MSK Flashcards
(368 cards)
1
Q
2 major divisions of arthritis
A
OA (degenerative)
inflammation
2
Q
3 main causes of joint inflammation
A
- infection
- crystal arthritis
- immune mediated (autoimmune)
3
Q
which one is primary joint inflammation
A
autoimmune
4
Q
which one is secondary joint inflammation
A
infection and crystal arthritis
5
Q
examples of infection in joint inflammation (2)
A
septic arthritis
TB
6
Q
examples of crystals arthritis in joint inflammation (2)
A
gout
pseudogout
7
Q
which are sterile joint inflammation
A
crystal arthritis
autommune
8
Q
which are non sterile joint inflammation
A
septic arthritis
TB
9
Q
speed of onset of OA
A
slow
10
Q
speed of onset of immune mediated arthritis
A
subacute
11
Q
speed of onset of crystal arthritis and septic arthritis
A
rapid
12
Q
which arthritis has both CRP & WCC elevated
A
septic arthritis
13
Q
what is the key investigation of septic arthritis
A
joint aspiration and send fluid for gram stain and culture
14
Q
management of septic arthritis
A
lavage (joint washout) and IV antibiotics
15
Q
what are the 3 kinds of autoimmune arthritis
A
- lupus
- seronegative arthritis
- rheumatoid arthritis
16
Q
where is the primary site of pathology of RA
A
synovium
17
Q
where can synovium be found
A
synovial joints
tenosynovium surrounding tendons
bursa
18
Q
sex bias of RA
A
F:M = 2:1
19
Q
features of RA (4)
A
polyarthritis
chronic
pain, swelling, morning stiffness
joint erosions
20
Q
what are detected in blood in RA
A
autoantibodies
21
Q
what is the strongest genetic risk factor in RA
A
HLA-DR
22
Q
what are in HLA class 1
A
HLA class A, B , C
23
Q
what are in HLA class 2
A
HLA class D
24
Q
where are HLA class 1 expressed on
A
all cells
25
what are associated with HLA class 1
CD8 killer cells
26
where are HLA class 2 expressed on
only on APCs eg dendritic cells, macrophages, B cells
27
what are associated with HLA class 2
CD4 helper cells with B cells
28
HLA class 1 associate with which disease in RA
ankylosing spondylitis
29
which HLA associate with ankylosing spondylitis
HLA-B27
30
why autoantibodies in RA but no ankylosing spondylitis
HLA class 2 implicates CD4 T cells and B cells
31
RA pattern of joint involvement (symmetry or not, how many joints, large or small joint)
symmetrical
polyarthritis
always small joints invovled
32
where do RA most commonly affect
hand and feet
33
common affected joints by RA
MCPJ
PIPJ
wrists
knees
ankles
MTPJ
34
which arthritis associate with morning stiffness
RA
35
which arthritis associate with worse with activities
OA
36
which joints are affected by OA
DIPJ
PIPJ
thumb CMCJ
MCPJ
37
what are some systemic symptoms of RA
fatigue
fever
weight loss
38
what are some organ-specific extra-articular features of RA
subcutaneous nodules
lung diseases (ILD, fibrosis, pleuritis)
vasculitis
neuropathies
amyloidosis
ocular inflammation (eye episcleritis)
felty's syndrome
39
where are subcutaneous nodules found in RA
central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissues
40
what can be found in RA in blood
rheumatoid factors (Ab that bind to IgG)
anti CCP antibodies
41
what is pannus in RA
synovium becomes proliferated mass of tissue due to neovascularisation, lymphangiogenesis, inflammatory cells
42
what cells does healthy synovial membrane has
macrophage like (type A synoviocyte)
fibroblast like (type B synoviocyte)
type 1 collagen
43
what are different types of RA pathogenesis (cellular and molecular pathways)
autoreactive B cells
autoreactive T cells
cytokines (TNF alpha, IL-6, IL-1)
44
treatment for autoreactive B cells RA
rituximab
45
treatment for autoreactive T cells RA
abatacept
46
treatment for cytokine related RA
anti-TNF alpha, anti IL-6 receptor
47
which cytokine is dominant pro-inflammatory cytokine in rheumatoid synovium
TNF-alpha
48
pathogenesis of TNF-alpha RA
inflammtory cell recruitment, angiogenesis, lymphangiogenesis, --> pannus formation
matrix matalloproteases --> cartilage loss
osteoclast activation --> bone loss (osteopenia, erosions)
49
blood test findings in RA
increase ESR, CRP
autoantibodies
50
what does ACPA do in RA
