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formative 3b > MSK Peer Teaching > Flashcards

MSK Peer Teaching Flashcards

1
Q

what is the role of articular cartilage

A

friction reduction

shock absorption

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2
Q

what is the role of the synovial fluid

A

lubrication

shock absorption

nutrient distribution (since hyaline cartilage is avascular and relies on diffusion from SF)

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3
Q

what is the pathophysiology of osteoarthritis

A
  • this is non-inflammatory wear and tear resulting from loss of articular cartilage
  • there is an imbalance of cartilage damage and repair
    1. damage
    2. disordered repair
    3. fibrillations
    4. osteophytes
    5. sclerosis
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4
Q

risk factors for osteoarthritis

A

older

female

genes

obesity

previous joint trauma

RA

gout

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5
Q

name a disease that reduces the risk of osteoarthritis

A

osteoporosis

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6
Q

presentation of OA

A

mostly knee and hip but can be anywhere

pain on movement and at rest if severe

worse at the END of the day

minimal swelling

morning stiffness lasts <30 minutes

affects the DIPs

crepitus

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7
Q

osteoarthritis X ray findings

A
  • LOSS
    • loss of joint space
    • osteophytes
    • subchondral sclerosis
    • subchondral cysts
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8
Q

Ix for osteoarthritis

A
  • bloods: normal
  • X-Ray: Loss
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9
Q

treatment for osteoarthritis

A
  • conservative
    • weight loss
    • exercise
    • physio
    • hot/cold packs
  • medical
    • analgesic ladder
    • intra-articular steroids
    • PPI if long term NSAIDs
  • surgical
    • osteophyte removal
    • joint replacement
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10
Q

what is rheumatoid arthritis

A

it is chronic systemic inflammatory disease due to deposition of immune complexes in synovial joints which causes symetrical, deforming polyarthritis

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11
Q

how common is RA

A

common it’s ~ 0.5 - 1% of the population

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12
Q

rheumatoid arthritis risk factors

A

increasing age

female

premenopausal

smoking

stress

infection

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13
Q

what is the typical presentation of RA

A

symmetrical swollen, painful and stiff joints (hands and feet) which is worse in the morning for >1hr and in hot weather. symptoms ease off with use

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14
Q

name 4 deformities associated with RA

A

rheumatoid nodule on elbow

ulnar defiation

boutonniere

swan neck deformity

z thumb

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15
Q

signs of RA apart from deformities

A

MCP, PIP, MTP, DIP (sparingly) symmetrical swelling

muscle wasting

carpal tunnel syndrome

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16
Q

9 extra-articular manifestations of RA

A

weight loss

xeropthalmia

pulmonary fibrosis

pericarditis

sjorgen’s

raynaud’s

neuropathies

scleritis

increased CV event risk

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17
Q

diagnostic criteria for RA

A
  • You need 4 of the following 7
    • morning stiffness
    • arthritis of 3 or more joints
    • arthritis of hand joints
    • symmetrical
    • rheumatoid nodules
    • rheumatoid factor +ve
    • radiographic changes (LESS)
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18
Q

radiographic changes seen in RA

A
  • LESS
    • loss of joint space
    • erosions (peri-articular)
    • soft tissue swelling
    • soft bones (osteopenia)
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19
Q

Investigations for RA

A
  • rheumatoid factor (only 70% patients)
  • anti-CCP (anticitrulinated protein antibody)
    • very specific
  • FBC
    • high platelets
    • high CRP
    • high ESR
  • X-Ray
    • LESS
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20
Q

treatment for RA

A
  1. initially NSAIDS
    • give PPI
  2. refer to rheumatology
  3. early use of DMARDs reduces joint destruction
    • methotrexate
    • sulfasalazine
  4. biologics
    • rituximab
  5. encourage exercise and manage RF
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21
Q

