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phase 2a > MSK conditions > Flashcards

MSK conditions Flashcards

1
Q

what kind of condition is rheumatoid arthritis and what does it affect

A

autoimmune condition- affects the synovium (specialised connective tissue that lines inner surface of synovial joint capsules)

-chronic destruction of synovial lining of joints + tendon sheaths + bursa

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2
Q

is RA symmetrical and does it affect multiple or just one joint

A

symmetrical + affects multiple joints
- symmetrical polyarthritis

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3
Q

list 4 risk factors for rheumatoid arthritis

A

women (x3 mc. then M)
30-50 yrs
FHx
other autoimmune disorders

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4
Q

where does RA most commonly affect

A

wrist/hand, feet, knee, hip

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5
Q

symptoms of RA

A

joint pain- worse in morn, usually lasts more than 30 mins- gets better as day goes on + w movement
symmetrical distal polyarthropathy
fatigue
wt. loss
malaise
aches + cramps

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6
Q

signs of RA

A

swan neck thumb/fingers
Z shaped thumb
boutonniere deformity (button hole)
ulnar deviation
rhuematoid nodules

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7
Q

what are some extra-articular presentations of RA

A

Rheumatoid nodules (firm, painless lumps under the skin, typically on the elbows and fingers)
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis
Bronchiolitis obliterans (small airway destruction and airflow obstruction in the lungs)
Sjorgen’s
pulmonary fibrosis
anaemia of chronic disease

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8
Q

1st line investigations for RA

A

clinical exam
serology: anti CCP (positive) + Rheumatoid factor (positive- not diagnostic)

bloods: anaemia, CRP/ESR increased
x-ray= LESS
L- loss of joint space
E- erosions
S- soft tissue swelling
S- see through bones (osteopenia)

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9
Q

gold standard investigations for RA

A

clinical diagnosis + serology + inflammatory markers

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10
Q

management of RA (1st,2nd,3rd)

A
  1. Monotherapy with cDMARDS eg. methotrexate, leflunomide or sulfasalazine
  2. Combination treatment with multiple cDMARDs
  3. Biologic therapies (usually alongside methotrexate) eg infliximab, rituximab, etanercept

can use NSAIDS for pain

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11
Q

what kind of a disorder is osteoarthritis

A

degenerative joint disorder (it’s not inflammatory) @ synovial joints due to a combo of genetic factors + overuse & injury

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12
Q

what causes structural issues in the joint in osteoarthritis

A

an imbalance between cartilage breakdown vs chondrocytes repairing the joint leads to structural issues in joint

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13
Q

which joints are commonly affected in osteoarthritis

A

hips
knees
fingers
thumb
cervical spine

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14
Q

list 5 risk factors for osteoarthritis

A

high intensity labour
old age
female
obesity
genetic

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15
Q

presentation of osteoarthritis

A

painful joints- stiff for less than 30 mins in the morn, becomes worse throughout day + with activity
proximal Bouchard nodes (middle of joint)
distal heberden nodes (closet 2 fingernail)
squaring @ base of thumb (carpometacarpal saddle joint)
weak grip/reduced range of motion
popping/clicking on moving (crepitus)

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16
Q

investigations for osteoarthritis

A

x-ray= LOSS
L- loss of joint space
O- osteophytes (bony lumps)
S- subchondral sclerosis (increased density of bone along joint line
S- subchondral cysts (fluid filled holes in bone)

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17
Q

management of osteoarthritis

A

patient education + lifestyle changes- wt. loss, physio, orthotics

analgesia:
1. paracetamol, topical NSAIDS (diclofenac), topical capsaicin
2. oral NSAIDS + PPI to protect stomach
3. opiates eg codeine + morphine

-intra-articular injections
-joint replacement surgery

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18
Q

what are 2 types of crystal arthritis

A

gout & psuedogout

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19
Q

describe gout

A

chronically high uric acid levels= build up causes urate crystals to be precipitated out and deposited in joints- causing them to become hot + swollen + painful

