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Clinical Years / Progress Test > MSK Rheumatology > Flashcards

MSK Rheumatology Flashcards

1
Q

what is rheumatoid arthritis

mainstay of treatment

A

autoimmune condition that often affects the small joints (hands and feet) but can extend elsewhere and into other systems including cardiorespiratory

lifelong immunosuppression and sometimes surgery

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2
Q

what are the main deformations seen in rheumatoid arthritis

A

Z-thumb
Ulnar deviations
Boutonnaires
Swan neck finger deformities

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3
Q

how are T cells affected in autoimmunity

A

Regulatory T cells activity reduces

pathogenic T effector cells are upregulated

any part of the immune pathway dysregulated can cause autoimmunity

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4
Q

basics of immune response

A

dendritic cell presents antigens

T-helper cells (CD4+, MHC Class 2) release inflammatory interleukins and interferon and also activate humoral response (antibody mediated)

T-killer cells (CD8+, MHC Class 1) can also play a role

These processes all cause inflammation and tissue damage

T regulatory cells dampen the inflammation

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5
Q

differentiating between inflammatory and non inflammatory joint conditions

A

inflammatory such as RA tend to have morning stiffness that improves with activity
joint swelling is more indicative of inflammation with the exception of Nodal osteoarthritis and knee swelling which can be caused by trauma

non inflammatory such as OA tends to be pain more than stiffness and is exacerbated by activity

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6
Q

pattern/symmetry in RA

A

tends to be symmetrical and affects groups of joints e.g. all of the metacarpophalangeal joints

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7
Q

antibody tests useful in suspected connective tissue disorder

A

ANA

anti-DsDNA

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8
Q

antibody tests useful in suspected small/medium vessel vasculitis

A

ANCA

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9
Q

general management of inflammation in rheumatology

A

analgesia

anti-inflammatories

immunosuppression (steroids and biologics) - steroids are short term

Disease modifying drugs can also be used later (DMARDs)

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10
Q

protective treatment with steroids

A

in rheumatology always give bone protection with steroids from the start - vitamin D, calcium and bisphosphonates

gastroprotection also needed

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11
Q

names of DMARDs

A

azathioprine

methotrexate

hydroxychloriquine

sulfasalazine

lefunomide

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12
Q

azathioprine

A

inhibits DNA replication stopping proliferating cells

test for TPMT deficiency before as can cause toxicity

co-prescribing with allopurinol can cause toxicity

main adverse effect; bone marrow suppression –> pancytopenia and immunosuppression

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13
Q

methotrexate

A

dihydrofolate antagonist that targets proliferating cells

usually given once weekly and folic acid given on other days
folinic acid used as rescue therapy if OD

adverse effects; mouth ulcers, deranged LFTs, pneumonitis and bone marrow suppression

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14
Q

hydroxychloriquine adverse effects

A

photo sensitivity, retinal toxicity, haemolytic anaemia and bone marrow suppression

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15
Q

sulfasalazine adverse effects

A

haemolytic anaemia, azoospermia (avoid in young men), abnormal LFTs, bone marrow suppression

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16
Q

leflunomide adverse effects

A

alopecia, hypertension, pneumonitis, peripheral neuropathy, hepatotoxicity and bone marrow suppression

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17
Q

monoclonal antibodies in rheumatology

A

self injected or administered as infusions that can last for many weeks at a time
alternative to daily immunosuppressive medication but both are sometimes needed

only managed by specialists and need extensive screening before including blood tests, infection screens and ruling out latent TB

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18
Q

what is the common target of many monoclonal antibody medications

A

Tumour Necrosis Factor (TNF) - widespread immune mediator and a central role in inflammation

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19
Q

what do systemic symptoms e.g. weight loss, night sweats, reduced appetite suggest in a presentation of arthritis