name 6 groups involved in the RA MDT

A

GP

Rheumatolgy

OT

Physiotherapy

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22
Q

acute exacerbations of RA are treated how

A

with IM steroid like methylprednisolone

TNF-alpha blockers like etenercept if DMARDs aren’t working

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23
Q

how is the swelling different in RA and OA

A

in RA the swelling is usually due to joint effsions in OA it’s bony

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24
Q

what is osteoporosis

A

it is low bone mass, high bone fragility and increased fracture risk

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25
Q

what causes osteoporosis

A

it is due to increased resorption and inadequate formation

or it can be caused by inadequate peak bone mass

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26
Q

osteoporosis risk factors

A

elderly

female

family history

smoking

low BMI

alcohol excess

those with low calcium i.e. lactose intolerant

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27
Q

what sort of drugs might cause osteoporosis

A

cortico steroids

hormone therapy e.g. androgen deprivation therapy in prostate cancer

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28
Q

what other diseases can predispose to Osteoporosis

A
  • joint diseases
    • RA
    • SLE
  • hyperparathyroidism & pseudohyperparathyroidism (high bone turnover)
  • high cortisol e.g. cushing’s (causes high resorption and low osteoblast activity)
  • low oestrogen or testosterone (e.g. menopause)
  • renal disease (low vit D)
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29
Q

what is the difference between primary and secondary osteoporosis

A

primary is basically old age + menopause because oestrogen protects bones

secondary is due to other disease or drugs

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30
Q

causes of secondary osteoporosis

A
  • SHATTERRED
    • Steroid use
    • Hyperthyroid/hyperparathyroid
    • Alcohol/smoking
    • Thin (low BMI)
    • Testosterone low
    • Early menopause
    • Renal/liver disease
    • Relatives (FH)
    • Erosive bone disease (RA or Myeloma)
    • Dietary calcium low
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31
Q

diagnosis of osteoporosis

A
  • DEXA BMD scan T score:
    • -2.5 SDs = OP
    • between -1 and -2.5 SDs = osteopenia
    • more than -1 = normal
  • bloods will be normal
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32
Q

1st, 2nd and 3rd line treatments for osteoporosis

A
  • 1st: bisphosphonates = alendronate
  • 2nd: another bisphosphonate = risendronate
  • 3rd: strontium ranelate
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33
Q

what antibody might be present in antiphospholipid syndrome

A

anti-cardiolipin antibody

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34
Q

primary prevention of osteoporosis

A

Adcal D3 (vitD with calcium)

calcium rich diet (dairy, sardines, white beans)

HRT

if they’re on corticosteroids consider prophylactic bisphosphonates

regular weight bearing exercise

reduce smoking and alcohol consumption

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35
Q

how do bisphosphinates work

A

bind calcium

is absorbed by osteoclasts

stimulate osteoclast apoptosis

reduce bone resorption

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36
Q

what is SLE

A
  • systemic lupus erythematosus
    • a multi-systemic disease in which autoantibodies are produced by B cells
    • these target a variety of autoantigens leading to formation of immune complexes at various sites
    • this activates complement system and an influx of neutrophils causing inflammation in those tissues
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37
Q

what are the risk factors for SLE

A

women in 90% cases

peak onset 20-40yrs

afro-carribeans 10x more likely than caucasians

hereditary

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38
Q

triggers for SLE

A

UV light

EBV

drugs e.g. isoniazid

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39
Q

presentation of SLE

A
  • typically relapsing remitting
  • very non specific symptoms
    • fatigue
    • myalgia and arthralgia
    • skin problems
    • fever
    • lymhadenopathy
    • weight loss
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40
Q

diagnostic criteria of SLE

A
  • 4 of the following 11 are required
    • MD SOAP BRAIN
      • Malar rash (30%)
      • Discoid rash
      • Serositis
      • Oral ulcers
      • Arthritis
      • Photosensitivity
      • Blood (all low - anaemia and leukopenia)
      • Renal disorder (proteinuria)
      • ANA +VE (90%)
      • Immunological disorder (anti-dsDNA)
      • Neurological symptoms (seizures)
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41
Q

Ix for SLE

A

screen for ANA (sensitive but not specific)

anti-dsDNA (specific but not sensitive)

inflammatory markers (ESR high but CRP may be normal)

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42
Q

two other conditions that SLE is associated with

A

raynaud’s

anti-phospholipid syndrome

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43
Q

4 complications of SLE

A

migraine

IHD

stroke

non-infective endocarditis

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44
Q

what is antiphospholipid syndrome

A

it occurs secondarily to SLE and is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies.