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20
Q

what are gouty tophi

A

SC uric acid deposits typically affecting small joints + connective tissues of hands, elbows and ears

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21
Q

list 4 risk factors for gout

A

increase in purines in diet (meat + seafood)
increased cell turnover
CKD
diuretics

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22
Q

presentation of gout

A

monoarticular (often big toe/DIPs/wrist/thumb)
acute, swollen, hot painful joints
tophi- SC deposits of uric acid affecting small joints + tissues

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23
Q

investigations for gout

A

joint aspiration (increased uric acid) + polarised light microscopy- MONOSODIUM URATE CRYSTALS, NEEDLE-SHAPED AND NEGATIVELY BIREFRINGENT of polarised light

others= joint x-ray- maintained joint space, lytic lesions, punched out erosions w. sclerotic borders or overhanging edges

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24
Q

management of gout (lifestyle changes, acute flares, prevention)

A

lifestyle changes: decreased purines, more dairy

acute flare= 1st NSAIDS, 2nd colchicine, 3rd corticosteroids

prevention= allopurinol (xanthine oxidase inhibitor > reduces uric acid)

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25
Q

what is pseudogout

A

damage 2 joint caused by the formation of calcium pyrophosphate crystals- deposited in joints

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26
Q

list 6 risk factors for psuedogout

A

females 70+
hyper(para)thyroidism
excess Fe or Ca
diabetes
metabolic diseases

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27
Q

presentation of psuedogout

A

older adult w.
symptoms= hot, swollen, tender joint- usually knees
signs= recent injury to joint in Hx

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28
Q

investigations for psuedogout

A

joint aspiration + polarised light:
-RHOMBOID SHAPED CRYSTALS
-POSITIVE BIREFRINGENT OF POLARISED LIGHT
-Ca PHOSPHATE CRYSTALS

x-ray= chondrocalcinosis (thin white line in middle of joint space caused by Ca deposition)

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29
Q

management of psuedogout

A

symptoms usually resolve spontaneously over several weeks

if symptomatic:
-NSAIDS
-colchicine
-corticosteroids/intra-articular steroid injections

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30
Q

what is osteoporosis (and osteopenia)

A

osteoporosis= reduction in bone density

osteopenia= less severe reduction in bone density

-increases likelihood of fractures

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31
Q

risk factors for osteoporosis (SHATTERED)

A

Steroids
Hyper(para)thyroidism
Alcohol + tabacco use
Thin (BMI <18.5)
Testosterone
Early menopause- women after menopause (oestrogen= protective)
Renal/liver failure
Erosive/inflammatory bone disease eg myeloma
Dietary low Ca/malabsorption

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32
Q

which 2 investigations would you do for osteoporosis

A

DEXA bone scan- measures bone mineral density- measure @ hip
T score=
normal= T >-1
osteopenia= T= -1 to -2.5
osteoporosis= T<-2.5

FRAX score- 10yr probability of major osteoporotic fracture/hip fracture

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33
Q

management of osteoporosis

A

Lifestyle: excercise, wt. loss, decrease alcohol + smoking, avoid falls

1st= vit D + Ca supplementation
bisphosphonates (reduce osteoclast activity) eg dendronate, ritendronate, zolendronic acid

2nd= denosumab (monoclonal antibody that blocks activity of osteoclasts)

HRT- esp 4 early menopausal women

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34
Q

describe spondyloarthropathies

A

group of chronic inflammatory diseases- mc affect sacroiliac joint + axial skeleton
- all associated with HLA B27 gene

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35
Q

name 4 spondyloarthropathies

A

ankylosing spondylitis
psoriatic arhritis
reactive arthritis
enteric arhritis

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36
Q

list the common features of spondyloarthropathies (SPINE ACHE)

A

Sausage fingers (dactylitis)
Psoriasis
Inflammatory back pain
NSAIDs (have good response to them)
Enthesitis (heel)

