis

what causes Raynaud’s phenomenon

A

vasoconstriction of the vessels supplying the fingers

353
Q

Systemic Sclerosis

what is Oesophageal dysmotility caused by

A

connective tissue dysfunction in the oesophagus

354
Q

Systemic Sclerosis

what sx are in oesophageal dysmotility

A

swallowing difficulties

acid reflux

oesophagitis

355
Q

Systemic Sclerosis

what is systemic and pulmonary HTN caused by

A

connective tissue dysfunction in the systemic and pulmonary arterial systems

worsened by renal impairment

356
Q

Systemic Sclerosis

which condition can occur in severe systemic sclerosis

A

pulmonary fibrosis

(gradual onset dry cough and SOB)

357
Q

Systemic Sclerosis

what is scleroderma renal crisis

A

acute

severe HTN + renal failure

358
Q

Systemic Sclerosis

which autoantibodies are positive in most patients

A

Antinuclear antibodies (ANA)

but not specific to systemic sclerosis

359
Q

Systemic Sclerosis

which antibodies are most associated with limited cutaneous systemic sclerosis

A

Anti-centromere antibodies

360
Q

Systemic Sclerosis

which antibodies are most associated with diffuse cutaneous systemic sclerosis

A

Anti-Scl-70 antibodies

they are associated with more severe disease.

361
Q

Systemic Sclerosis

what is nailfold capillaroscopy

A

a technique where the nailfold is magnified and examined

362
Q

Systemic Sclerosis

nailfold capillaroscopy: what will indicate systemic sclerosis

A

Abnormal capillaries, avascular areas and micro-haemorrhages

363
Q

Systemic Sclerosis

how to differentiate patients with primary Raynaud’s and Systemic Sclerosis

A

patients with primary Raynaud’s will have normal nailfold capillaries

364
Q

Systemic Sclerosis

what is dx based on

A

meeting a number of criteria for clinical features, antibodies and nailfold capillaroscopy.

365
Q

Systemic Sclerosis

mnx for diffuse disease and complications such as pulmonary fibrosis

A
  • MDT
  • steroids + immunosuppressants
366
Q

Systemic Sclerosis

non-medical mnx

A
  • Avoid smoking
  • Gentle skin stretching to maintain range of motion
  • Regular emollients
  • Avoiding cold triggers for Raynaud’s
  • Physio + occupational therapy
367
Q

Systemic Sclerosis

what medical trx for Raynaud’s

A

Nifedipine

368
Q

Systemic Sclerosis

medical trx

A

focuses on treating symptoms and complications:

e.g analgesia, PPIs, abx, ACEi

369
Q

what is enteropathic arthritis

A

seronegative spondylarthropathy occurring in 10-20% of patients with inflammatory bowel disease (IBD)

370
Q

what is associated with Polyarteritis nodosa

371
Q

Polymyalgia Rheumatica

which condition is this strongly associated with

A

giant cell arteritis

372
Q

Polymyalgia Rheumatica

demographics

A

>50y

women

Caucasians

373
Q

Polymyalgia Rheumatica

what are the core features

A
  • Bilateral shoulder pain that may radiate to the elbow
  • Bilateral pelvic girdle pain
  • Worse with movement
  • Interferes with sleep
  • Stiffness for at least 45 minutes in the morning
374
Q

Polymyalgia Rheumatica

how long should core features be present for

A

at least 2w

375
Q

Polymyalgia Rheumatica

other features

A
  • Systemic symptoms: weight loss, fatigue, low grade fever, low mood
  • Upper arm tenderness
  • Carpel tunnel syndrome
  • Pitting oedema
376
Q

Polymyalgia Rheumatica

how is dx made

A
  • clinically
  • response to steroids
  • exclude other conditions
377
Q

Polymyalgia Rheumatica

what inx should you do to exclude other conditions

A
  • FBC, U&Es, LFTs. TFTs
  • Ca (hyperparathryoidism, osteomalacia)
  • Serum protein electrophoresis (myeloma)
  • CK (myositis)
  • RF
  • urine dipstick
378
Q

Polymyalgia Rheumatica

what are pts initially started on

A

15mg prednisolone/day

assess 1w after. Stop if poor response

379
Q

Polymyalgia Rheumatica

when you assess 3-4w later after starting steroids, what would you expect to see in PMR

A

a 70% improvement in symptoms and inflammatory markers to return to normal

380
Q

Polymyalgia Rheumatica

If 3-4 weeks of steroids has given a good response, what regime should you start

A

a reducing regime with the aim of getting the patient off steroids

can take 1-2y

381
Q

Polymyalgia Rheumatica

additional measures for pts on long term steroids

A

Don’t STOP

Don’t: risk of adrenal crisis if steroids are abruptly withdrawn

Sick day rule: increase dose if unwell

Treatment card: to alert others they are steroids dependent

Osteoporosis: consider bisphosphonates, Ca + Vit D

PPI: consider gastric protection

382
Q

what needs to be screened for first before starting biologics like infliximab?

