MSK conditions Flashcards
(155 cards)
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
2
Q
is RA symmetrical and does it affect multiple or just one joint
A
symmetrical + affects multiple joints
- symmetrical polyarthritis
3
Q
list 4 risk factors for rheumatoid arthritis
A
women (x3 mc. then M)
30-50 yrs
FHx
other autoimmune disorders
4
Q
where does RA most commonly affect
A
wrist/hand, feet, knee, hip
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
6
Q
signs of RA
A
swan neck thumb/fingers
Z shaped thumb
boutonniere deformity (button hole)
ulnar deviation
rhuematoid nodules
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
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)
9
Q
gold standard investigations for RA
A
clinical diagnosis + serology + inflammatory markers
10
Q
management of RA (1st,2nd,3rd)
A
- Monotherapy with cDMARDS eg. methotrexate, leflunomide or sulfasalazine
- Combination treatment with multiple cDMARDs
- Biologic therapies (usually alongside methotrexate) eg infliximab, rituximab, etanercept
can use NSAIDS for pain
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
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
13
Q
which joints are commonly affected in osteoarthritis
A
hips
knees
fingers
thumb
cervical spine
14
Q
list 5 risk factors for osteoarthritis
A
high intensity labour
old age
female
obesity
genetic
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)
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)
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
18
Q
what are 2 types of crystal arthritis
A
gout & psuedogout
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
20
Q
what are gouty tophi
A
SC uric acid deposits typically affecting small joints + connective tissues of hands, elbows and ears
21
Q
list 4 risk factors for gout
A
increase in purines in diet (meat + seafood)
increased cell turnover
CKD
diuretics
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
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
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)
25
what is pseudogout
damage 2 joint caused by the formation of calcium pyrophosphate crystals- deposited in joints
26
list 6 risk factors for psuedogout
females 70+
hyper(para)thyroidism
excess Fe or Ca
diabetes
metabolic diseases
27
presentation of psuedogout
older adult w.
symptoms= hot, swollen, tender joint- usually knees
signs= recent injury to joint in Hx
28
investigations for psuedogout
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)
29
management of psuedogout
symptoms usually resolve spontaneously over several weeks
if symptomatic:
-NSAIDS
-colchicine
-corticosteroids/intra-articular steroid injections
30
what is osteoporosis (and osteopenia)
osteoporosis= reduction in bone density
osteopenia= less severe reduction in bone density
-increases likelihood of fractures
31
risk factors for osteoporosis (SHATTERED)
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
32
which 2 investigations would you do for osteoporosis
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
33
management of osteoporosis
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
34
describe spondyloarthropathies
group of chronic inflammatory diseases- mc affect sacroiliac joint + axial skeleton
- all associated with HLA B27 gene
35
name 4 spondyloarthropathies
ankylosing spondylitis
psoriatic arhritis
reactive arthritis
enteric arhritis
36
list the common features of spondyloarthropathies (SPINE ACHE)
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)
37
describe ankylosing spondylitis
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
38
presentation of ankylosing spondylitis
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)
39
1st line investigations for ankylosing spondylitis
CRP + ESR increased
HLA B27 genetic test
Schober's test
40
gold standard investigation for ankylosing spondylitis
x-ray of spine + sacrum:
-bamboo spine
-sacroilitis
-squaring of vertebral bodies
-subchondral sclerosis and erosions
41
management of ankylosing spondylitis
NSAIDS (naproxen, indomethacin, ibuprofen)
steroids during flares
anti-TNF drugs eg etanercept ,infliximab
physio + lifestyle advice
surgery 4 deformities
42
describe psoriatic arthritis and what screening tool is used
inflammatory arthritis associated w psoriasis (1/5 w psoriasis have it- annual screening tool= PEST TOOL)
43
presentation of psoriatic arthritis
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
44
1st line investigations for psoriatic arthritis
CRP/ESR raised
rheumatoid factor=negative
anti-CCP= negative
joint aspiration= negative
45
gold standard investigation for psoriatic arthritis
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
46
management of psoriatic arthritis
NSAIDs for pain (naproxen, ibuprofen, indomethacin)- intra-articular corticosteroid injection if severe
DMARDS (methotrexate, sulfasalazine)
TNF inhibitor (etanercept, adalimumab, infliximab)
47
complications of psoriatic arthritis
arthritis mutilans- most severe form of arthritis - osteolysis of bones around joints in digits> progressive shortening> skin folds as digit shortens > telescopic finger
48
describe reactive arthritis
immune-mediated response to certain GI or GU infections eg shigella, chlamidiya, campylobacter jejuni
49
presentation of reactive arthritis
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
50
investigations for reactive arthritis
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)
51
management of reactive arthritis
1st= Abxs, until septic arthritis excluded
NSAIDS= naproxen, ibuprofen, indomethacin
steroid injections into affected joints
DMARDS (sulfasalazine)
TNF inhibitors
52
what is enteric arthritis/ IBD associated arthritis
arthritis secondary to IBD
bacterial aetiology
53
which joints does enteric arthritis mainly affect
peripheral joints, esp lower limbs
54
presentations of enteric arthritis
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
55
1st line investigations for enteric arthritis
joint aspiration
stool culture
colonoscopy + biopsy
increased faecal- calprotectin
FBC- anaemia- malabsorption, increased WCC, CRP/ESR increased
joint x-ray
56
gold standard investigations for enteric arthritis
clinical diagnosis + symptoms + medical history
57
management of enteric arthritis
DMARDs- methotrexate, leflunomide, sulfasalazine
NSAIDs= naproxen, ibuprofen, indomethacin
TNF inhibitors= etanercept, infliximub
treat UC/crohn's
58
what are 2 types of infective arthritis
septic arthritis
osteomyelitis
59
what is septic arthritis
infection of 1 or more joints caused by pathogenic inoculation of microbes- via either direct inoculation or haematogenous spread
!emergency!