Arthritis
Crohn’s/colitis/CRP (elevated but can be norm)
HLA B27
Eye (uvetitis)

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37
Q

describe ankylosing spondylitis

A

chronic inflammatory disorder- mainly affects sacroiliac joints + vertebral column + causes progressive stiffness & pain

inflammatory arthritis of spine + ribcage= formation on new bone + stiffness of joints

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38
Q

presentation of ankylosing spondylitis

A

progressively worse lower back pain + stiffness (worse w rest- improves w movement)
worse @ morning + night
sacroiliac pain (buttock region)
flares of worsening symptoms
decreased lumbar flexion due 2
fusion of spine + sacroiliac joints

anterior uvetitis
dactylitis
enthesitis (inflammation of where tendon/ligament meets bone)

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39
Q

1st line investigations for ankylosing spondylitis

A

CRP + ESR increased
HLA B27 genetic test
Schober’s test

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40
Q

gold standard investigation for ankylosing spondylitis

A

x-ray of spine + sacrum:
-bamboo spine
-sacroilitis
-squaring of vertebral bodies
-subchondral sclerosis and erosions

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41
Q

management of ankylosing spondylitis

A

NSAIDS (naproxen, indomethacin, ibuprofen)
steroids during flares
anti-TNF drugs eg etanercept ,infliximab

physio + lifestyle advice
surgery 4 deformities

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42
Q

describe psoriatic arthritis and what screening tool is used

A

inflammatory arthritis associated w psoriasis (1/5 w psoriasis have it- annual screening tool= PEST TOOL)

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43
Q

presentation of psoriatic arthritis

A

inflammatory joint pain
plaques of psoriasis- behind ear, nails, scalp
onycholysis (separation of nail from nail bed)
dactylics
enthesitis
nail pitting
anterior uvetitis
conjunctivitis
aortitis
amyloidosis

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44
Q

1st line investigations for psoriatic arthritis

A

CRP/ESR raised
rheumatoid factor=negative
anti-CCP= negative
joint aspiration= negative

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45
Q

gold standard investigation for psoriatic arthritis

A

joint x-ray:
-erosion in DIP joints
-osteolysis + dactylics
-pencil in cup deformity- central erosions of bone beside joint> 1 bone appears hollow + other bone = narrow + sits up in cup like a pencil

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46
Q

management of psoriatic arthritis

A

NSAIDs for pain (naproxen, ibuprofen, indomethacin)- intra-articular corticosteroid injection if severe

DMARDS (methotrexate, sulfasalazine)

TNF inhibitor (etanercept, adalimumab, infliximab)

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47
Q

complications of psoriatic arthritis

A

arthritis mutilans- most severe form of arthritis - osteolysis of bones around joints in digits> progressive shortening> skin folds as digit shortens > telescopic finger

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48
Q

describe reactive arthritis

A

immune-mediated response to certain GI or GU infections eg shigella, chlamidiya, campylobacter jejuni

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49
Q

presentation of reactive arthritis

A

symptoms begin 1-4 weeks after infection
asymmetrical oligoarthritis (joint swelling + stiffness in large joint eg knee)
painful, swollen, red + stiff joints
dactylitis
classic triad= conjunctivitis + urethritis + arthritis (can’t see, can’t pee, can’t climb a tree)
Reiter’s syndrome

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50
Q

investigations for reactive arthritis

A

ESR + CRP= raised
ANA= negative
rheumatoid factor= negative

x-ray= sarcolitis (pain in joints) or enthesopathy (inflamed entheses)

joint aspirate= negative (excludes septic arthritis + gout)

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51
Q

management of reactive arthritis

A

1st= Abxs, until septic arthritis excluded
NSAIDS= naproxen, ibuprofen, indomethacin
steroid injections into affected joints
DMARDS (sulfasalazine)
TNF inhibitors