causes chronic joint destruction and systemic inflammation
51
Xray features in RA (3)
soft tissue swelling
peri-articular oeteopenia
bony erosions
52
which is better scan for RA
USS
53
USS features of RA
synovial thickening (synovial hypertrophy)
increased blood flow (doppler signal)
can detect erosion not found on RA
54
why not MRI for RA
expensive
time consuming
55
why need aggressive pharmacological treatment for RA
suppress inflammation
56
pharmacological treatment for RA
glococorticoid (steroids)
DMARDs(disease modifying anti-rheumatic drug)
57
first line pharmacological treatment for RA
combine DMARD therapy (methotrexate+hydroxychloroquine +/or sulfasalazine) and IM or oral steroid short course
58
second line pharmacological treatment for RA
biological therapies eg anti-TNF alpha blockade
59
methods to administer steroid in RA (4)
oral prednisolone
IM methyl prednisolone
IV
Intra - articular (IA)
60
steroid side effects
cushing's syndrome
61
what is the scoring system for RA
DAS28 score
62
components of DAS28 scoring in RA
number of tender joints
number of swollen joints
patient visual analogue score (VAS)
ESR/ CRP
63
what are some biological therapies targeting cytokines in RA
inhibit TNF-alpha and IL-6
64
antibiotics to inhibit TNF-alpha
infliximab
adalimumab
golimumab
cetrolizumab
65
antibodies to inhibit IL-6 receptor
tocilizumab
sarilumab
66
biological therapies targeting lymphocytes
B cell depletion
block T cell co-stimulating
67
example of biological therapies to target B cell depletion
Rituximab (IV infusion)
68
example of biological therapies to target blocking T cell co-stimulation
adatacept
69
what is seronegative inflammatory arthritis
RF CCP antibodies not present in blood
but are immune mediated
70
examples of seronegative inflammatory arthritis (3)
psoriatic arthritis
reactive arthritis
ankylosing spondylitis
71
what is psoriatic arthritis
immune mediated disease affecting skin
72
where does psoriatic arthritis mainly affect
skin
extensor surfaces (elbow, knees)
some also has joint inflammation
73
dominant pathogenic pathway in psoriatic arthritis
IL17-IL23
74
what are some clinical signs of psoriatic arthritis
nail pitting
onycholysis (nail separate from nail bed)
75
which joints do psoriatic arthritis affect
IPJs
tendon insertions (enthesitis), can hv sausage finger
76
is psoriatic arthritis symmetrical
can be both
asymmetric in IPJ
symmetric in small joints
77
what are some manifestations of psoriatic arthritis
spinal and sacroiliac joint inflammation
oligoarthritis of alrge koints
arthritis mutilans
symmentric involvement of small joints
78
what is reactive inflammation
sterile inflammation followed by infection elsewhere in body
79
what are some common infections causing reactive
urogenital infections
gastrointestinal infection (eg salmonella)
80
extra-articular manifestations in reactive arthritis
enthesitis (tendon inflammation)
skin inflammation
eye inflammation
81
reactive arthritis can be first manifestation of which disease
HIV
Hepatitis C infection
82
is septic arthritis same as reactive arthritis
no
83
difference between septic arthritis and reactive arthritis in terms of synovial fluid culture
septic: positive
reactive: sterile
84
difference between septic arthritis and reactive arthritis in terms of antibiotic therapy
septic: yes, IV
reactive: no (but yes for treating underlying infection of STI)
85
difference between septic arthritis and reactive arthritis in terms of joint lavage
septic: yes
reactive: no
86
In trauma, what are the 3 main components in hold
plaster
external fixator
internal fixator
87
how long is rehab in truama
~6 weeks
88
ABCD in truama
airway
breathing
circulation
disability
89
what to look for when assessing fractures
pain
swelling
crepitus
deformity
collateral (nerve, vessel)
90
imaging for investigations in fractures
XRay
CT
MRI
91
what is CT for in assessing fractures (2)
assess pattern and make diagnosis
92
how to describe a fracture radiograph (6)
Location: which bone and which part of bone?
Pieces: simple/multifragmentary?
Pattern: transverse/oblique/spiral
Displaced/undisplaced?
Translated/angulated?
