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Year 4 > Medicine - Rheumatology > Flashcards

Medicine - Rheumatology Flashcards

1
Q

Features of RA on X-ray

A 
SPADES
soft tissue swelling
periarticular erosions
absent osteophytes
deformity
erosions
subluxation
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2
Q

Features of OA on X-ray

A 
LLOSS
loss of joint space
loss of articular cartilage
osteophytes (bone lipping)
subchondral cysts
sclerosis
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3
Q

Side effects of methotrexate

A

ILD

Hepatitis

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4
Q

What is Felty’s syndrome?

A

RA
Splenomegaly
neutropenia/thrombocytopenia

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5
Q

Examples of anti-TNF drugs

A

Etanercept

Infliximab

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6
Q

Example of anti-CD20 drug

A

Rituximab

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7
Q

Example of JAK inhibitor

A

Tofacitinib

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8
Q

Example of anti-IL6 drug

A

Tocilizumab

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9
Q

Genetics involved in psoriatic arthritis?

A

HLA-B27 (one of the seronegative spondyloarthropathies)

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10
Q

How can PA be distinguished from RA at presentation?

A

PA has DIP involvement, and dactylitis

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11
Q

What nail changes are found in PA?

A

Hyperkeratosis
Onycholysis
Nail pitting

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12
Q

What is the CASPAR criteria used for?

A

Classifying Psoriatic arthritis

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13
Q

What is the PSARC criteria used for?

A

Monitoring response to treatments in PsA

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14
Q

Treatment options in PsA?

A 
NSAIDs
Joint injections (corticosteroid)
DMARDs
Anti-TNF drugs
Biologics
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15
Q

Common causes of infection in septic arthritis:

A

Can be mono or polymicrobial:

  • staph. aureus
  • haemophilus influenza
  • neisseria gonorrhoea
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16
Q

Risk factors for septic arthritis?

A 
Prosthesis
DM
Steroids
RA
Alcohol/IVDU
Ulcers
Joint injections
Surgery
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17
Q

What antibiotics are commonly used for septic arthritis treatment?

A

IV flucloxacillin + gentamicin (N)

IV vancomycin + gentamicin (P)

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18
Q

What are the contraindications to joint aspirations? (arthrocentesis)

A 
Haemarthrosis
Prosthetic joint
Overlying skin infection
Immunocompromised
Clotting disorder
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19
Q

What type of crystals are found in gout?

A

Monosodium urate (negatively birefringent needle-shaped)

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20
Q

What type of crystals are found in pseudogout?

A

Calcium pyrophosphate (positively birefringent rhomboid-shaped)

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21
Q

Risk factors for gout?

A 
DM
Obesity
HTN
Haematological malignancy
Diuretics
Rich diet
Chemotherapy
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22
Q

Risk factors for pseudogout?

A

Hypothyroidism
Hypophosphataemia
Hypomagnesaemia

Hyperparathyroidism
Haemochromatosis
FHx
Older age
Prior joint injury
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23
Q

What blood tests would you request if you suspected gout?

A

FBC, CRP, serum urate

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24
Q

What blood tests would you request if you suspected pseudogout?

A

FBC, CRP, (high) calcium and PTH, (low) Mg and PO4, (high) T3/4

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25
Q

What are the X-ray features of gout?

A

soft tissue swelling
tophi formation
rat-bite erosions in long-standing disease

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26
Q

What are the X-ray features of pseudogout?

A

chondrocalcinosis (almost diagnostic!)

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27
Q

What are the causes of GCA?

A
  • primary = autoimmune issue (a type of large vessel vasculitis)
  • secondary = to infection (hepatitis) or drugs
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28
Q

What is the definition of osteoporosis?

A

Reduction in bone mass (resorption > deposition)

matrix composition maintained but BMD reduced

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29
Q

What are the RFx for OP development?