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45
Q

what are the signs of Antiphospholipid syndrome

A
  • CLOT
    • Coagulation defects
    • Levido reticularis (pink-blue mottling)
    • Obstetric: recurrent miscarriages
    • Thrombocytopaenia
  • Also there will be anti-cardiolipin antibody present
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46
Q

what is the treatment for anti-phosopholipid syndrome

A
  • manage CVS risk factors
    • smoking
    • weight
    • diet
    • exercise
    • DM
    • HTN
    • hyperlipidaemia
  • warfarin or LMWH if trying to conceive
  • aspirin
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47
Q

what is sjorgen’s syndrome

A

it’s a chronic inflammatory autoimmune disease

it is either primary fibrosis of exocrine glands or it is secondary to another connective tissue disorder such as SLE, RA or systemic sclerosis

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48
Q

what are the clinical features of sjorgen’s syndrome

A
  • dry eyes and mouth, aka sicca complex
  • parotid swelling i.e. englarged salivary glands
  • other glands and affected too causing dyspareunia and dry cough etc
  • arthralgia
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49
Q

Ix of Sjorgen’s syndrome

A

Schirmer’s test - measures conjunctival dryness

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50
Q

treatment for Sjorgen’s syndrome

A
  • Sicca: treat with artificial tears and artificial saliva
  • NSAIDs for arthralgia
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51
Q

What is crest syndrome and what are the clinical features

A
  • it is systemic sclerosis that is limited rather than diffuse
  • SKIN INVOLVEMENT IS LIMITED TO THE HANDS, FACE AND THE FEET
  • CREST
    • Calcinosis - calcium deposits in skin
    • Raynaud’s phenomenon
    • Eosphageal dysfunction - acid reflux or decrease in motility
    • Sclerodactyly - thickening and tightening of skin on hands
    • Telangiectasias - dilation of capillaries showing red marks on surface of skin
  • Also
    • beak like nose
    • microstomia
    • potentially fatal pulmonary hypertension
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52
Q

what is diffuse systemic sclerosis

A

it is where crest syndrome is diffuse

all organs have fibrosis

anti-topoisomerase and anti-ro antibodies

there is poor prognosis

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53
Q

treatment for crest syndrome and systemic sclerosis

A

there is no cure

treat the organs involved

for raynaud’s give CCBs e.g. nifedipine

for pulmonary HTN give prostaglandins e.g. iloprost

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54
Q

what is ankylosing spondylitis

A

it is a chronic inflammatory disease of the spine and sacro-iliac joints

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55
Q

what HLA haplotype is ankylosing spondylitis associated with?

A

HLA-B27

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56
Q

pathophysiology of ankylosing spondylitis

A

enthesitis

excessive and erosive repair phase follows

this leads to formation of syndesmophytes

these then fuse (ankylosis)

this prevents flexion and rotation

bamboo spine = end stage

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57
Q

ankylosing spondylitis associated features

A
  • SPINEACHE
    • Sausage digit
    • Psoriasis
    • Inflammatory back pain
    • NSAID good response
    • Enthesitis
    • Arthritis (asymmetrical, large joint oligoarthritis)
    • Crohns, UC and high CRP
    • HLA-B27
    • Eye: anterior uveitis
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58
Q

typical ankylosing spondylitis patient

A

man

16-30

gradual onset back/buttock pain

axial involvement

relieved by exercise

radiates to hip/buttocks

decreased chest expansion

kyphosis

hips and knees flexed

question mark posture

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59
Q

what is enthesitis

A

inflammation of the entheses, the sites where tendons or ligaments insert into the bone

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60
Q

what is kyphosis

A

Kyphosis (from Greek κυφός kyphos, a hump) is an abnormally excessive convex curvature of the spine as it occurs in the thoracic and sacral regions.