A

more likely to be CTD/vaculitis/malignancy

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20
Q

symptoms to ask about to determine seronegative forms of arthritis

A

GI symptoms - IBD associated?
eye symptoms - iritis
psoriasis symptoms

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21
Q

what syndrome is commonly associated with rheumatoid arthritis

A

Sjrogen’s syndrome - ask about symptoms of dry eyes, dry mouth

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22
Q

what does boggy swelling indicate

A

suggests synovitis which occurs in inflammatory arthritis

in OA swelling is bony

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23
Q

what is the typical joint pattern in rheumatoid arthritis

A

inflammatory small joint polyarthritis affecting the hands, feet and wrists in a symmetrical distribution
in the hands tends to affect the metacarpophalangeal (MCP ) and proximal interphalangeal joints whereas in OA the distal interphalangeal joints are more likely to be affected

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24
Q

swan neck deformity (RA)

A

hyperextension of the PIPJ and flexion of the DIPJ

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25
Q

boutonnière deformity (RA)

A

flexion of the PIPJ and hyperextension of the DIPJ

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26
Q

guttering deformity (RA)

A

muscle wasting seen over the dorsum of the hand

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27
Q

management of suspected RA

A

analgesia and urgent referral to rheumatology
needs rapid and aggressive suppression of inflammation to reduce joint damage, maintain function and quality of life and prevent disability

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28
Q

investigations in suspected RA

A
  • FBC, liver and renal function for baselines
  • inflammatory markers
  • thyroid function; can present with joint pain
  • immune markers; rheumatoid factor and anti-CCP antibody may suggest rheumatoid arthritis, anti-nuclear antibody may indicate connective tissue disease
  • plain film x-rays
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29
Q

anti-CCP compared to RF in diagnosing RA

A

anti-CCP is more specific and sensitive for RA

RF can be raised in other conditions including Sjrogen’s syndrome, other rheumatic conditions, malignancies and chronic infections

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30
Q

hand xray in RA

A

often normal in early disease

later may have periarticular osteopenia, erosions, joint space narrowing (usually uniform) and deformity

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31
Q

SoB in RA

A

respiratory conditions associated with RA including pulmonary fibrosis and pleural effusions can cause SoB. lung nodules also associated but wouldn’t cause SoB

consider concurrent conditions too; asthma, COPD, infection

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32
Q

criteria to diagnose RA

A

diagnostic criteria which covers joint involvement, serology, acute phase proteins and duration of symptoms
score of 6 or more needed

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33
Q

epidemiology RA/explanation

A

chronic autoimmune condition - immune system attacking own body causing inflammation in joints and can also affect other parts of the body

affects around 1 in 100 women and 1 in 200 men

needs long term treatment and often aggressive treatment to aim to control symptoms and prevent joint damage and disability

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33
Q

epidemiology RA/explanation

A

chronic autoimmune condition - immune system attacking own body causing inflammation in joints and can also affect other parts of the body

affects around 1 in 100 women and 1 in 200 men

needs long term treatment aim to control symptoms and prevent joint damage and disability

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34
Q

how is disease activity monitored in RA

A

Disease Activity Score (DAS 28) provides a score out of 10 and has categories of severity

uses:
- joint tenderness score
- number of joints
- patient global assessment (VAS out of 100)
- acute phase response (ESR/CRP)

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35
Q

how to check for swelling if synovitis not obvious on examination

A

USS - identifies swelling and bone erosions

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36
Q

treating active newly diagnosed rheumatoid arthritis

A

start a DMARD such as methotrexate, sulfasalazine, or leflunomide with pt education before

steroid therapy for symptom relief

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37
Q

extra-articular features in RA

A
  • Scleritis and episcleritis
  • dry eyes and dry mouth (esp Sjrogen’s)
  • lymphadenopathy and splenomegaly
  • vasculitis
  • pericardial effusion and pleural effusion
  • carpal tunnel
  • palm and nail changes
  • FBC changes; Normochromic normocytic anaemia; leukopenia; pancytopenia
  • amyloidosis
  • systemic symptoms; fatigue, weight loss, low grade fever
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38
Q

synovial changes in RA

A
  • thickening and inflammation
  • proliferative synovitis
  • angiogenesis occurs –> more inflammatory cells infiltrate
  • synovial fluid becomes fibrinous inflammatory exudate, containing many neutrophils
  • local enzyme and mediator release can damage cartilage and cause bone erosion
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39
Q

treatment if doesn’t respond to initial DMARDs in RA

A

biologic therapy with a monoclonal antibody drug such as Rituximab or Tocilizumab or another biologic such as Abatacept and Baracitinib