X/Y/Z plane
93
what are the 4 types of displacement in trauma fractures
translation
angulation
rotation
impaction
94
what kind of translation of displacement in trauma fracture (4)
medial
lateral
dorsal
volar
95
what kind of angulation of displacement in trauma fracture (2)
valgus
varus
96
when is direct fracture healing possible? (3)
1.anatomical reduction
2. absolute stability / compression
3. no callus or deformity
97
when is indirect fracture healing possible? (3)
1. Sufficient reduction
2. Micromovement
3. Callus
98
3 stages of indirect fracture healing
1. inflammation
2. repair
3. remodelling
99
what is wolff's law in indirect fracture healing
Bone Grows and Remodels in response to the forces that are placed on it
100
steps in indirect fracture healing (4)
1. haematoma formation
2. fibrocartiliginous callus formation
3. bony callus formation
4. bone remodelling
101
what is involved in inflammation stage in indirect fracture healing (3)
1. Haematoma formation
2. Release of Cytokines
3. Granulation tissue and blood vessel formation
102
what is involved in repair stage in indirect fracture healing (2)
1. Soft Callus formation
(Type II Collagen - Cartilage)
2. Converted to hard callus
(Type I Collagen - Bone)
103
what is involved in remodelling stage in indirect fracture healing (2)
1. Callus responds to activity, external forces, functional demands and growth
2. Excess bone is removed
104
2 kinds of reduction in management of fractures
closed
open
105
3 kinds of hold in management of fractures
Plaster/splint
External fixation
Internal fixation
106
3 kinds of rehabiliate in management of fractures
Early / late
Weight bearing
Physiotherapy
107
2 kinds of closed reduction in management of fractures
manipulation
traction
108
2 kinds of open reduction in management of fractures
mini incision
full exposure
109
how to describe fixations (3)
internal/external
intra/extra medullary
mono/multiplanar
110
general fracture complication examples
Fat embolus
DVT
Infection
Prolonged immobility (UTI, chest infections, sores)
111
specific fracture complication examples
Neurovascular injury
Muscle/tendon injury
Non union/mal union
Local infection
Degenerative change (intraarticular)
Reflex sympathetic dystrophy
112
what are mechanical factors affecting healing (2)
movement
forces
113
what are biological environment factors affecting healing (4)
blood supply
immune function
infection
nutrition
114
causes of fractured of neck of femur (3)
Osteoporosis (older)
Trauma (younger)
Combination
115
what's important in history for fractured neck of femur
Age
Comorbidity respiratory/cardiovascular/diabetes/cancer
Preinjury mobility independent/shopping/walking/sports
Social hx: relatives, stairs, alcohol
116
what are different types of neck of femur fractures
subcapital
transcervical
basicervical
subtrochanteric & intertrochanteric (both not femur fractures technically)
117
which of the femur fractures is intracapsular
subcapital
118
which of the femur fractures is extracapsular
transcervical
basicervical
119
what are the 2 types of problems arouse from neck of femur fracture for blood supply compromised
avascular necrosis
non-union(broken bone fails to heal)
120
exeample of management of neck of femur fractures for extracapuslar fractures
DHS (dynamic hip screw)
121
presentation of shoulder dislocation
pain
restricted movement
loss of normal shoulder contour
related to direct trauma usually
122
which neurovascular status need to be assessed in shoulder dislocation
axillary nerve
123
investigation for shoulder dislocation
x-ray to identify fracture (humeral neck, glenoid etc)
124
what is the safest management for shoulder dislocation
traction countertraction +/- gentle internal rotation to disimpact humeral head
125
management of shoulder dislocation
adequate analgesia , vigorous/twisted manipulation should be avoided to avoid fractures
traction
126
what are the 3 views for xray in shoulder dislocation
AP
true AP
Y-view
127
what is hill-sachs defect in shoulder dislocation
defect at humerus head under glenoid
128
temporary management of any distal radius fracture
reduction of fracture and placement into cast until definitive fixation
129
exrtra-articular secpfic distal radiu fracture management
MUA and K-wire fixation
130
distal radius fracture not suitable for K-wires or intra-articular fracture management
Open Reduction Internal Fixation (ORIF) with plate and screws