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52
Q

what is enteric arthritis/ IBD associated arthritis

A

arthritis secondary to IBD
bacterial aetiology

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53
Q

which joints does enteric arthritis mainly affect

A

peripheral joints, esp lower limbs

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54
Q

presentations of enteric arthritis

A

asymmetric joint involvement
bone deformity
painful, red, hot, swollen joints
stiffness + reduced motion
SPINE ACHE

(IBD associated Sx)
abdo pain
blood in stool
diarrhoea
wt. loss

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55
Q

1st line investigations for enteric arthritis

A

joint aspiration
stool culture
colonoscopy + biopsy
increased faecal- calprotectin
FBC- anaemia- malabsorption, increased WCC, CRP/ESR increased
joint x-ray

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56
Q

gold standard investigations for enteric arthritis

A

clinical diagnosis + symptoms + medical history

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57
Q

management of enteric arthritis

A

DMARDs- methotrexate, leflunomide, sulfasalazine
NSAIDs= naproxen, ibuprofen, indomethacin
TNF inhibitors= etanercept, infliximub

treat UC/crohn’s

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58
Q

what are 2 types of infective arthritis

A

septic arthritis
osteomyelitis

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59
Q

what is septic arthritis

A

infection of 1 or more joints caused by pathogenic inoculation of microbes- via either direct inoculation or haematogenous spread
!emergency!

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60
Q

name 4 bacterias that can cause septic arthritis

A

staphylococci (mc)
streptococci
N. gonorrhoea
E. coli

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61
Q

list 7 risk factors for septic arthritis

A

joint replacement/joint prothesis
pre-existing joint disease
IVDU
immunosuppression
intra-articular corticosteroid injection
alcohol misuse
diabetes

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62
Q

presentations of septic arthritis

A

acutely hot, swollen. painful joint
onset <2 weeks
stiffness + decreased range of motion
mc in <4yrs/older adults
fever + lethargy
sepsis (tachycardia, HTN, cold, clammy, shaking)

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63
Q

investigations for septic arthritis

A

aspirate joint 4 microscopy + culture (polarised light microscopy 2 identify organism)
in synovial fluid- increased WCC
ESR/CRP= increased

64
Q

management of septic arthritis

A

aspirate joint (drainage)
pathogen directed Abxs:
-empirical antibiotic eg flucloxacillin (E.coli)
-vancomycin (MRSA, S.aureus)
- IM ceftriaxone, azithromycin (N. gonorrhoea)
analgesia (NSAIDS)

65
Q

what is osteomyelitis

A

inflammatory condition of bone + bone marrow
caused by infectious organism (mc S.aureus)

Haematogenous osteomyelitis= pathogen carried thru blood + seeded in bone

66
Q

list 7 risk factors for osteomyelitis

A

open fractures
orthopaedic ops (esp prosthetic joints)
diabetes
peripheral artery disease
IVDU
immunosuppression
children> upper resp tract or varicella infections

67
Q

acute presentations of osteomyelitis

A

limp or reluctance to weight bear (children)
hot, erythema + swollen joint
dull, non specific pain @ site of infection
bone oedema
low grade fever + fatigue

68
Q

chronic presentations of osteomyelitis

A

sequestra (deep ulcers- necrotic bone embedded in pus)

69
Q

1st line investigations for osteomyelitis

A

FBC= increased WCC + ESR/CRP, blood culture MC + Serology

x-ray= localised osteopenia + periosteal reaction (changes 2 bone surface)

MRI= bone marrow oedema

70
Q

gold standard investigation for osteomyelitis

A

bone marrow biopsy + culture 2 identify organism

71
Q

management of osteomyelitis

A

immobilise + abxs:
vancomycin (MRSA, S.aureus)
fusidic acid (S.aureus)
flucloxacillin (salmonella)

surgery= debridement of infected bone + tissue

72
Q

what is vasculitis and give the name of small, medium and large vasculitis

A

vasculitis= group of diseases causing inflammation of blood vessels

large- giant cell arteritis
medium-polyarteritis nodosa
small- granulomatosis with polyangiitis