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40
Q

joints affected by OA

A

weight bearing joints; cervical spine, lumbar spine, hip, knees, ankles

hands; wrist, DIP joints and PIP joints

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41
Q

what drug class increases risk of gout

A

diuretics especially thiazide

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42
Q

examination findings in OA

A

effusion
painful flexion
crepitus
weakness +/- muscle wasting
joint line tenderness
deformity
bony swelling
instability
antalgic gait

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43
Q

nodes in OA

A

Bouchard’s nodes - PIP joints
Heberdens’s nodes - DIP joints

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44
Q

any investigations needed to diagnose OA?

A

clinical diagnosis but consider
Bloods
- to rule out inflammatory arthritis
- U+Es to get baseline for diclofenac use
Xray affected joints

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45
Q

management of OA
- conservative
- pharmacological
- surgical

A

Conservative;
Patient education
Weightloss
Exercise/physiotherapy

Pharmacological;
Analgesia:
- topical anti-inflammatories/capaiscin cream
- WHO Ladder – paracetamol, NSAIDs (also COX2), opiods
Intra-articular steroid injection for moderate to severe pain

Surgical (joint replacement);
only if refractory to medical management and significant impact on life

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46
Q

OA pathophysiology

A

Dysregulation of tissue turnove
Focal articular cartilage damage leads to
- hypertrophy of subchondral bone
- marginal osteophytes
- synovitis
- thickening of joint capsule and ligaments

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47
Q

main modifiable risk factor in OA

other risk factors

A

obesity

increasing age
F>M
previous joint injury
intense sport activity
occupation
alignments and muscle strength
genetic factors

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48
Q

when to suspect secondary OA (due to another cause)

A

suspect in presentation <40 years, atypical joint distribution,

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49
Q

causes of secondary OA

A

Metabolic; crystal, Wilson’s, haemachromatosis, haemaglobinopathies, collagenopathies, acromegaly

Traumatic

Anatomical/congenital; slipped femoral epiphysis
epiphyseal dysplasia, congenital dislocated hip, unequal leg length, hyper mobility

neuropathic; syphilis, diabetes

inflammatory; septic or any other inflammatory A

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50
Q

steroid injections in OA

A

after topical anitinflammatories and analgesia

can have two injections in a joint if first worked but if severe after that consider joint replacement

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51
Q

differentials hot, painful, swollen joint

A

septic arthritis - must not miss
gout
psuedogout
haemarthrosis
psoriatic arthritis
reactive arthritis

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52
Q

gout risk factors

A

male
alcohol
high BMI
high purine intake - red meat, oily fish, marmite
other features of metabolic syndrome e.g. diabetes

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53
Q

investigations in an acutely hot, swollen joint

A

FBC and inflammatory markers - reactive/septic
Joint aspiration and synovial fluid analysis - gold standard for gout diagnosis
Blood cultures
Renal and Liver function

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54
Q

acute treatment of gout

A

fast acting NSAIDs such as Naproxen first line (coprescribe a PPI)

Colchicine if can’t have NSAIDs e.g in renal impairment

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55
Q

when and what prophylactic treatment should be used in gout

A

urate lowering therapy such as allopurinol which is lifelong

start when attacks are recurrent (>2 in 12 months) as can damage the joint, plus consider these factors:
- tophi
- joint damage
- renal impairment or Hx of kidney stones
- diuretic therapy
- gout starting at a young age

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56
Q

when after an attack should urate lowering therapy be started

A

2-4 weeks after an acute attack

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57
Q

how is Allopurinol given
+ MoA, dose and S/Es

A

allopurinol is a xanthine oxidase inhibitor

start at 100mg daily and tirade every 2-5 weeks (start at 50mg if CKD stage 4)
max dose 900mg but lower in renal impairment

side effects:
10% of patients develop a rash
serious side effect; allopurinol hypersensitivity syndrome may occur and carries a mortality of 20-25%. more likely in south Asian or Japanese heritage - has a specific HLA-B association