131
main function of proximal tibial
key weightbearing surface of knee joint
132
what can cause tibial plateau fracture
valgus or varus force
axial loading across knee
impaction pf femoral condyles cause soft bone of tibial plateau
133
non-operative management of tibial plateau fracture
CT imaging
134
operative management of tibial plateau fracture
restore articular surface using combination of plate and screws
bone graft or cement to prevent further depression after fixation
135
non operative management of ankle fracture
non-weightbearing below knee cast for 6-8 weeks, can transfer to walking boot then PT
136
what is weber A fracture
below syndesmosis and thought to be stable
137
what is weber B fracture
fracture at same level of syndesmosis
138
do weber A or B need operative management
no
weber B if no instability then no need
139
operative management for ankle fracture
Open reduction internal fixation (ORIF)
140
what is weber C fracture
above level of syndesmosis therefore unstable
141
curvature of cervical and lumbar in spine
normal lordosis
142
curvature of thoracic spine
kyphosis
143
how many bones do vertebrae of spine have
24 (7C, 12 T, 5L)
144
function of intervertebral discs (2)
shock absorber
allow segmentation and multi-directional movement
145
what does the spinal column made up of (4)
vertebrae
muscles
intervertebral joints
facet joints
146
which level does spinal cord end
L2 vertebrae
147
where do we do lumbar puncture
L3-4
148
what is the most distal part of spinal cord called
conus medullaris
149
what are the movements of the spine (4)
flexion
extension
lateral flexion
rotation
150
what is important to distinguish in terms of back pain (2)
mechanical back pain and serious pathology
151
which type of back pain is usually self limiting
acute back pain
152
characteristic of mechanical back pain (2)
reproduced
worse with movement
153
common causes of mechanical back pain (4)
-Muscular tension (e.g. chronic poor posture, weak muscles)
-Acute muscle sprain/spasm
-Degenerative disc disease
-Osteoarthritis of facet joints
154
what is sciatica
pain radiating down one leg
155
causes of sciatica
disc herniation contacting the exiting lumbar nerve root
156
causes of back pain (7)
tumor
infection
inflammatory spondyloarthropathy
fracture
large disc prolapse
referred pain (pancreas, kidney, aortic aneurysm)
157
bacteria that cause back pain
Staphylococcus, streptococcus, tuberculosis (TB)
158
infection causes of back pain (4)
Discitis
Vertebral osteomyelitis
Paraspinal abcess
Microbiology: Staphylococcus, streptococcus, tuberculosis (TB)
159
inflammatory causes of back pain
ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease (IBD)-associated
160
what are the red flags of back pain
Pain at night or increased pain when supine
Constant or progressive pain
Thoracic pain
Weight loss
Previous malignancy
Fever/night sweats
Immunosuppressed
Bladder or bowel disturbance (Sphincter dysfunction)
Leg weakness or sensory loss
Age <20 or >55 yrs
161
symptoms or signs of cauda equina syndrome
Saddle anaesthesia (loss of sensation)
Bladder/bowel incontinence
Loss of anal tone on PR
Radicular leg pain
Ankle jerks may be absent
162
investigation of cauda equina syndrome
MRI L spine
163
causes of cauda equina syndrome
large disc herniation, bony mets, myeloma, TB, paraspinal abcess
164
treatment for cauda equina syndrome
surgery
165
do we need investigations in absence of red flags
no
166
what are the treatment for low back pain without red flags
analgesia (NSAIDS, ibuprofen, paracetamol, codeine)
avoid bed rest
Physiotherapy
167
blood tests components to test for back pain
ESR
CRP
FBC
ALP
calcium
PSA
168
increase ESR indications in back pain
increase in myeloma
chronic inflammation
TB
169
increase alkaline phosphatase(ALP) indication
bony metastases
170
imaging investigations for back pain
X-ray
CT
MRI
171
advantages and disadvantages of using MRI for back pain
-Best visualization of soft tissue structures like tendons and ligaments
-Best for spinal imaging: can see spinal cord and exiting nerve roots
-Expensive and time-consuming
172
173
treatment for herniated disc
1. Conservative as for LBP without sciatica
-Analgesia especially NSAIDs
-Physiotherapy to improve core strength and treat associated muscle spasm
2. Nerve root injection (local anaesthetic and glucocorticoid)