73
Q

describe giant cell arteritis

A

affects aorta and/or its major branches (carotid + vertebral arteries)
temporal artery often involved- temporal arteritis

74
Q

list 4 risk factors for giant cell arteritis

A

50+ yrs
northern european
females
Hx of polymyalagia rheumatica

75
Q

presentations of giant cell arteritis (4)

A

headache- new onset, unilateral over temporal area
scalp tenderness
jaw claudication
visual disturbances= blurred vision, diplopia, amaurosis fugax (transient vision loss)
blindness

76
Q

1st line investigations for giant cell arteritis

A

increased ESR >50mm/hr and/or CRP
Halo sign on ultrasomography of temporal + axillary artery

77
Q

gold standard investigation for giant cell arteritis

A

temporal artery biopsy- giant cells + granulomatous inflammation

78
Q

management of giant cell arteritis

A

high does corticosteroid eg prednisolone 40-60mg

comps= blindness, irreversible neuropathy

79
Q

which blood vessels does polyarteritis nodosa affect and where

A

affects medium sized blood vessels @ skin, GIT, kidneys and heart

80
Q

what is polyarteritis nodosa associated with

A

hep B + developing countries

81
Q

list 6 presentations of polyarteritis nodosa

A

peripheral neuropathy
cutaneous/SC nodules
abdo pain
unilateral orchitis (characterisitc feature, inflammation of testis)
livedo reticular- mottled purple, lace like rash
HTN

82
Q

1st line investigations for polyarteritis nodosa

A

increased ESR and/or CRP
HBsAg (Hep B antigen)
CT angiogram (beaded appearance- aneurysms)

83
Q

gold standard investigation for polyarteritis nodosa

A

biopsy eg kidney shows transmural fibrinoid necrosis

84
Q

management of polyarteritis (hep B neg vs pos)

A

Hep B negative= corticosteroids + cyclophosphamide (DMARDS)

hep B positive= antiviral agent, plasma exchange & corticosteroids

85
Q

which blood vessels does Wagner’s granulomatis/granulomatosis with polangitis affect

A

small blood vessels @ ENT, lungs and kidneys
young adults

86
Q

list 6 presentations of Wagner’s granulomatis

A

saddle shaped nose- due 2 perforated septum
nose bleeds
crusty nasal/ear secretions
hear loss
sinusitis
cough, wheeze, haemoptysis, dyspnoea

87
Q

1st line investigations for Wagner’s granulomatis

A

FBC= raised eosinophils, raised ESR/CRP
histology= granulomas
CT chest= lung nodules

88
Q

gold standard investigation for Wagner’s granulomatis

A

positive c-ANCA test

89
Q

management of Wagner’s granulomatis

A

corticosteroids (prednisolone) + immunosuppression (rituximab, cyclophosphamide)

comps= glomerularnephritis

90
Q

what is systemic lupus erythematosus (SLE)

A

inflammatory autoimmune disorder affecting multiple organs

91
Q

describe the mechanism of antibodies in SLE

A

anti-nuclear antibodies (aNA) + anti double-stranded DNA (aDsDNA) antibodies attack proteins in the cell nucleus
>generates inflammatory response + damage

92
Q

list 3 risk factors for SLE

A

young/middle aged
female
black/asian

93
Q

presentations of SLE

A

photosensitive red butterfly rash across cheeks + nose
wt. loss
fever + fatigue
joint pain
mouth ulcers
hair loss
correctable ulnar deviation
Raynaud’s

94
Q

1st line investigations for SLE

A

FBC- anaemia, leukopenia, thrombocytopenia
norm CRP, raised ESR
raised U&Es

urine dipstick= haematuria, proteinuria

95
Q

gold standard investigation for SLE

A

ANA + aDsDNA antibodies present
other= renal USS (nephritis)

96
Q

management of SLE

A

give hydroxychloroquine
severe/resistant lupus= methotrexate
no-response= rituximab