58
Q

what is second line for gout prophylaxis

A

febuxostat - offer if unable to take allopurinol

59
Q

initial period of therapy with urate lowering drugs can

A

in first six months can increase risk of gout attacks so initially prescribe alongside an NSAID or colchicine for this first 6 months

60
Q

screening and lifestyle advice in recurrent gout

A

lifestyle; weight, alcohol, red meat , compliance with treatment

screening; for CVD, hyperlipidemia, HTN, diabetes

61
Q

what is the target urate serum level

A

300 micromoles/L

62
Q

Red Flags childhood hip pain

A

Nocturnal pain, night sweats, weight loss - Acute Lymphoblastic Leukaemia

Holding leg abducted and fever - septic arthritis

High fever, non weight bearing - osteomyelitis of femur/pelvis

changeable history/unsual mechanism - non-accidental injury

63
Q

where can hip pain be referred from

A

Abdomen, including hernia orifices and testicles, [enlarged liver spleen, mass – malignancy], the knee

64
Q

Transient synovitis of the hip

A

aka irritable hip

more common in boys
typically age 4-8
acute onset limp +/- pain with reduced hip movements
systemically well
self limiting condition
often preceded by a viral URTI or gastroenteritis

65
Q

Septic arthritis/osteomyelitis of hip

A

any age

associated with fever, systemic upset, acute onset pain which is non-weight bearing and extreme on movement

immediate referral to hospital

66
Q

hip fracture presentation

A

any age but more likely in elderly from fall from standing height

in younger patients associated with traumatic injury

acute onset of pain and reduced movement/non-weight bearing

67
Q

Slipped Upper Femoral Epiphysis (SUFE) presentation

A

more common in boys typically >10 years of age

risk factors obesity and hypothyroidism

2 possible presentations:
- acutely with sudden onset pain and non-weightbearing
- gradual onset vague pain that may be referred to the knee and a limp

68
Q

cause of a slipped upper femoral epiphysis

A

proximal femoral growth plate becoming unstable and the epiphysis and diaphysis can slip

69
Q

Developmental Dysplasia of the Hip (DDH) presentation

A

more common in girls

usually detected at birth but can present later with delayed developmental milestones

older children may present with gradual onset of a painless limp

70
Q

signs of developmental dysplasia of the hip

A
  • asymmetrical skin folds
  • leg length discrepancies
  • buttock flattening
  • walking with the affected leg in external rotation
71
Q

Juvenile Idiopathic Arthritis (JIA) presentation

A

can present at any age

different types; determine if inflammatory
note pain or limping can also be caused by ankle or knee swelling and arthritides

72
Q

bone tumour hip pain presentation

A

red flags of malignancy

nocturnal bone pain which responds to NSAIDs

bone swelling may be evident

73
Q

abdominal pathology hip pain

A

Testicular torsion/inguinal hernia/appendicitis

pain in the hip, non-weightbearing with or without abdominal pain, nausea, or reduced appetite

74
Q

haematological malignancy hip pain

A

Red flag symptoms

typically affects younger children

Abdominal mass with splenomegaly may be present.

75
Q

what is perthes disease

A

childhood condition whereblood supply to the femoral head of the hip joint is temporarily interrupted and the bone begins to die

usually in 4-10 years old
gradual onset pain

76
Q

safety netting transient synovitis of the hip

A

should improve in a few days - use paracetamol and ibuprofen in the mean time
follow up in GP in a few days and if not better consider other causes

safety net parents to attend A&E if signs of sepsis ie. fever, loss of appetite, not passing urine as often

77
Q

what is the cut off for acute vs chronic symptoms

A

6 weeks

78
Q

ethnicity risk factor in lupus

A

African-American women are three times more likely to get lupus than white women. Lupus is also more common in Hispanic, Asian, and Native American and Alaskan Native women

79
Q

broadly two causes of nephrotic syndrome

A

systemic conditions; amyloidosis, lupus, diabetes

primary renal disorders

80
Q

what is nephrotic syndrome

A

heavy proteinuria >3-5g/24hr, hypoalbumineaemia, oedema,

81
Q

acute nephritic syndrome

A

haematuria, proteinuria (usually <2g/24hr), hypertension, oliguria, uraemia, oedema (periorbital, sacral, pedal)