60
name 4 bacterias that can cause septic arthritis
staphylococci (mc)
streptococci
N. gonorrhoea
E. coli
61
list 7 risk factors for septic arthritis
joint replacement/joint prothesis
pre-existing joint disease
IVDU
immunosuppression
intra-articular corticosteroid injection
alcohol misuse
diabetes
62
presentations of septic arthritis
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)
63
investigations for septic arthritis
aspirate joint 4 microscopy + culture (polarised light microscopy 2 identify organism)
in synovial fluid- increased WCC
ESR/CRP= increased
64
management of septic arthritis
aspirate joint (drainage)
pathogen directed Abxs:
-empirical antibiotic eg flucloxacillin (E.coli)
-vancomycin (MRSA, S.aureus)
- IM ceftriaxone, azithromycin (N. gonorrhoea)
analgesia (NSAIDS)
65
what is osteomyelitis
inflammatory condition of bone + bone marrow
caused by infectious organism (mc S.aureus)
Haematogenous osteomyelitis= pathogen carried thru blood + seeded in bone
66
list 7 risk factors for osteomyelitis
open fractures
orthopaedic ops (esp prosthetic joints)
diabetes
peripheral artery disease
IVDU
immunosuppression
children> upper resp tract or varicella infections
67
acute presentations of osteomyelitis
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
chronic presentations of osteomyelitis
sequestra (deep ulcers- necrotic bone embedded in pus)
69
1st line investigations for osteomyelitis
FBC= increased WCC + ESR/CRP, blood culture MC + Serology
x-ray= localised osteopenia + periosteal reaction (changes 2 bone surface)
MRI= bone marrow oedema
70
gold standard investigation for osteomyelitis
bone marrow biopsy + culture 2 identify organism
71
management of osteomyelitis
immobilise + abxs:
vancomycin (MRSA, S.aureus)
fusidic acid (S.aureus)
flucloxacillin (salmonella)
surgery= debridement of infected bone + tissue
72
what is vasculitis and give the name of small, medium and large vasculitis
vasculitis= group of diseases causing inflammation of blood vessels
large- giant cell arteritis
medium-polyarteritis nodosa
small- granulomatosis with polyangiitis
73
describe giant cell arteritis
affects aorta and/or its major branches (carotid + vertebral arteries)
temporal artery often involved- temporal arteritis
74
list 4 risk factors for giant cell arteritis
50+ yrs
northern european
females
Hx of polymyalagia rheumatica
75
presentations of giant cell arteritis (4)
headache- new onset, unilateral over temporal area
scalp tenderness
jaw claudication
visual disturbances= blurred vision, diplopia, amaurosis fugax (transient vision loss)
blindness
76
1st line investigations for giant cell arteritis
increased ESR >50mm/hr and/or CRP
Halo sign on ultrasomography of temporal + axillary artery
77
gold standard investigation for giant cell arteritis
temporal artery biopsy- giant cells + granulomatous inflammation
78
management of giant cell arteritis
high does corticosteroid eg prednisolone 40-60mg
comps= blindness, irreversible neuropathy
79
which blood vessels does polyarteritis nodosa affect and where
affects medium sized blood vessels @ skin, GIT, kidneys and heart
80
what is polyarteritis nodosa associated with
hep B + developing countries
81
list 6 presentations of polyarteritis nodosa
peripheral neuropathy
cutaneous/SC nodules
abdo pain
unilateral orchitis (characterisitc feature, inflammation of testis)
livedo reticular- mottled purple, lace like rash
HTN
82
1st line investigations for polyarteritis nodosa
increased ESR and/or CRP
HBsAg (Hep B antigen)
CT angiogram (beaded appearance- aneurysms)
83
gold standard investigation for polyarteritis nodosa
biopsy eg kidney shows transmural fibrinoid necrosis
84
management of polyarteritis (hep B neg vs pos)
Hep B negative= corticosteroids + cyclophosphamide (DMARDS)
hep B positive= antiviral agent, plasma exchange & corticosteroids
85
which blood vessels does Wagner's granulomatis/granulomatosis with polangitis affect
small blood vessels @ ENT, lungs and kidneys
young adults
86
list 6 presentations of Wagner's granulomatis
saddle shaped nose- due 2 perforated septum
nose bleeds
crusty nasal/ear secretions
hear loss
sinusitis
cough, wheeze, haemoptysis, dyspnoea
87
1st line investigations for Wagner's granulomatis
