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Medicine > Rheum > Flashcards

Rheum Flashcards

1
Q

What is polymyositis?

How does it present?

A

Inflammation and destruction of type I and II muscle fibres due to cytotoxic lymphocytes

usually develops over 3-6 months with progressive, symmetrical proximal muscle wasting, tenderness + weakness
symmetrical non-erosive arthritis affects knees, wrists + hands - often morning stiffness

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2
Q

Who is affected by polymyositis? What causes it?

A

affects those in 20s
maybe autoimmune, coxsackie virus has been implicated

can be associated with SLE, RA and Sjogrens
can be non-metastatic complication of malignancy

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3
Q

How does dermatomyositis differ from polymyositis?

A

Cutaneous rash

can affect children

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4
Q

What are the endocrine causes of myopathy?

A

Corticosteroid-induced (Cushing’s or exogenous)
Thyroid (hypo + hyper)
Osteomalacia
B12/ folate deficiency

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5
Q

What are other secondary causes of myopathy?

A

Viral myalgias

Toxic myopathies: alcohol, drugs, statins, lithium

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6
Q

Investigations for widespread MSK pain

A

ESR: high in PMR, inflammatory arthritis, SLE, malign
Serum calcium: low in osteomalacia, high in malign
PTH
Serum ALP: raised in Paget’s and in response to inflamm
Immunology screen

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7
Q

How to approach widespread MSK pain

A

Do the joints look/ move normally? If not, consider inflamm arthritis

If yes, is their proximal myopathy?

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8
Q

How many fibromyalgia trigger points?

A

18

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9
Q

Management of fibromyalgia

A

Education/ reassurance
Physio/ exercise
CBT
Trial TCAs, meds for neuropathic pain

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10
Q

What age does SLE develop?

A

15-40 years

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11
Q

What % SLE sufferers have ANAs?

A

90%

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12
Q

Define SLE

A

Characterised by autoantibody to nuclear material

Widespread vasculitis that can affect most body systems

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13
Q

What involvement of SLE sufferers have skin involvement?

A

75%
malar rash
annular lesions
alopecia

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14
Q

What is drug-induced SLE: causes and presentation?

A

COCP and others
Milder than normal SLE
Kidney-sparing
settles on withdrawal of drug

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15
Q

What are the systemic features of SLE?

A

MSK: arthritis - myalgia - myositis

CNS: headaches - psychosis, depression, anxiety - seizures - neuropathies - chorea

CVS: pericarditis - myocarditis - endocarditis (Libmans-Sacks: non-infective vegetations)

Resp: pneumonitis (mimics pneumonia) - effusion - infarction

Renal: GN (late stages: important to monitor)

Haem: anaemia - thrombocytopenia

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16
Q

What kind of arthritis in SLE?

A

Polyarticular

deformity not due to joint erosion, due to tenosynovitis and fibrosis

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17
Q

What can cause flare-ups in SLE?

A

Stress - skin exposure - infection - COCP - other drugs

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18
Q

What are life-threatening conditions that can be caused by SLE flare-up?

A

Renal failure

Cerebral vasculitis

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19
Q

Investigations for SLE

A

Anti-dsDNA (v specific)
ANA (detected in most)
Anti-histone antibodies: often positive in drug-induced SLE (v specific)
Anti-Ro/La - associated with secondary Sjogens and pulm fibrosis (not v specific)
Antiphospholipid and anticardiolipin antibobodies (positive in 10-20% pts)

Urine for signs of nephritis

FBC: penias
U&Es: renal function
ESR/ CRP: may be high during flare-ups or even when feeling well

Others: skin biopsy, complement C3/4 (low), renal biopsy….