97
Q

what is fibromyalgia

A

chronic pain syndrome characterised by widespread pain in the body for 3+ months + tenderness in 11/18 designated sites

98
Q

list 4 risk factors for fibromyalgia

A

women
low socioeconomic status
20-50
stressed + depressed

99
Q

presentation of fibromyalgia

A

widespread chronic pain + tenderness
fatigue + insomnia
morning stiffness
headaches
IBS
fibro-fog (problems w memory + concentration)

100
Q

investigations for fibromyalgia

A

11/18 tender points in 9 pairs of sites for at least 3+ months

101
Q

management of fibromyalgia

A

patient education
tricyclic antidepressants eg amitriptyline
exercise + relaxation + CBT
analgesia- paracetamol, tramadol, codeine

102
Q

what is sjogrens syndrome and what does it cause

A

autoimmune condition affecting mostly salivary and lacrimal glands causing dry mucous membranes

103
Q

how primary and secondary sjogrens occur

A

primary= occurs in isolation
secondary= comp of SLE/RA

104
Q

list 3 risk factors for sjogrens

A

FHx
female
40+ yrs

105
Q

presentations of sjogrens

A

dry mucous membranes
-dry mouth
-dry eyes
-dry vagina

106
Q

investigations for sjogrens

A

prescence of anti-Ro and anti-La antibodies
schirmer test- tears travel <10mm on filter paper

107
Q

management + comps of sjogrens

A

artificial tears, artificial saliva, vaginal lubricant
hydroxychloroquine 2 halt progression

comps=
eye infections- conjunctivitis, corneal ulcers
oral problems- dental cavities
vaginal problems- sexual dysfunction

108
Q

what is anti-phospholipid syndrome associated with and what does it cause

A

associated with anti-phospholipid antibodies
-cause blood to become prone 2 clotting= hyper coagulable state

109
Q

how primary and secondary anti-phospholipid syndrome occur

A

primary= idiopathic
secondary= autoimmune condition of SLE

110
Q

list 7 risk factors for anti-phospholipid syndrome

A

young females
diabetes
HTN
obesity
autoimmune conditions
smoking
oestrogen therapy

111
Q

presentations of anti-phospolipid syndrome

A

thrombosis= DVT, PE/stroke, MI
recurrent miscarriages
livedo reticularis- purple, lace-like rash
balance issues + headaches + double vision

112
Q

investigations for anti-phospholipid syndrome

when can a diagnosis be made

A

Hx of thrombosis/ pregnancy comps + serology
serology:
- anticardiolipin antibodies
- lupus anticoagulant
- anti-beta-2-glycoprotein 1 antibodies

$- diagnosis only made after x2 abnormal blood tests, 12 weeks apart

113
Q

management of anti-phospholipid syndrome (long term + pregnant)

A

long term:
- low dose aspirin (if norm antiplatelets eg clopidogrel)
- warfarin (HX of clots)

pregnant:
LMWH + aspirin

114
Q

define polymyositis

A

chronic inflammation of muscles

115
Q

define dermatomyositis

A

connective tissue disorder where there is chronic inflammation of skin + muscles

116
Q

presentations of polymyositis/dermatomyositis

A

symmetrical wasting of shoulder muscles + pelvic girdle

dermatomyositis:
gottron lesions (scaly erythematous patches on knuckles + elbows + knees)
purple rash on face + eyelids
photosensitive erythematous rash on back, shoulders and neck
preorbital oedema
subcutaneous calcinosis
musc pain + fatigue + weakness

117
Q

1st line investigations for dermatomyositis

A

clinical presentation:
-photosensitive erythematous rash on back
-purple rash on face + eyelids

increased:
Lactate dehydrogenase
AST + ALT
myoglobin
creatinine kinase

sereology=
anti-Jo1 antibodies
anti Mi2 antibodies (dermatomyositis)
ANA (dermatomyositis)
electromyograph

118
Q

gold standard investigation for dermatomyositis

A

muscle fibre biopsy- inflammation + necrosis

119
Q

management of dermatomyositis (1st, 2nd, 3rd)