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61
Q

what is a differential for ankylosing spondylitis and how would you differentiate

A
  • mechanical back pain
  • can differentiate because in AS
    • onset of pain is gradual
    • wakes patients from sleep
    • pain is relieved by exercise
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62
Q

what is the major investigation for ankylosing spondylitis

A

sacroiliitis is the first visible sign on x ray/MRI

enthesitis also visible

if advanced: syndesmophytes and bamboo spine

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63
Q

diagnosis of ankylosing spondylitis

A

sacroiliitis on x ray/mri with at least one of the spineache features

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64
Q

why do you get anaemia in chronic disease

A
  • In chronic infection, chronic immune activation, and malignancy
  • These conditions all produce massive elevation of Interleukin-6,
  • This stimulates hepcidin production and release from the liver
  • This reduces the iron carrier protein ferroportin so that access of iron to the circulation is reduced
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65
Q

first, second and third line treatments for Ankylosing Spondylitis

A
  • 1st line: exercise and physio
  • 2nd line: NSAIDs
  • 3rd line: anti-TNF alpha e.g. etanercept
    • these stop syndesmophytes forming
    • once they’re formed, nothing will reverse/stop the progress

ANKYLOSING SPONDYLITIS DOES NOT RESPOND TO DMARDS

66
Q

How much of the population have psoriasis

A

2-3%

67
Q

how many of the patients with psoriasis have psoriatic arthritis

A

10-40%

68
Q

psoriatic arthritis is associated with which HLA type

A

HLA B27

69
Q

how does psoriatic arthritis present

A
  • arthritis in:
    • DIPJ
    • Spine - sacroilliac joint (asymetrically)
  • skin - psoriatic plaques
  • sausage digit (‘dactylitis’)
  • nail involvement in 80%
    • onycholysis
    • hyperkeratosis
    • pitting
70
Q

Ix for psoriatic arthritis

A
  • bloods:
    • anaemia
    • high ESR
    • Rh F -ve
  • X ray
    • erosive changes (pencil in cup deformity of fingers)
71
Q

management of psoriatic arthritis

A
  • NSAIDs
  • DMARDs
    • methotrexate
    • sulfasalazine
    • ciclosporin
  • exercise
72
Q

what is reactive arthritis

A
  • it is typically an oligoarthritis of lower limbs caused by sterile inflammation of synovial membranes that follows an infection that is typically GI or STI
    • shigella
    • chlamydia
    • gonorrhoea
    • salmonella
    • campylobacter
73
Q

which HLA type is reactive arthritis typically associated with

A

HLA B27

74
Q

what is the triad of symptoms associated with reactive artheritis and what is it called

A
  • Reiter’s triad
    • can’t see - conjunctivitis
    • can’t pee - urethritis
    • can’t climb a tree - arthritis
75
Q

Ix for reactive arthritis

A
  • bloods:
    • high ESR and CRP
  • stool culture if diarrhoea
  • STI screen
  • joint aspirate
    • if it’s not sterile it’s septic arthritis
  • X-ray
76
Q

what is vasculitis

A

it is an inflammatory disorder of the blood vessel walls which can affect any organ causing destruction or stenosis of a vessel

77
Q

management of reactive arthritis

A

treat cause of infection

rest and splint the joint

NSAIDs

consider the use of methotrexate and sulfasalazine as steroid sparing agents

78
Q

what are two types of ANCA +ve vasculitis

A

Wegener’s

Churg-Strauss syndrome

79
Q

what are two types of ANCA -ve vasculitis

A

Henoch Schonlein purpura

Goodpastures (anti-glomerular basement membrane antibodies)

80
Q

in whom is Giant Cell Arteritis more common in

A

women and those over 50

81
Q

presentation of Giant Cell Arteritis

A

headache

scalp tenderness (pain combing hair)

jaw claudication

acute visual changes (amaurosis fugax)

82
Q

diagnosis of giant cell arteritis

A
  • 3 of the following:
    • Age >50 y/o
    • New headache
    • Temporal artery tenderness
    • ESR >50
    • Abnormal artery biopsy
83
Q

Ix for giant cell arteritis

A

temporal artery biopsy

ESR

84
Q

Treatment of Giant cell arteritis

A

steroids: prednisolone

visual changes: urgent IV methyprednisolone and refer to opthalmologist

85
Q

what is polymyalgia rheumatica

A

autoinflammatory process that affects joints and muscles

often coexists with GCA

causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips.