82
Q

presentation/ associated symptoms of CTD such as Lupus

A

can present very non-specifically

Joint pains - inflammatory in nature
Rash
Can present with nephrotic syndrome

associated symptoms;
- Raynaud’s
- hair loss
- mouth ulcers
- fatigue
- weight loss
- ask about cardiorespiratory/GI/GU symptoms

83
Q

what is systemic lupus erythematous (SLE)

A

inflammatory autoimmune connective tissue disease
systemic - multiple organ systems affected
erythematous - characteristic photosensitive malar rash on the face

presents with varying and non-specific symptoms usually in young to middle age and more common in women

84
Q

what antibodies characterise systemic lupus erythematous

A

anti nuclear antibodies (ANA) - 85% pts with lupus will be ANA positive but can can also be positive in other conditions

Anti-double stranded DNA (anti-dsDNA) is specific to SLE

antiphospholipid antibodies can occur secondary to SLE

85
Q

what course does SLE tend to take

A

relapsing remitting course with periods of severe inflammation
death usually occurs due to infection or cardiorespriaotry involvement

86
Q

investigations in SLE

A
  • autoantibodies
  • FBC; can see leukopenia, normocytic anaemia, autoimmune haemolytic, thrombocytopenia
  • complement levels; decreased in active disease
  • CRP and ESR
  • urine dip and urine protein:Cr ratio
  • renal biopsy can be done for lupus nephritis
  • MSUS looking for casts
  • LFTs (albumin)
87
Q

diagnosing SLE

A

the ACR diagnostic criteria uses antibodies and a number of the other investigations/clincial features where a score of 10 or more fulfils the criteria

88
Q

using ESR or CRP in diagnosing SLE

A

ESR better - raises in active SLE whereas CRP tends to stay around normal

raised CRP may suggest another infection or inflammation in present

89
Q

what other conditions can ANA be raised in

what is the significance of a negative ANA test

A

many other rheumatological and autoimmune conditions including Sjrogen’s and dermomyositis and 5% of the healthy population has ANA - note there are many different types of antinuclear antibodies

but if negative almost certainly rules out SLE

90
Q

treatment for lupus nephritis

A

corticosteroids and immunosuppressants

91
Q

pregnancy in SLE

A

pregnancy should be planned in a period of disease stability

immunosuppressants should be changed to ones safe in pregnancy

presence of particular antibodies needs to be known; Ro(SSA), La(SSB) and antiphospholipid antibodies - can cross the placenta and cause neonatal lupus

92
Q

what can neonatal lupus cause

A

lupus rash, complete heart block and blood abnormalities such as cytopaenias

93
Q

what is antiphospholipid syndrome

A

systemic autoimmune disease characterized by elevated antiphospholipid antibodies and an acquired thrombophilia or clotting tendency

94
Q

what is needed to diagnose antiphospholipid syndrome

A

positive antiphospholipid antibodies present (lupus anticoagulant, anticardiolopin antibody, anti -β2 gylcoprotein) on two or more occasions at least 12 weeks apart
AND
vascular thrombosis OR pregnancy morbidity

95
Q

how is the stage of lupus nephritis decided

A

by histology in line with WHO classification stage I-V

96
Q

what categories of symptoms are included in the diagnostic criteria for lupus

A

Constitutional

Haematological

Neuropsychiatric

Mucocutaenous

Serosal (pleurisy or pericardial)

MSK

Renal

Antiphosphoplipid Abs

Complement proteins

SLE specific antibodies

97
Q

first line treatments SLE

A

NSAIDs
Steroids (prednisolone)
Hydroxychloriquine (1st line for mild SLE)
SPF and sun avoidance for photosensitive rash

98
Q

treatments SLE

A

NSAIDs
Steroids (prednisolone)
Hydroxychloriquine (1st line for mild SLE)
SPF and sun avoidance for photosensitive rash

if resistant to first line/more severe try other anti rheumatic drugs (methotrexate, leflunomide, azathioprine) and then if still resistant biologic therapies such as rituximab