3. Surgery if neurological compromise or symptoms persist
174
examples of inflammatory spondyloarthritis (SpA)
ankylosing spondylitis
psoriatic arthritis
IBD
175
where are the most common inflammation site of Spondyloarthritis
spine (spondylitis) and sacro-iliac joints (sacro-iliitis), peripheral joints, entheses (tendon insertions)
176
what are some extra-articular manifestations of inflammatory spondyloarthritis (4As)
Anterior uveitis (iritis) – ocular inflammation
Apical lung fibrosis
Aortitis/aortic regurgitation
Amyloidosis – due to chronically serum amyloid A (SAA) depositing in organs
177
major characteristic of ankylosing spondylitis
enthesitis
loss of spinal movement
178
strongest genetic risk factor of ankylosing spondylitis
HLA-B27
179
is ankylosing spondylitis mono or poly genetic
polygenetic
180
what are the cytokines that are important in ankylosing spondylitis (3)
1. tumour necrosis factor alpha (TNF-alpha)
2. interleukin-17 (IL-17)
3. interleukin-23 (IL23)
181
what features on MRI of sacroiliac joint suggest inflammation of bone marrow
white on either side of sacroiliac joint
182
features of untreated ankylosing spondylitis
Spinal enthesitis
Bridging syndesmophytes
(new bone growth between adjacent vertebra)
Spinal fusion
183
what feature on MRI suggest ankylosing spondylitis
shiny corners
184
management of ankylosing spondylitis
1. physiotherapy
2. Medicine (NSAIDs, biological therapies)
185
examples of pharmacological treatment for ankylosing spondylitis
1st line: NSAIDs
-e.g. ibuprofen,
-Selective COX2 inhibitors (e.g. celecoxib) reduce GI ulcer risk
2nd line: ‘Biological’ therapies
Therapeutic monoclonal antibodies (mAbs) targeting specific molecules
Use if inadequate disease control after trying 2 NSAIDs
Anti-TNF-alpha (e.g. infliximab, golimumab)
Anti-IL17 (e.g. secukinumab)
186
what are overlap symptoms in autoimmune connective tissue disorders
have both lupus and inflammatory
187
examples of autoimmune connective tissue disorders
SLE
scleroderma
autoimmune inflammatory muscle disease
sjogren's syndrome
188
where is main site of inflammation in RA
synovium
189
what are the autoantibodies associated with RA (2)
Rheumatoid factor
anti CCP(citrullinated peptide) antibodies
190
does ankylosing spondylitis have autoantibodies
no, it is seronegative
191
examples of seronegative inflammatory arthritis
Ankylosing spondylitis
Reactive Arthritis
Arthritis associated with psoriasis (psoriatic arthritis)
Arthritis associated with gastrointestinal inflammation (enteropathic arthritis)
192
where is site of inflammation in ankylosing spondylitis
spinal inflammation
enthesis (tendon, ligament, joint capsule)
193
does SLE affect innate or adaptive immune system
both
194
where are site of inflammation of SLE
multi-site
joints
skin
kidney
195
what is raynaud's phenomenon
color change in hand and feet
196
what is typical color change in raynaud's phenomenon and what do colors mean (3)
WHITE -> Vasospasm leads to blanching of digit
BLUE -> Cyanosis as static venous blood deoxygenates
RED -> Reactive hyperaemia
197
describe the color change in raynaud's phenomenon
triphasic color changes
198
why are serum autoantibodies in autoimmune connective tissue disorders important
Useful diagnostically
Some correlate with disease activity
May be directly pathogenic
199
are arthralgia and arthritis erosive
no
200
is male or female more common in SLE
female
9:1 ratio
201
typical onset of age of SLE
15-45
202
in SLE, do X-ray show bony erosiion
no
203
typical clinical features of SLE
swan neck deformity
arthritis and deformity of fingers
204
causes of deformity in SLE
soft tissue damage
205
swan neck deformity is characteristic of which RA
SLE
206
skin and mucosa clinical features of SLE
Skin and mucosa:
Malar rash – erythema that spares the nasolabial fold
Photosensitive rash
Mouth ulcers
Hair loss
207
vascular clinical features of SLE
raynaud's phenomenon
208
MSK clinical features of SLE
arthralgia
arthritis
usually non-erosive
209
haematological clinical features of SLE
autoimmune thrombocytopenia (low platelets)
haemolytic anaemia
Lymphopenia
210
systemic clinical features of SLE
renal disease(glomerulonephritis)
cerebral disease
serositis
myocarditis
211
is lymphadenopathy clinical features of SLE
yes
212
which antibody can be found in SLE (2)
anti-nuclear antibodies (ANA)
antiphospholipid antibodies(APL)
213
is ANA found in all SLE patients