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20
Q

Management of SLE

A

Education: long sleeves, sunscreen

Mild: NSAIDs or anti-malarials

More severe: CS or clever stuff

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21
Q

Features of anti-phospholipid syndrome

A

Venous thrombosis
Arterial thrombosis
Spontaneous miscarriage
Thrombocytopenia (not severe enough to cause haemorrhage)

Others: migraine, epilepsy, chorea, leg ulcers, cardiac valve abnormalities

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22
Q

Management of antiphospholipid syndrome

A

Lifestyle advice to manage risk factors for thrombosis

If no clinical features, dont need to treat
If thrombosis, needs lifelong warfarin

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23
Q

What is Sjogrens?

A

Chronic autoimmune disease charactised by inflammation of exocrine glands: predominantly salivary and lacrimal

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24
Q

What is sicca syndrome?

A

Dry eyes/ mouth due to non-immune causes, eg smoking

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25
Q

Causes of Sjogrens

A

Primary

or secondary in association with RA, SLE, systemic sclerosis, polymyositis, PBC, chronic active hepatitis

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26
Q

Symptoms of Sjogrens

A

Keratoconjunctivitis, often bacterial infections

Xerostomia, caries

Vaginal dryness

Low GI mucus: gastritis, oesophagitis

Primary Sjogrens is systemic and can develop symptoms similar to SLE

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27
Q

Investigations for Sjogrens

A

RhF, and ANA often raised
Sometimes antiphospholipids raised
Anti-Ro/La and Ig often v high

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28
Q

Vasculitis with different BP in both arms

A

Takayasu arteritis

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29
Q

Presentation of osteogenesis imperfecta

A

V varying degrees

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30
Q

What is osteopetrosis?

A

Marble bone disease
Failure of osteoclasts to resorb bones
(bone marrow transplant is curative)

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31
Q

What is the T score?

A

Bone mineral density (osteoporosis)

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32
Q

Describe the histology in osteoporosis?

A

Increased osteoclastic resorption
slowed osteoblast formation
thinning of bone cortex
trabeculae are attenuated with big Heversian canals

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33
Q

Modifiable risk factors for osteoporosis

A

poor calcium and vit D
lack of exercise
smoking
alcohol excess

34
Q

Non-modifiable risk factors for osteoporosis

A 
Age
Race (Caucasian, Asian)
Female
Early menopause
Small size
Family hx
35
Q

Meds that can cause osteoporosis

A

CS, anticonvulsants, heparin

36
Q

What does DEXA scan measure?

A

Bone density of lumbar spine and proximal femur

need 30% loss before seen on radiograph

37
Q

What does serum biochemistry show in osteoporosis?

A

No abnormalities

38
Q

Mx osteoporosis

A

Lifestyle
Bisphosphonates
other clever stuff

39
Q

Rarer cause of rickets

A

Phosphate depletion (renal disease, liver failure, others)

40
Q

Causes of vit D deficiency

A

low dietary intake, insufficient sun exposure, deranged liver or kidney metabolism, malabsorption (coeliac disease, small bowel resection)

41
Q

Clinical features of rickets

A

Bowing of legs
Overgrowth of costochondral junctions (forming a ‘rachitic rosary’)
Widened epiphyses
Flattened ‘bossed’ square skull or craniotabes (skull snaps back when pressed)

42
Q

Clinical features of osteomalacia

A

Muscle and bone pain
Spontaneous incomplete fractures in long bone and pelvis
Proximal myopathy with waddling gait and Gower’s sign

43
Q

Biochem in Pagets

A

Raised ALP
(ca, phos normal)

Hydroxyproline in urine

44
Q

Mx of Pagets

A

Bisphosphonates if symptomatic

Maybe surgery (v vascular)

45
Q

10% Pagets leads to which ca?

A

Osteosarcoma

poor prognosis, may need to amputate/ chemo

46
Q

Why can Pagets lead to high-output HF?

A

New blood vessels forming shunts

47
Q

Most common bug cause of osteomyelitis?

Others

A

Staph aureus
(also strep spp, haemophilus influenzae)
If immunocompromised: E.coli, Klebsiella, Pseudomonas etc.

48
Q

How is osteomyelitis usually caused?