A

1st- corticosteroid (prednisolone) + IV immunoglobulin
2nd- cDMARDs: methotrexate, azathioprine
3rd- rituximab or cyclophosphamide

120
Q

what is scleroderma and describe the 2 types

A

excess collagen production- leads to thickening + tightening of skin> causes vascular damage

2 types=
1. limited cutaneous systemic sclerosis (CREST syndrome
2. diffuse cutaneous systemic sclerosis

121
Q

list 4 risk factors for scleroderma

A

women
30-50 yrs
FHx
exposure 2 environmental substances and toxins (silicon dust, solvents)

122
Q

what are the presentations In CREST syndrome and what are the 1st signs that present

A

C- calcinosi (enalrged nodules under the skin)
R- raynauds
E- oesophageal dysmotility (strictures, food gets stuck on swallowing)
Sclerodactyly (tightening + thickening of skin over fingers distal to MCP joint)
T- telangiectasia (prominent dilated capillaries- particularly in cheeks)

1st Sxs= skin becoming tight, fingers becoming stiff + inflexible + Raynaud’s

123
Q

what investigations would you do for scleroderma

A

anti-nuclear antibodies may be present
present=
anti-centromere antibodies
anti-SCL70

other= norm FBC + U&E + CRP
pulmonary func. tests

124
Q

management of scleroderma

A

no treatment- immunosuppressants 2 slow progression eg cyclophosphamide

treat symptoms:
analgesia
CCB 4 Raynaud’s
PPI for oesophageal reflux
topical emolient
ACEi for kidneys

125
Q

name the 3 most common bone tumours

A

chondrosarcoma
osteosarcoma
Ewing sarcoma (bone marrow)

126
Q

list 4 risk factors for bone tumours

A

previous radiotherapy
previous cancer
paget’s disease
benign bone lesions

127
Q

which tumours most commonly metastasise to bone

A

BLT KP
Breast
Lungs
Thyroid
Kidney (renal cell)
Prostate

128
Q

presentations of bone cancers

A

mc in males + long bones
bone pain:
-worse at night, constant or intermittent
-resistant 2 analgesia
-may increase in intensity
atypical bony or soft tissue swellings/masses + easy bruising
inflammation + tenderness over bone
systemic symptoms
mobility issues

129
Q

1st + gold standard investigations for bone cancers

A

1st= x-ray
gold= bone biopsy

other= bloods + CT of chest/abdo/pelvis

130
Q

management of bone cancers

A

chemo
radio
surgey- limb sparing amputation

131
Q

describe osteomalacia

A

poor bone mineralisation- leads 2 soft bones due 2 lack of Ca2+ in adults

132
Q

describe rickets

A

inadequate mineralisation of the bone + epiphyseal cartilage in the growing skeleton of CHILDREN

133
Q

list 6 risk factors for osteomalacia

A

malabsorption disorders (eg IBD)
CKD- causes vit D deficiency
darker skin
decreased exposure to sunlight
hyperparathyroidism- increased calcium release from bone
anticonvulsant drugs

134
Q

give 4 presentations of osteomalacia + 2 presentations of rickets

A

osteomalacia:
bone pain + tenderness
dull ache that is worse w. weight bearing exercises
fractures (esp neck of femur)
must weakness- waddling gait + difficulty w. stairs

rickets:
growth retardation
hypotonia, knock-kneed, bow-legged

135
Q

investigations for osetomalacia

A

x-ray- loss of cortical bone- defective mineralisation
DEXA: shows low bone density
Bloods= low Ca phosphate
low serum 25-hydroxyvitamin D

136
Q

management of osteomalacia

A

vit D supplements

137
Q

describe Paget’s disease

A

disorder of bone tumour
areas of patchy bone due 2 excessive osteoclast + osteoblast activity
-leads to areas of sclerosis (high density) and lysis (low density)