yes, so absence of ANA rules out SLE
but ANA not specific to SLE
214
what antibodies can be present in SLE (5)
Anti-ds-DNA antibodies
Anti-Ro
Anti-La
Anti-Smith (Sm)
Anti-RNP
215
what are APL (antiphospholipid)antibodies associated with increase risk of
thrombosis (arterial -- stroke, venous -- DVT)
pregnancy loss
216
what does Persistent presence of APL + a clinical event mean
anti-phospholipid antibody syndrome
217
what is primary anti-phospholipid antibody syndrome
Anti-phospholipid antibody syndrome absence in SLE
218
which antibodies are specific to SLE
anti-dsDNA
Anti-Sm
219
which antibodies in SLE are specific to SLE and serum level correlates to disease activity
anti-dsDNA
220
which antibodies in SLE are specific to SLE and serum level DONT correlates to disease activity
anti-Sm
221
which immunopathology in SLE is innate immunity (2)
Overactivity of type 1 interferon pathway
Complement pathway abnormalities
222
which immunopathology in SLE is adaptive immunity
autoreactive B & T cells
223
in SLE how did immune system generate a response to nuclear antigen
1. Apoptosis leads to translocation of nuclear antigens to membrane surface
2.Impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells
3. B cell autoimmunity
4. Tissue damage by antibody effector mechanisms e.g. complement activation and Fc receptor engagement
224
what is the hypothesis called in SLE to describe the stimulation of immune system to generate a response to nuclear antigen
waste disposal hypothesis
225
what are the key investigations to do in SLE
bloods
urine
imaging
226
blood results in SLE
high ESR
normal CRP (unless infection/serositis/arthritis)
227
why need to check urine in SLE
glomerulonephritis
urinalysis + quantify urine protein:creatinine ratio
228
what are some immunological findings to test for in SLE
Antinuclear antibodies (ANA)
Anti-dsDNA antibodies
Complement consumption – e.g. low C4 and C3
antiphospholipid antibodies (APL)
229
relationship of complement C3 and C4 and anti-dsDNA in SLE patients
when C3 & C4 reduce
anti-dsDNA increase
230
kidney findings to test for SLE
creatinine in blood
creatinine in urine
eGFR
protein in urine
Protein:Creatinine ratio (PCR)
CKD EPI
albumin in blood
231
haemological findings to test for SLE
Hb
platelet
lymphocyte
reticulocyte
232
what are the treatment goals in SLE
remission or low disease activity and prevention of flares
Balance of controlling disease vs avoiding iatrogenic harm (especially steroids)
233
steroids side effects when treat SLE
Infection
Osteoporosis
Avascular necrosis (AVN) - often affects hips: higher incidence in lupus, especially in presence of APL Abs
234
medication for mild SLE
Hydroxychloroquine (main)
steroids for acute flare (but aim withdraw asap)
235
medication for serious SLE
immunomodulatory agents (mycophenolate, methotrexate, azathioprine)
236
medication for SLE + kidney disease
Mycophenolate +/- rituximab
237
SLE B-cell targeted therapies
Rituximab = anti-CD20 monoclonal antibody: depletes B cells
Belimumab = anti-BAFF antibody (BAFF = a B cell survival factor/cytokine)
238
myocarditis + SLE medication
iv steroids + iv cyclophosphamide (+/- rituximab)
239
Patients with SLE and antiphospholipid antibody syndrome medications
anticoagulation (warfarin)
240
what is an emerging therapy for SLE
anifrolumab (interferon receptor blockade)
241
what needs to be considered when treating SLE women with pregnancy
Consider both risk of disease & drugs to both mother and to fetus
aim get to remission first
242
medical treatment for SLE pregnant women
Hydroxychloroquine, azathioprine, low molecular weight heparin (LMWH) safe
243
which antibody in SLE can cause miscarriage
APL
244
what medication can help reduce miscarriage risk in SLE
aspirin or heparin
245
where are heberden's nodes
at DIPJ
246
where are bouchard's nodes
at PIPJ
247
if we see symmetrical small joint polyarthritis affecting DIPJs and PIPJs, and patient's hand cannot grip properly, what's likely diagnosis
OA
248
treatment for OA
analgesia
hand therapy
249
are there any disease modifying therapy for OA
no
250
raynaud's phenomenon is a characteristic of what disease
SLE
251
positional chest pain in context of SLE is what
might suggest pericarditis
may come from soft tissue pr ribs
252
pain on inspiration in context of SLE implication
maybe pulmonary embolism as SLE patients have APL antibodies which predispose them to thrombosis