A 
S - steroids
H - hyperthyroid/parathyroid/calciuria
A - alcohol/smoking
T - low testosterone
T - thin (BMI <19)
E - early menopause
R - renal/liver failure
E - erosive/inflammatory bone disease
D - diet (low calcium/vit D, malabsorption, DM)
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30
Q

What is used to investigate OP and describe its results:

A

FRAX score (fracture risk assessment tool)

DEXA scan: gives a t-score

greater than -1 = normal
-1 to -2.5 = osteopenia
less than -2.5 = osteoporosis
less than - 2.5 with fractures = defined OP

Remember: T-score (compares to a healthy thirty year old), Z-score (compares to an age matched individual)

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31
Q

Name some of the pharmacological treatments for OP:

A

HRT
SERM e.g. raloxifene
Bisphosphonates e.g alendronate
Teriparatide (synthetic PTH)
Strontium ranelate (reduces OC and increases OB activity)
Denosumab (monoAb against RANK-L, stops OC recruitment)

32
Q

Describe the signs/symptoms of ankylosing spondylitis

A
  • lower back pain
  • worse at night, better towards the end of the day
  • pain better with exercise and worse with rest
  • pain radiates from hip -> buttocks
  • dyspnoea (if costochondral involvement)
  • uveitis
  • enthesitis (achilles tendonitis, plantar fasciitis)
33
Q

How is Ank Spond diagnosed?

A
  • clinical + radiological criteria
  • MRI or X-ray used as imaging
  • X-ray may show bamboo spine (syndesmophytes present)
34
Q

What are three features of poor prognosis in Ank Spond?

A
  • smoking
  • high ESR/CRP
  • syndesmophytes present
35
Q

What autoantibodies are found in SLE?

A
  • ANA (sensitive but not specific)

- anti-ds-DNA (more specific)

36
Q

What are the signs/symptoms of SLE?

A 
S - serositis (pleuritis, pericarditis)
O - oral ulcers
A - arthritis
P - photosensitivity
B - blood (low WCC, RBC and plts)
R - renal (glomerulonephritis)
A - ANA
Immunological - anti-ds-DNA
N - neurological (confusion, seizures)
M - malar rash (butterfly, non-scarring)
D - discoid rash (scarring)
37
Q

Name the large vessel vasculitides

A
  • GCA
    (- PMR)
  • Takayasu arteritis
38
Q

Describe Takayasu arteritis

A

Large vessel vasculitis
aortic-arch syndrome/pulseless disease
inflammation of aorta and primary branches
common in females 15-25yrs
presents - fever, malaise, night sweats, weight loss, bruits, absent/reduced/assymmetrical pulses
Investigate with CT/MRI/angiography

39
Q

Name the medium vessel vasculitides

A

PAN

Kawasaki disease

40
Q

Describe PAN

A

Medium vessel vasculitis
Polyarteritis nodosa
a Necrotising vasculitis which causes aneurysms and thrombi
can cause infarction in all organ systems

41
Q

Describe Kawasaki disease

A 
Medium vessel vasculitis
common in children and babies
aneurysm formation in medium/large arteries, commonly affecting:
- cardiac
- axillary
- iliac
- popliteal arteries
Presents with:
- fever
- conjunctivitis
- mucositis (strawberry tongue)
- peeling skin
- lymphadenopathy
42
Q

Describe the different types of ANCA:

A

Anti-neutrophil cytoplasmic antibodies
2 types:
- C-ANCA (cytoplasmic) = against proteinase 3 (PR3)
- P-ANCA (perinuclear) = against myeloperoxidase (MPO)

43
Q

Describe the ANCA associated vasculitides

A

small vessel vasculitidies
- microscopic polyangitis: P-ANCA associated, necrotising inflammation in many organs including kidneys