86
Q

what is the presentation of polymyalgia rheumatica

A

symmetrical aching and tenderness

morning stiffness in shoulders and proximal limb muscles

87
Q

what is the Ix for polymyalgia rheumatica

A

high crp and esr

normal creatinine kinase

high alkaline phosphatase

88
Q

what is the treatment for polymyalgia rheumatica

A

steroids like prednisolone

89
Q

what is wegener’s vasculitis aka

A

granulomatosis with polyangiitis

90
Q

what is granulomatosis polyangiitis and what tissues does it normally affect

A
  • aka wegener’s vasculitis
  • normally affects the arterioles and capillaries
91
Q

what is the presentation of wegener’s vasculitis

A
  • upper resp tract
    • sinusitis
    • nasal crusting
  • lungs
    • pulmonary nodules
  • Kidney
    • glomerulonephritis, destruction of basement membrane
92
Q

Ix for wegener’s vasculitis

A

high ESR

CXR nodules

c-ANCA positive

93
Q

management of granulomatosis polyangiitis

A

high dose steroids

cyclophosphamide

94
Q

what does ANCA stand for

A

Antineutrophil cytoplasmic antibodies

95
Q

is gout more common in men or women and what is the typical age of presentation

A

men 40-60

96
Q

what are the crystals that cause gout

A

monosodium urate crystals

97
Q

what dietary factor causes gout, what metabolises this and what is it turned into and where is this excreted

A
  • purines from the diet
  • turned to uric acid
  • catalysed by xanthine oxidase
  • excreted by the kidneys
98
Q

what causes gout

A
  • high purine diet
    • alcohol
    • red meat
    • seafood
    • fructose
  • genetics
  • renal disease
  • diuretics
  • high insulin levels
99
Q

investigations for gout

A
  • polarised light microscopy
    • NEGATIVELY birefringent NEEDLE shaped monosodium urate crystals
  • high serum urate but it may be normal
  • JOINT ASPIRATE FOR ANY RED HOT JOINT
    • R/O septic arthritis
100
Q

acute treatment for gout

A
  • NSAIDs
  • Colchicine if NSAIDs contraindicated
101
Q

why might NSAIDs be contraindicated

A

peptic ulcer

diabetes

renal disease

102
Q

gout prevention: lifestyle

A
  • lifestyle
    • calorie restriction
    • modify diet
    • weight loss
    • reduce alcohol consumption
    • dairy is protective
103
Q

medical prevention of gout

A
  • allopurinol
    • it’s a xanthine oxidase inhibitor
  • YOU MUST NOT USE IN AN ACUTE ATTACK AS IT’S PARIDOXICALLY PROLONGS THE PAIN
104
Q

What is the crystal in pseudogout

A

calcium pyrophosphate crystals

105
Q

what are the risk factors for pseudogout

A

old age (70s) (older than for gout)

hyperparathyroidism

haemochromatosis

hyperphosphataemia

diabetes

106
Q

Investigations for pseudogout

A

aspirate joint to R/O septic arthritis

polarised light microscopy shows POSITIVELY birefringent RHOMBOID shaped crystals