253
urine tests in SLE
urinalysis (urine dip)
UPC ratio to quantify proteinuria
254
bloods in SLE (need test what)
FBC
ESR, CRP
ANA, APL antibodies
complements C3 and C4
255
imaging for SLE
CXR ( look for pleural effusion, enlarged contour of heart if large pericardial effusion)
echocardiogram (look for pleural effusion)
CT pulmonary angiogram
256
symmetrical polyarthritis affecting both large and small joints suggest what
RA
lupus (so needa check antibodies)
257
is arthralgia or arthritis more common in SLE
arthralgia
258
RA treatment
DMARDs(disease modifying antirheumatic drugs) eg methotrexate, hydroxychloroquine)
short course of oral steroids for acute inflammation but avoid long term steroids
259
how many bones do a child skeleton has
270
260
how many bones do adult hv
206
261
where do long bone growth occurs post-natally
physis (at proximal and distal end)
262
bone development step for flat bone
intramembranous mesenchymal cells --> bone --> flat bones
263
bone development step for long bone
endochondral mesenchymal --> cartilage --> bone --> long bones
264
steps for intramembranous ossification
1. condensation of mesenchymal cells then differentiate into oesteoblasts where ossification centre forms
2. secreted osteoid traps osteoblasts which become osteocytes
3. trabecular matrix and periosteum form followed by angiogenesis
4. compact bone develops superficial to cancellous bone
5. crowded blood vessels condense into red bone marrow
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how many ossification centre do endochondral ossification involve
2
primary and secondary
266
does flat bone formation involve 1 or 2 ossification centre
1
267
does long bone formation involve 1 or 2 ossification centre
2
268
what is primary ossification centre
Sites of pre-natal bone growth through endochondral ossification from the central part of the bone
269
what is secondary ossification centre
Occurs post-natal after the primary ossification centre and long bones often have several (the physis)
270
steps for endochondral primary ossification formation
1. mesenchymal differentiation at primary ossification centre
2. cartilage model of future bony skeleton forms
3. angiogenesis, capillaries penetrate cartilage
4. calcification at primary ossification centre to form spongy bone
5. perichondrium transform into periosteum
6. cartilage and chondrocytes continue to grow at ends of bone to form secondary ossification centre
271
where does post bone growth happen
secondary ossification centre (physis)
272
what are the 6 parts at growth plate / physis
1. growth plate zones
2. reserve zone
3. proliferative zone
4. maturation and hypertrophy
5. calcified matrix
6. zone of ossification
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what happens at the growth plate/ physis
1. Zone of elongation in long bone
2. Contains cartilage
3. Epiphyseal side – hyaline cartilage active and dividing to form hyaline cartilage matrix
4. Diaphyseal side – Cartilage calcifies and dies and then replaced by bone
274
where do prenatal bone growth occur
primary ossification centre
275
in what 4 ways are children's skeleton differ to adult
1. elasticity
2. physis
3. remodelling potential
4. speed of healing
276
why children's bone can bend more than adult
have a higher proportion of cartilage and collagen
277
why children bone more prone to plastic deformity, buckle fracture, greenstick injury
higher density of haversian canals
278
which 3 injuries are children more prone to
plastic deformity(bends before break)
buckle fracture(compress out)
greenstick injury (like a tree)
279
when does growth of physis stop for girls and boys
Girls 15-16
Boys 18-19
280
what are the classification for physeal injuries
salter-harris
281
what can physeal injury lead to
growth arrest, then deformity
282
causes of physeal injury
trauma
tumor
chemo
283
what do speed of healing and remodeling potential of skeleton depend on
location and the age of the patient
284
physis at which part grows more (2)
knee
extreme of upper limb (shoulder/ wrist)
285
what are the 4 common children's congenital conditions in skeleton fracture
1. developmental dysplasia of hip(DDH)
2. club foot
3. achondroplasia
4. osteogenesis imperfecta
286
what is developmental dysplasia of hip(DDH)
Group of disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
287