99
Q

what is the triad of symptoms in reactive arthritis

A

triad of arthritis, urethritis and conjunctivitis/uveitis

100
Q

what is the relevance of plasma viscosity

A

measures the thickness of the blood which is increased in inflammatory processes

101
Q

what antibodies are raised in vasculitis

A

ANCA - anti-neutrophil cytoplasmic antibody
points more to a small vessel vasculitis

102
Q

what plain film X-ray signs may you see in
- RA
- Gout
- Pseudogout

A

RA - marginal erosions

Gout - juxta-articular erosions

Pseudogout - chondrocalcinosis

103
Q

what is vasculitis
how can it be categorised

A

inflammation of blood vessels which presents with a multi-systemic picture including joints, lungs, skin, kidneys and nerves

small, medium and large vessel vasculitis
The size of the vessel affected can correlate with the symptoms and pathology

104
Q

examples of large vessel vasculitis

A

Giant Cell Arteritis
Takasayu’s arteritis

105
Q

examples of medium vessel vasculitis

A

Polyarteritis nodosa
Kawasaki’s disease
Eosinophilic granulomatosis with polyantitis (churg-strauss disease)

106
Q

examples of small vessel vasculitis

A

microscopic polyangitis

eosinophilic granulomatosis with polyantitis (churg-strauss disease)

Granulomatosis with polyangitis (Wegener’s granulomatosis)

107
Q

two types of ANCA + their targets

A

p-ANCA and c-ANCA

differences are between the target of the antibody and staining produced

c-ANCA = cytoplasmic antibody
more likely to be raised in granulomatosis with polyangiitis (GPA)
Ab target is proteinase-3

p-ANCA = perinuclear
more likely to be found in microscopic polyangiitis and in eosinophilic granulomatosis with polyangiitis
Ab target is myeloperoxidase

108
Q

key features of granulomatosis with polyangiitis

A

nasal crusting, cavitating lesions in the lung and a saddle-nose deformity

109
Q

what is the diagnostic triad of eosinophilic granulomatosis with polyangiitis

A

asthma, eosinophilia and multi-organ involvement (Lanham criteria)

110
Q

investigations in vasculitis

A

CXR
Urinalysis

111
Q

what type of nephritis is associated with ANCA vasculitis

A

crescentic glomerulonephritis - aka rapidly progressive glomerulonephritis

can present with both nephrotic and nephritic features clinically

high dose immunosuppression required

112
Q

inducing remission in a small cell vasculitis

A

depends on if organs threatened

if not consider methotrexate

if organs threatened glucocorticoid + cyclophosphamide or rituximab
if life-threatening same but add plasma exchange

113
Q

maintenance therapy in a small cell vasculitis condition such as EGPA

A

taper Glucocorticoid

either continue rituximab if already on it
if not switch to azathioprine or methotrexate

in the long term try to taper these

114
Q

considerations when starting a patient on high dose steroids

A

bone protection

gastro protection

screen for diabetes

monitor blood pressure and weight

115
Q

multi-system presentations and complications in EGPA

A

Respiratory - allergic rhinitis, polyps, paranasal sinus involvement, asthma, haemoptysis, pneumonitis

Cardio - pericardial effusion, myocarditis, myocardial infarction

Skin - purpura, livedo reticularis (mottled look)

Renal - Crescentic glomerulonephritis, hypertension and renal failure

Neurological - Mononeuritis monoplex and stroke

Ophthalmology - anterior uveitis

Gastro - Mesenteric infarction and bowel perforation

116
Q

What drug classically causes an exacerbation of asthma symptoms in someone with EGPA?