A

haematogenous spread

can also occur from infected wounds, open fractures, surgery

49
Q

How to investigate for osteomyelitis?

A

Blood cultures
Inflammatory markers
Pus should be aspirated for MC&S

x-ray may look normal for 7-10 days

50
Q

What is Pott’s disease?

A

TB osteomyelitis in thoracic or lumbar vertebrae

51
Q

Causes primary OA

A

idiopathic

general wear and tear

52
Q

How does OA appear o/e?

A

Swelling and effusion
Joint deformity
Creps on movement
Wasting of supporting muscles due to limited use of joints

53
Q

How does RA show on x-ray?

A

Soft tissue swelling, narrowing of joint spaces, subchondral cysts, juxta-articular erosions, may have osteopenic adjacent bone

54
Q

Mx ank spond

A

NSAIDs

DMARDs have no place

55
Q

What is reactive arthritis?

A

Aseptic, in response to infection at different site

GI, urinary, Reite’s…

56
Q

What is enteropathic arthritis?

A

Related to IBD (20% pts)
Peripheral asymmetrical mono-oligoarthritis
Varies with severity of disease (eg bowel resection improves sx)
Most x-rays/ bloods are normal
mx by improving IBD

Different to sacroilitits where unrelated to disease severity

57
Q

Why do crystal arthropathies cause swelling?

A

neutrophils attack crystals

58
Q

Causes of secondary gout?

A 
Increased production of uric acid (increased cell turnover in ca, leukaemias after chemo)
Impaired excretion (renal failure, chronic booze, diuretics)
High dietary intake of purines
59
Q

Where does urate come from?

A

Breakdown of DNA

60
Q

What is chronic gouty arthritis?

A

After recurrent attacks - cartilage degeneration, synovial hyperplasia, secondary OA

61
Q

Gout:
Mx
Prophylaxis

A

NSAIDs, eg colchine

allopurinal is prophylaxis

62
Q

Describe crystals of pseudogout

A

Brick-shaped crystals that are positively bifringe…wotevs

gout are needle-shaped

63
Q

Mx pseudogout

A

Pain relief

Joint aspiration/ CS

64
Q

Where is the pain in De Quervain’s tenosynovitis?

A

Radial styloid

65
Q

What causes mallet finger?

A

Extensor tendon damage - DIP cannot fully extend

66
Q

What causes dropped finger?

A

Extensor tendon rupture at wrist, so MCP cannot extend

primary or secondary to RA

67
Q

Which elbow: tennis and golfer’s

A

Tennis: lateral epicondylitis
Golfers: medial (GM)

68
Q

MoA bisphosphonates

A

Osteoclast inhibition

69
Q

mx OA

A

lifestyle

paracetamol and topical NSAIDs (knee, hand)

oral NSAID/ PPI

CS injection

surgery

70
Q

what can be reactivated with biological agents?

A

TB, hep B

71
Q

what should be given for gout in renal disease?

A

CS

72
Q

keratoderma blenorrhagica and circinate balanitis are associated with what

A

reactive arthritis

73
Q

mx reactive arthritis

A

NSAIDs

74
Q

which malignancy linked with SLE

A

non–Hodgkins

75
Q

CREST

A 
calcinosis
raynauds
oesophageal dysmotility
sclerosis
telangiectasia

this is limited sclerosis.

also diffuse systemic sclerosis

76
Q

antibodies associated with CREST

A

ant-centromere

77
Q

antibodies associated with diffuse systemic sclerosis

A

anti-Scl-70

78
Q

Raynaud disease vs syndrome

A

Disease is idiopathic

syndrome part of underlying condition

79
Q

bloods to arrange in raynauds

A

ANA (90%)
anti-centromere (CREST)
Anti Scl-70 (diffuse)
Anti-RNA polymerase III (increased risk of renal crises)

80
Q

antibodies in polymyositis

A

anti-Jo-1

and elevated CK

81
Q

p-ANCA

A

Churg-Strauss (associated with asthma)

Medicine (30 decks)

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