X-Ray shows chondrocalcinosis

107
Q

what are the symptoms of pseudogout

A

acute pain in joint - sudden onset

typically larger joints e.g. knee

108
Q

treatment for acute attacks of gout

A

rest

ice packs

intra-articular steroids

NSAIDs ± Colchicine may prevent the acute attacks

109
Q

treatment for chronic pseudogout

A

methotrexate of sulfasalazine if inflammatory changes continue

110
Q

what is fibromyalgia

A

it is a non-specific muscular disorder with unknown cause

pain with no signs of inflammation

111
Q

rfs for fibromyalgia

A

female (10x more common)

middle age

low household income

divorced

112
Q

fibromyalgia is associated with

A

IBS

chronic headache

depression

chronic fatigue

113
Q

presentation of fibromyalgia

A
  • widespread symptoms that have lasted >3 months
    • pain worse with stress or cold weather
    • morning stiffness >1hr
    • non-restorative sleep
    • headache and diffuse abdo pain
    • neurocognitive features
      • mood disorder, poor sleep, poor concentration etc
114
Q

Ix and Dx of fibromyalgia

A

all Ix normally normal

diagnosis is based on pain in >11/18 palpitation sites

115
Q

management of fibromyalgia

A
  • reassure that there’s no serious pathology
  • non pharma: CBT, exercise and education
  • manage pain: with analgesia and acupuncture
  • improve sleep: amitriptyline
    • this is an antidepressant
116
Q

red flags for lower back pain

A
  • TUNAFISH
    • Trauma, TB
    • Unexplained loss of weight/night sweats
    • Neurological deficits (e.g. incontinence)
    • Age <20 or >55
    • Fever
    • IVDU
    • Steroid use or immunocompromised
    • History of cancer
117
Q

risk factors for lower back pain (lumbago)

A

manual labour work

low socioeconomic status

poor working conditions

older age

smoking

118
Q

when would you Ix lower back pain

A

only if it is chronic i.e. >12 weeks

119
Q

what are the Ix for lower back pain

A

if young then CRP and ESR to check for tumour, myeloma or infection

only X ray if there are red flags

120
Q

Tx for lower back pain and prognosis

A

90% will resolve within 6 weeks

continue normal activity - don’t rest

lifestyle

analgeisic ladder and diazepam if insufficient

physio

acupuncture

CBT

lifestyle advice –> better lifting, heat pads, slouching etc

121
Q

mechanical vs inflammatory back pain table

A
122
Q

major cause of inflammatory back pain?

A

ankylosing spondylitis

123
Q

5 causes of mechanical back pain

A

degenerative discs

osteoarthritis

muscular imbalance

disc herniation

vertibral fracture

124
Q

what is the most common causative organism in septic arthritis

A

staph aureus

125
Q

name 4 organisms that can cause septic arthritis and some examples of situations in which they are more common

A
  • staph aureus (most common)
  • N. gonorrhoea (if young and sexually active)
  • Staph epidermidis (joint replacement)
  • E.coli (if immunocompromised)
126
Q

presentation of septic arthritis

A
  • any red hot swollen joint is septic arthritis until proven otherwise
  • knee in 50% cases
  • 90% monoarthritis
  • fever
127
Q

risk factors for septic arthritis

A
  • any pre-existing joint disease
  • DM
  • recent joint surgery
  • immunosuppression
  • penetrating trauma
  • skin breaks or ulcers
  • elderly >80
128
Q

management of septic arthritis

A
  • urgent aspiration for M, C &S
    • they must have been off abx at this point
  • then empiricle Abx followed by abx for known organism
  • rest
  • analgesia
  • stop immunosuppressive drugs
129
Q

three causes of osteomyelitis

A

haematogenous origin (80%) e.g. from a boil

direct innoculation to bone (trauma/surgery)

contigous spread of infection to bone from adjacent tissues

130
Q

what is the major causative organism in osteomyelitis and what is another one in a specific situation