138
Q

presentations of Paget’s disease

A

bone pain
bone deformity
fractures
hearing loss (if bones of ear are affected)

139
Q

investigations for paget’s disease

A

Bloods:
-raised ALP, other LFTs= normal
-normal Ca + phosphate

X-ray:
bone enlargement deformity
osteoporosis circumscripta ( well defined osteolytic lesions)
cotton wool appearance of skull (poorly defined areas of sclerosis + lysis)
v-shapd defects in bones

140
Q

management of paget’s disease

A

bisphosphonates
NSAIDs 4 bone pain
Ca + vit D supplements
surgery 2 correct bone deformity

141
Q

describe polymyalgia rheumatica and which condition is it strongly associated with

A

inflammatory condition causing pain + stiffness in shoulders + pelvic girdle + neck

strong association w. giant cell arteritis
-both conditions respond well to treatment w steroids

142
Q

list 5 presentations of polmyalgia rheumatica

A

bilateral shoulder pain radiating to elbow
bilateral pelvic girdle pain
worse w. movement
insomnia
rapid response to steroids
-symptoms must have been present for 2+ weeks

143
Q

investigations for polmyalgia rheumatica

A

clinical presentation
increased inflammatory markers (ESR + CRP)
response 2 steroids

144
Q

management of polymyalgia rheumatica

A

1st- 15mg oral prednisone daily- should see rapid improvement
-assess 1 week after starting steroids- if poor response, probs not PMR
-assess @ 3-4 weeks- should see 70% improvement in symptoms + inflammatory markers have returned to normal

145
Q

describe Marfan’s (inheritance what Is affected)

A

autosomal dominant condition
-affects gene responsible for fibrillin production (important part of connective tissue)

146
Q

presentation of Marfan’s

A

tall stature
long limbs/neck
long fingers
hypermobility
pectus carinatum (breast bone juts out)/pectus excavaton (breast bone sunken into chest)
high arch palate
heart murmur/aortic comps
poor eyesight

147
Q

1st line investigations for Marfan’s (including Ghent criteria)

A

physical exam
echocardiogram
MRI
eye exam

Ghent criteria:
MAJOR- enlarged aorta, lens dislocation, FHx, at least 4 skeletal problems
MINOR- myopia, loose joints, high arched palate

148
Q

gold standard investigation for Marfan’s

A

genetic testing

149
Q

management of Marfan’s

A

Lifestyle- avoid intense + caffeine
Meds- BBs/ARBs
physio- strengthen joints
surgery- aortic dissection, lens correcta, bone problems

yearly echocardiogram, opthalmologist

150
Q

list 7 comps of Marfan’s

A

mitral/aortic valve prolapse
aortic aneurysms
aortic dissection
lens dislocation
GORD
pneumothorax
scoliosis

151
Q

what is Ehlers-Danlos syndrome (type of mutation)

A

umbrella term for a group of inherited connective tissue disorders causing defects in collagen- results in hyper mobility of joints + abnormalities in connective tissue

autosomal dominant mutation
x13 subtypes, mc= hypermobile EDS

152
Q

presentations of Ehlers-Danlos

A

varies btwn types by generally:
joint hypermobility
easily stretched skin
easy bruising
chronic joint pain
re-occurring dislocations
cardiovascular comps

153
Q

investigations for Ehlers-Danlos

A

GS= physical exam
Beighton score to assess hyper mobility
collagen mutations
exclude marfan’s

154
Q

management of Ehlers-Danlos

A

no cure
focus on maintaining healthy joints + strength training
via physiotherapy + occupational therapy + psychological support

155
Q

what are the red flags of back pain (TUNA FISH)

A

Trauma- osteoporosis
Unexplained wt. loss- cancer
Neurological symptoms- cauda equina syndrome
Age >50 or <20- 2ndary bone cancer, ankylosing spondylitis, herniated disc

Fever- infection
IVDU- infection
Steroid use- infection
History of cancer- cancer metastasised to spine

phase 2a (12 decks)

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