FBC= raised eosinophils, raised ESR/CRP
histology= granulomas
CT chest= lung nodules
88
gold standard investigation for Wagner's granulomatis
positive c-ANCA test
89
management of Wagner's granulomatis
corticosteroids (prednisolone) + immunosuppression (rituximab, cyclophosphamide)
comps= glomerularnephritis
90
what is systemic lupus erythematosus (SLE)
inflammatory autoimmune disorder affecting multiple organs
91
describe the mechanism of antibodies in SLE
anti-nuclear antibodies (aNA) + anti double-stranded DNA (aDsDNA) antibodies attack proteins in the cell nucleus
>generates inflammatory response + damage
92
list 3 risk factors for SLE
young/middle aged
female
black/asian
93
presentations of SLE
photosensitive red butterfly rash across cheeks + nose
wt. loss
fever + fatigue
joint pain
mouth ulcers
hair loss
correctable ulnar deviation
Raynaud's
94
1st line investigations for SLE
FBC- anaemia, leukopenia, thrombocytopenia
norm CRP, raised ESR
raised U&Es
urine dipstick= haematuria, proteinuria
95
gold standard investigation for SLE
ANA + aDsDNA antibodies present
other= renal USS (nephritis)
96
management of SLE
give hydroxychloroquine
severe/resistant lupus= methotrexate
no-response= rituximab
97
what is fibromyalgia
chronic pain syndrome characterised by widespread pain in the body for 3+ months + tenderness in 11/18 designated sites
98
list 4 risk factors for fibromyalgia
women
low socioeconomic status
20-50
stressed + depressed
99
presentation of fibromyalgia
widespread chronic pain + tenderness
fatigue + insomnia
morning stiffness
headaches
IBS
fibro-fog (problems w memory + concentration)
100
investigations for fibromyalgia
11/18 tender points in 9 pairs of sites for at least 3+ months
101
management of fibromyalgia
patient education
tricyclic antidepressants eg amitriptyline
exercise + relaxation + CBT
analgesia- paracetamol, tramadol, codeine
102
what is sjogrens syndrome and what does it cause
autoimmune condition affecting mostly salivary and lacrimal glands causing dry mucous membranes
103
how primary and secondary sjogrens occur
primary= occurs in isolation
secondary= comp of SLE/RA
104
list 3 risk factors for sjogrens
FHx
female
40+ yrs
105
presentations of sjogrens
dry mucous membranes
-dry mouth
-dry eyes
-dry vagina
106
investigations for sjogrens
prescence of anti-Ro and anti-La antibodies
schirmer test- tears travel <10mm on filter paper
107
management + comps of sjogrens
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
what is anti-phospholipid syndrome associated with and what does it cause
associated with anti-phospholipid antibodies
-cause blood to become prone 2 clotting= hyper coagulable state
109
how primary and secondary anti-phospholipid syndrome occur
primary= idiopathic
secondary= autoimmune condition of SLE
110
list 7 risk factors for anti-phospholipid syndrome
young females
diabetes
HTN
obesity
autoimmune conditions
smoking
oestrogen therapy
111
presentations of anti-phospolipid syndrome
thrombosis= DVT, PE/stroke, MI
recurrent miscarriages
livedo reticularis- purple, lace-like rash
balance issues + headaches + double vision
112
investigations for anti-phospholipid syndrome
| when can a diagnosis be made
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
management of anti-phospholipid syndrome (long term + pregnant)
long term:
- low dose aspirin (if norm antiplatelets eg clopidogrel)
- warfarin (HX of clots)
pregnant:
LMWH + aspirin
114
define polymyositis
chronic inflammation of muscles
115
define dermatomyositis
connective tissue disorder where there is chronic inflammation of skin + muscles
116
presentations of polymyositis/dermatomyositis
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
1st line investigations for dermatomyositis
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
gold standard investigation for dermatomyositis
muscle fibre biopsy- inflammation + necrosis
119
management of dermatomyositis (1st, 2nd, 3rd)
1st- corticosteroid (prednisolone) + IV immunoglobulin
2nd- cDMARDs: methotrexate, azathioprine
3rd- rituximab or cyclophosphamide
120
what is scleroderma and describe the 2 types
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
list 4 risk factors for scleroderma