A

Montelukast - bear in mind if stepped up to this for asthma then suddenly gets worse

117
Q

pathophysiology of EGPA

A

genetic determinants - HLA genes and IL-10

acquired determinants - allergens, infections, drugs etc

appears to be T cell mediated producing interleukins and cytokines which attract eosinophils
humoral system also has some role and produces ANCA

118
Q

what infection is polyarteritis nodosa associated with

A

hepatitis B

119
Q

vasculitis screen

A

FBC, U+Es, LFTs, TFTs, PV, CRP, ANA and ANCA with a chest x-ray and urine dip

120
Q

how many joints make a
- oligoarthritis
- polyarthritis

A

oligo 2-5
poly >5

121
Q

what is polymyalgia rheumatica

A

inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck
strong association to giant cell arteritis and often occur concurrently

122
Q

polymyalgia rheumatica epidemiology

A

usually older adults
more common in women
more common in caucasians

123
Q

core diagnostic features of polymyalgia rheumatica

A

clinical diagnosis with important diagnoses of exclusion
response to steroids also used to diagnose

core features present > 2 weeks:
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

124
Q

treatment of polymyalgia rheumatica

A

steroids
if good response after 1 week prednisolone 15mg daily, then taper up

after 3-4 weeks start reducing regime

if symptoms recurring then may need to stay on steroids

125
Q

gonococcal arthritis + treatment

A

most common presentation; dermatitis, polyarthritis and tenosynovitis

treatment is IV ceftriaxone

126
Q

what joint is most commonly affected in septic arthritis

A

knee in adults

127
Q

Raynaud’s

A

exaggerated vasoconstrictive response of digital arteries in response to cold or emotional stress

primary - typically young women, bilateral

secondary - underlying disease such as CTD, malignancy + others - suggested by later onset, unilateral, autoantibodies, rash

128
Q

Raynaud’s treatment

A

all should be referred to secondary care

1st line; calcium channel blocker e.g. nifidipine

2nd line; IV prostacyclin infusions, effect can last several months

129
Q

what is dermatomyositis

A

inflammatory disorder that causes symmetrical proximal muscle weakness and characteristic skin lesions

can be idiopathic or associated with a connective tissue disorder

130
Q

what is polymyositis

A

inflammatory disorder of symmetrical proximal muscle weakness
similar to dermatomyositis but without the skin features

131
Q

features of antiphospholipid syndrome

A

venous/arterial thrombosis

recurrent fetal loss

lived reticularis (mottled skin)

thrombocytopenia

prolonged APTT

132
Q

management of antiphospholipid syndrome

A

primary thromboprophylaxis - low dose aspirin

secondary thromboprophylaxis - lifelong warfarin

133
Q

systemic sclerosis / scleroderma

A

autoimmune inflammatory fibrotic connective tissue disease where the skin and other mucosa harden

134
Q

patterns of disease systemic sclerosis

A

limited cutaneous (CREST syndrome)
Calcinosis (calcium under skin)
Raynaud’s
Oesophageal dysmotility
Sclerodactyly
Telangiectasia (small dilated vessels)

Diffuse Cutaneous - all CREST features + affects internal organs causing CVD, lung disease and kidney disease

135
Q

autoantibodies systemic sclerosis

A

ANA - not specific

Anticentromere antibodies - limited SS

Anti-Scl 70 antibodies - diffuse SS and more severe disease

136
Q

systemic sclerosis treatment

A

no standardised treatment

steroids and immunosuppressants can be used in diffuse or severe disease

gentle skin stretching, emollients, avoiding cold, physiotherapy and occupational therapy

can treat symptoms and complications medically

137
Q

Still’s disease

A

arthralgia
spiking fevers
elevated serum ferritin
lymphadenopathy
RF and ANA negative

manage with NSAIDs and steroids

138
Q

what condition are anti-Ro antibodies associated with

A

Sjrogen’s syndrome

139
Q

drug induced lupus

A

arthralgia, myalgia and rash (usually no renal or nervous system involvement)

ANA positive
anti-histone antibody positive
anti-DsDNA negative

common causes: procainamide, hydralazine
less common causes: isionizad, phenytoin, minocycline

140
Q

dermomyositis associated antibody

A

anti-Jo-1

141
Q

what is Sjögren’s syndrome

A

autoimmune condition that affects the exocrine glands resulting in dry mucous membranes e.g. mouth, eyes, vagina

primary - occurs in isolation
secondary - SLE or RA associated

anti-Ro and anti-La antibodies

142
Q

the As of ankylosing spondylitis

A

apical fibrosis
anterior uveitis
aortic regurg
achilles tendonitis
AV node block
amyloidosis

Clinical Years / Progress Test (24 decks)

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