  • granulomatosis with polyangitis: C-ANCA associated, granulomatous inflammation, triad of upper respiratory/lower respiratory/kidney issues
  • eosinophilic granulomatosis with polyangitis: P-ANCA associated, necrotising and granulomatous inflammation causing asthma, eosinophilia and peripheral neuropathy
44
Q

Describe the immune-complex vasculitides:

A

HSP (Henoch Schonlein purpura)

  • commonest childhood vasculitis
  • median age ~4yrs

Cryoglobulinaemic vasculitis
- autoimmune where the cold triggers immunoglobulins called cryoglobulins reversibly precipitate at <37oC in serum

45
Q

Describe reactive arthritis:

A 
Seronegative spondyloarthropathy (RF-ve, HLA-B27 +ve)
inflammatory arthropathy after infection (antigen cross reacts from infection to self-tissue in joint)
Commonly pts have preceding venereal/diarrhoeal infection
46
Q

What common infections can cause reactive arthritis

A

Venereal:

  • shigella
  • chlamydia
  • salmonella
  • yersinia

Diarrhoeal:
- campylobacter

47
Q

What investigations would you want to carry out if reactive arthritis was suspected?

A
  • bloods (ESR, CRP, RF, U&E)
  • urinalysis and stool cultures
  • joint aspirate
  • STI check
  • X-ray
48
Q

Define Paget’s disease of bone

A

Also called ‘Osteitis deformans’
increased bone turnover (more OB and OC)
Rare <40yrs
bone remodelling and enlargement = deformity and weakness

49
Q

Describe the pathophysiology of Paget’s disease of bone

A

3 distinct phases:

1) Initial short-lived burst of OC activity and bone resorption
2) Mixed phase of OC and OB activity (increased bone turnover and structurally abnormal bone)
3) Chronic sclerotic phase = bone formation > deposition

50
Q

Describe primary and secondary bony lesions

A

Primary e.g. myeloma

  • much more rare
  • lytic usually

Secondary e.g. mets from lungs, breast, prostate, kidney, thyroid

  • commoner
  • usually sclerotic
51
Q

Describe compartment syndrome and its causes

A
  • increased interstitial pressure in a closed fascial compartment
  • pressure can be increased due to internal cause (haematoma, iatrogenic cannula) or external cause (casts, burns, bandages)
52
Q

What is the indication for a fasciotomy in compartment syndrome?

A

If myoglobin (released from ischaemic muscle) is high as this it toxic to the kidneys and can cause kidney damage

53
Q

What are the important time points for managing compartment syndrome?

A 
1-4hrs = reversible
>8hrs = irreversible (muscle ischaemia and necrosis)
54
Q

What genetic HLA type is common in RA?

A

HLA DR4

55
Q

Describe the features of RA (articular and extra-articular)

A 
symmetrical deforming polyarthritis
DIP sparing
peak onset ~40yrs
swan neck/boutonnieres deformities
ulnar deviation
swelling, heat, pain
tenosynovitis
(Extra-articular)
nodules
lungs - ILD, fibrosis, pneumonia
heart - IHC, pericarditis
eyes (scleritis, episcleritis)
kidneys - amyloidosis
feltys syndrome
56
Q

Describe the pathophysiology of RA

A

Genetics (DR4) + environmental (smoking increases PAD, increased anti-CCP antibodies, hormones and infections)

57
Q

What common HLA type in seen in AnkSpond

A

HLA-B27, RF- (as it is a seronegative spondyloarthropathy!)

58
Q

Describe GCA and how it presents

A

large vessel vasculitis (also called temporal arteritis)
affects extra-cranial branches of the carotid artery
can be primary (autoimmune) or secondary (drugs/infection e.g. hepatitis)

headache, temporal tenderness, jaw claudication, malaise, weight loss, depending on nearby nerves affected = amaurosis fugax, tongue tingling, confusion

59
Q

How is GCA investigated and treated?