A

staph aureus in 90% cases

salmonella in sickle cell anaemia

131
Q

what are the risk factors for osteomyelitis

A
  • the same as for septic arthritis
    • pre-existing joint disease
    • DM
    • recent surgery
    • immunosuppression
    • penetrating trauma
    • skin breaks/ulcers
    • elderly >80yrs
132
Q

osteomyelitis presentation

A

fever and dull, localised bone pain

made worse on movement

overlying tenderness and erythema

commonly occurs in the metaphysis of long bones in children

133
Q

Ix for osteomyelitis

A
  • bloods: wcc, CRP, ESR
  • imaging: X-ray or MRI
  • Bone biopsy is diagnostic
134
Q

management of osteomyelitis

A

surgical drainage of abscess

debridement of dead bone

IV Abx

135
Q

what does osteomyelitis lead to if untreated

A

bone death

136
Q

name three types of primary bone tumour

A

osteosarcoma

ewings sarcoma

chondrosarcoma

137
Q

who is affected by osteosarcoma and where in the body mostly

A

kids, and adults <20yrs

in the knees and humerus

pagets is a RF

138
Q

who gets ewing’s sarcoma and where in the body is it

A

<25yrs old

mostly hips and long bones

139
Q

symptoms of primar bone malignancy

A

bone pain that is nocturnal

local red and swelling - maybe painful or painless

fatigue, weight loss and anaemia

unexplained bone fractures

140
Q

Ix for bone tumours

A

x ray

mri

biopsy

141
Q

treatment for bone tumours

A
  • chemo ± radiotherapy
    • useful in ewing’s but not chondrosarcoma
  • surgery
  • bisphosphonates
    • decrease pain and fracture rates
142
Q

pathology of myeloma

A
  • increased RANKL causes increased osteoclast activity
  • CRAB
    • high ca2+
    • renal failure
    • anaemia
    • bone lytic lesion (i.e. pepper pot skull)
  • bone marrow infiltration –> fatigue, infection and bruising/bleeding
143
Q

who should you screen for myeloma

A

all patients over 50 with new back pain

screen with serum electropheresis and ESR

144
Q

investigation of myeloma

A

serum electrophoresis - single Ig band

bence jones protein in urine

bone marrow aspirate

x ray - pepper pot skull

145
Q

management of myeloma

A

analgesia - avoid NSAIDs (renal failure)

bisphosphinates

EPO transfusions for anaemia

chemotherapy

they don’t tend to transplant for myeloma

146
Q

what is RF and where would you find it

A

rheumatoid factor seen in rheumatoid arthritis and other autoimmune conditions with low specificity

147
Q

what is anti-ccp and where would you find it

A

anti cyclic citrullinated peptide

it’s seenin RA with good specificity

148
Q

what are ANA antibodies, what is an example and when would you find it

A

anti nuclear antibodies

an example is anti-dsDNA antibody

found in SLE

149
Q

what are ANA antibodies, what is an example and when would you find it

A

anti nuclear antibodies

an example is anti-dsDNA antibody

found in SLE

150
Q

when is anti-ro found

A

sjorgen’s

151
Q

c-ANCA what is it and when would you find it

A

it is cytoplasmic anti neutrophil cytoplasmic antibodies

found in wegener’s

152
Q

what is p-ANCA and when is it found

A

perinuclear anti-neutrophil cytoplasmic antibodies,

found in churg-strauss

153
Q

when is anti-centromere/anti-topoisomerase antibody found?

A

in CREST or systemic sclerosis

154
Q

what is anti-GBM and when is it found?

A

it is anti glomerular basement membrane antibody and it is found in goodpasture’s

155
Q

what are the two antibodies associated with coeliac

A

anti-endomysial antibodies of the immunoglobulin A (Anti-EMA)

Anti-transglutaminase antibodies (Anti-tTG)

156
Q

what is bence jones protein

A

A Bence Jones protein is a monoclonal globulinprotein or immunoglobulin light chain found in the urine.

Detection of Bence Jones protein may be suggestive of multiple myeloma

157
Q

which hand joint is more affected in OA than in RA

A

DIP

158
Q
A
159
Q

in which condition would you see hebarden’s nodes and bouchard’s nodes and which one is which

A

osteoarthritis (RA much more rarely)

outer hebredes

160
Q

what are the antibodies present in diffuse systemic sclerosis

A

anti-topoisomerase and anti-ro antibodies

formative 3b (18 decks)

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