A

TB due to the SE of it being reactivated

383
Q

why is hydroxychloroquine CI’d is psoriasis

A

SE: it worsens it

384
Q

what is Still’s disease

A

an idiopathic autoinflammatory condition

385
Q

pyrexia (often very high and of uncertain origin at first) , arthralgia and a fine nonpruritic salmon pink rash, elevated serum ferritin. What is it?

A

Still’s disease

386
Q

Giant Cell Arteritis

aka

A

temporal arteritis

387
Q

Giant Cell Arteritis

which condition is it strongly linked with

A

polymyalgia rheumatica

388
Q

Giant Cell Arteritis

which patients are at higher risk

A

white females

>50y

389
Q

Giant Cell Arteritis

key complication

A

vision loss

390
Q

Giant Cell Arteritis

sx

A
  • Severe unilateral headache typically around temple and forehead
  • Scalp tenderness noticed when brushing hair
  • Jaw claudication
  • Blurred or double vision
391
Q

Giant Cell Arteritis

diagnosis

A
  • Clinical presentation
  • Raised ESR: usually 50 mm/hour or more
  • Temporal artery biopsy findings
392
Q

Giant Cell Arteritis

what is found on temporal artery biopsy

A

Multinucleated giant cells

393
Q

Giant Cell Arteritis

what is it

A

a systemic vasculitis of the medium and large arteries.

394
Q

Giant Cell Arteritis

what may FBC show

A

normocytic anaemia and thrombocytosis (raised platelets)

395
Q

Giant Cell Arteritis

what may LFTs show

A

raised ALP

396
Q

Giant Cell Arteritis

result of c reactive protein

A

usually raised

397
Q

Giant Cell Arteritis

what will duplex US of the temporal artery show

A

hypoechoic halo sign

398
Q

Giant Cell Arteritis

initial mnx

A

high dose steroids immediately before confirming diagnosis

399
Q

Giant Cell Arteritis

what other meds should you consider apart from prednisolone

A
  • aspirin 75mg daily
  • PPI for gastric protection whilst on steroids
400
Q

Giant Cell Arteritis

ongoing mnx

A
  • continue high dose steroids (40-60mg) until the symptoms have resolved
  • slowly wean off steroids (can take several years)
401
Q

Giant Cell Arteritis

early complications

A
  • vision loss
  • stroke
402
Q

Giant Cell Arteritis

late complications

A
  • relapses
  • steroids SEs
  • stroke
  • aortitis –> aortic aneurysm –> aortic dissection
403
Q

which is more sensitive or more specific for RA?

anti-CCP
RF

A

RF - most sensitive

anti-CCP - most specific

404
Q

(PIP) joints are hyper-extended but this is reducible when she extends her fingers from a fist position.

what is it

A

Jaccoud’s arthropathy in SLE

405
Q

young footballer, lower back pain worse in morning. pain in his buttocks which alternates from left to right. He has a localised pain over his right achilles tendon

what is it

A

sacroilitis

406
Q

what is in arthrotec (an NSAID sometimes used to treat joint pain)

A

Misoprostol and diclofenac

407
Q

what SE can misoprostol cause

408
Q

does SLE cause low and high complement

409
Q

does SLE cause exudative or transudative pleural effusions

410
Q

what needs to be screened for and treated first before starting biologics

411
Q

which cancer is dematomyositis associated with

412
Q

What anatomical area is inflamed in the joints of an inflammatory arthritis

A

Synovium (synovial fluid and membrane)

413
Q

red hot swollen joint. Gram stain negative. No crystals. Temperature and WCC high. What is it and how to treat

A

septic arthritis

gram
stain is positive in 50%, so a negative gram stain does not
mean there is no infection.

IV antibiotics should be started pending
culture results.

Finals (47 decks)

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