women
30-50 yrs
FHx
exposure 2 environmental substances and toxins (silicon dust, solvents)
122
what are the presentations In CREST syndrome and what are the 1st signs that present
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
what investigations would you do for scleroderma
anti-nuclear antibodies may be present
present=
anti-centromere antibodies
anti-SCL70
other= norm FBC + U&E + CRP
pulmonary func. tests
124
management of scleroderma
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
name the 3 most common bone tumours
chondrosarcoma
osteosarcoma
Ewing sarcoma (bone marrow)
126
list 4 risk factors for bone tumours
previous radiotherapy
previous cancer
paget's disease
benign bone lesions
127
which tumours most commonly metastasise to bone
BLT KP
Breast
Lungs
Thyroid
Kidney (renal cell)
Prostate
128
presentations of bone cancers
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
1st + gold standard investigations for bone cancers
1st= x-ray
gold= bone biopsy
other= bloods + CT of chest/abdo/pelvis
130
management of bone cancers
chemo
radio
surgey- limb sparing amputation
131
describe osteomalacia
poor bone mineralisation- leads 2 soft bones due 2 lack of Ca2+ in adults
132
describe rickets
inadequate mineralisation of the bone + epiphyseal cartilage in the growing skeleton of CHILDREN
133
list 6 risk factors for osteomalacia
malabsorption disorders (eg IBD)
CKD- causes vit D deficiency
darker skin
decreased exposure to sunlight
hyperparathyroidism- increased calcium release from bone
anticonvulsant drugs
134
give 4 presentations of osteomalacia + 2 presentations of rickets
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
investigations for osetomalacia
x-ray- loss of cortical bone- defective mineralisation
DEXA: shows low bone density
Bloods= low Ca phosphate
low serum 25-hydroxyvitamin D
136
management of osteomalacia
vit D supplements
137
describe Paget's disease
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
presentations of Paget's disease
bone pain
bone deformity
fractures
hearing loss (if bones of ear are affected)
139
investigations for paget's disease
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
management of paget's disease
bisphosphonates
NSAIDs 4 bone pain
Ca + vit D supplements
surgery 2 correct bone deformity
141
describe polymyalgia rheumatica and which condition is it strongly associated with
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
list 5 presentations of polmyalgia rheumatica
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
investigations for polmyalgia rheumatica
clinical presentation
increased inflammatory markers (ESR + CRP)
response 2 steroids
144
management of polymyalgia rheumatica
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
describe Marfan's (inheritance what Is affected)
autosomal dominant condition
-affects gene responsible for fibrillin production (important part of connective tissue)
146
presentation of Marfan's
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
1st line investigations for Marfan's (including Ghent criteria)
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
gold standard investigation for Marfan's
genetic testing
149
management of Marfan's
Lifestyle- avoid intense + caffeine
Meds- BBs/ARBs
physio- strengthen joints
surgery- aortic dissection, lens correcta, bone problems
yearly echocardiogram, opthalmologist
150
list 7 comps of Marfan's
mitral/aortic valve prolapse
aortic aneurysms
aortic dissection
lens dislocation
GORD
pneumothorax
scoliosis
151
what is Ehlers-Danlos syndrome (type of mutation)
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
presentations of Ehlers-Danlos
varies btwn types by generally:
joint hypermobility
easily stretched skin
easy bruising
chronic joint pain
re-occurring dislocations
cardiovascular comps
153
investigations for Ehlers-Danlos
GS= physical exam
Beighton score to assess hyper mobility
collagen mutations
exclude marfan's
154
management of Ehlers-Danlos
no cure
focus on maintaining healthy joints + strength training
via physiotherapy + occupational therapy + psychological support
155
what are the red flags of back pain (TUNA FISH)
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