A

Bloods - high ESR/CRP
Temporal artery biopsy (beware of skip lesion)
Start steroids immediately = pred, or IV methyl-pred if visual changes
(usually need steroids for ~2yrs and then need to wean off)

60
Q

Describe PMR and its presentation

A

polymyalgia rheumatica
Rare <60yrs
not a true vasculitis, can develop from GCA
presents with painful proximal myopathy (pelvic, neck, shoulder pain)
NO MUSCLE WEAKNESS! (helps to distinguish from myositis’)

61
Q

What HLA type is PMR associated with?

A

HLA DRB1 (found in GCA-PMR concurrent cases, but NOT in PMR alone)

62
Q

How is PMR investigated and treated?

A

High ESR/CRP
lots of other bloods! (CK should be normal to distinguish from myositis’)

Treat with steroids (but not needed as urgently as in GCA)
Use methotrexate for relapsing disease

63
Q

Define polymyositis and its presentation

A

Idiopathic inflammatory myopathy characterised by striated muscle inflammation
Cause unclear
Presents: painful proximal myopathy + WEAKNESS
- malaise, weight loss, fever, dysphagia, palpitations, syncope

64
Q

How is polymyositis investigated?

A

Clinical features
Lab findings: high platelets, high CRP, high CK (50-100x ULN), anti-Jo antibodies
MRI shows muscle inflammation and oedema

65
Q

Define dermatomyositis and its presentation

A

Idiopathic inflammatory myopathy characterised by striated muscle inflammation (same as polymyositis) + rash

  • heliotrope rash (eyelids), periorbital oedema and Gottron’s papules
66
Q

Describe Sjogren’s syndrome and its associated HLA type

A

Systemic autoimmune disorder
presents with dry eyes and mouth
lymphocytic infiltration of lacrimal and salivary glands
9F : 1M

HLA B8/DR3

67
Q

How does Sjogren’s syndrome present?

A 
Sicca complex = reduced salivary and lacrimal gland excretion
Dry eyes (keratoconjunctivitis), red itchy eyelids (blepharitis)
Dry mouth (xerostomia) - pts often need to sip water to swallow food
68
Q

How Sjogren’s syndrome diagnosed and how can it be managed?

A 
Bloods: high ESR
Schirmers test (filter paper)
Salivary gland biopsy

lacrimal substitutes
artificial saliva/gels
chewing gum - stimulates saliva flow

69
Q

How do primary and secondary bone growths/mets differ

A 
Primary = lytic
Secondary = more sclerotic
70
Q

Describe compartment syndrome and its causes

A

Increased interstitial pressure in a closed fascial compartment
Causes nerve damage and cell death

causes:
increased internal pressure (bleeding/iatrogenic)
increased external pressure (burns, casts, bandages)

71
Q

What are the S/Sx of compartment syndrome?

A 
Pain
Pallor
Paraesthesia
Paralysis
Pulseless

shiny, swollen taught skin
increased autonomic responses (cause sweating and tachycardia)

72
Q

What conditions are associated with carpal tunnel syndrome

A

RA, CKD, DM, acromegaly, pregnancy

73
Q

What is the time at which the damage from compartment syndrome and the neuropraxia becomes irreversible

A

8hrs!

74
Q

How is compartment syndrome investigated and managed?

A

Measure compartment pressure (?20-30mmHg above diastolic BP then this is a strong indicator for fasciotomy

Treatment: remove external constriction, fasciotomy, may need to remove dead muscle and get skin grafts

75
Q

What is tendinopathy and common tendinopathes?

A

= general term for tendon degeneration with combination of: pain, swelling and impaired performance

Commonly: achilles, rotator cuff, tennis elbow (lateral) and golfers elbow (medial epicondyle)

76
Q

How is tendinopathy managed?

A 
NSAIDS/GTN patches
Physio
RICE
Stretching and strengthening
Extra-corporal shock wave therapy (causes microtrauma and increased healing in the local area?)

May need surgery

Year 4 (28 decks)

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