what does normal development of femur relies on
the concentric reduction and balanced forces through the hip
288
describe the spectrum of DDH (3)
dysplasia – subluxation – dislocation
289
risk factors of DDH
Female
First born
Breech
FHx
Oligohydramnios
Native American/Laplanders – swaddling of hip
Rare in African American/Asian
290
examination of DDH in baby
screening to check range of movement
291
investigation of DDH
USS (birth to 4 months)
Xray (after 4 months)
measure acetabular dysplasia and hip position
292
treatment for DDH
pavlik harness
293
what happens if failed pavlik harness when treating DDH
secondary changes to capsule and soft tissue
treat with MUA + Closed reduction and Spica
294
what is another name of clubfoot
Congenital Talipes Equinovarus
295
what is clubfoot/Congenital Talipes Equinovarus
congenital deformity of foot
296
risk factors of club foot
genetic
Highest in Hawaiians
M2:1F
297
what is the gene associated in Highest in clubfoot
PITX1 gene inactivation
298
mnemonic of deformity in Congenital Talipes Equinovarus / clubfoot
CAVE
299
what does CAVE stand for in deformity of Congenital Talipes Equinovarus
Cavus –high arch: tight intrinsic, FHL, FDL
Adductus of foot: Tight tib post and ant
Varus: Tight tendoachillies, tib post, tib ant
Equinous: tight tendoachilles
300
name and describe treatment for clubfoot
Ponseti method
1. First a series of casts to correct deformity
2. Many require operative treatment
, Soft tissue releases
3. Foot orthosis brace
4. Some will require further operative intervention to correct final deformity.
301
which is the most common skeletal dysplasia
achondroplasia
302
nature of achondroplasia
genetic
autosomal dominant
303
which gene mutation in achondroplasia
G380r mutation in FGFR3 (fibroblast growth factor receptor)
function abnormally, slowing down the growth of bone in the cartilage of the growth plate.
304
what happens in achondroplasia
inhibition of chondrocyte proliferation in the proliferative zone of the physis
results in defect in endochondral bone formation
305
which zone does achondroplasia affect in physis
proliferative zone
306
name of clinical presentation of achondroplasia
Rhizomelic dwarfism
307
what is Rhizomelic dwarfism
Humerus shorter than forearm
Femur shorter than tibia
Normal trunk
Adult height of approx. 125cm
Normal cognitive development
Significant spinal issues
308
what is another name of osteogenesis imperfecta
brittle bone disease
309
nature of osteogenesis imperfecta
Hereditary – autosomal dominant or recessive
310
which type of collagen in affected in osteogenesis imperfecta
decrease in type 1 collage
311
why is there decrease in type 1 collagen in osteogenesis imperfecta (2)
Decreased secretion
Production of abnormal collagen
312
consequence of reduced type 1 collagen
insufficient osteoid production
313
effects in bones in osteogenesis imperfecta
Fragility fractures
Short stature
Scoliosis (spine twists and curves to the side)
314
what are some non-orthopaedic manifestations in osteogenesis imperfecta
Heart
Blue Sclera
Dentinogenesis imperfecta – brown soft teeth
Wormian skull
Hypermetabolism
315
medical treatment for osteogenesis imperfecta
bisphosphonates (inhibit osteoclast)
denosumab (block RANKL to bind, inhibit osteoclast)
setrusumab
316
surgical rteatment for osteogenesis imperfecta
mechanical alignment
stabilisation
317
5 types of paediatric fractures (PAIDS)
pattern
anatomy
intra/extra-articular
displacement
salter-harris
318
5 types of pattern in paediatric fractures
transverse
oblique
spiral
comminuted (broken bone in at least 2 places)
avulsion (pulled off ligament)
319
how is anatomy of paediatric skeleton separated into 3 parts
proximal 1/3
middle 1/3 diaphysis
distal 1/3
*this is different to adult
320
is there callus formation in primary bone healing
no
321
steps in secondary bone healing
1. haematoma formation
2. fibrocartilaginous callus formation
3. bony callus formation
4. bone remodelling
322
what is primary bone ehaling
heals by direct union
323
what are the 2 bone healings in intra/extra articular fracture
primary and secondary bone healing
324
4 types of displacement in paediatric fracture
displaced
angulated
shortened
rotated
325
what are the 5 types of Salter Harris physeal injuries (SALT)
1. (Physeal)Separation
2. Fracture traverses physis and exits metaphysis (Above)
3. Fracture traverses physis and exits epiphysis (Lower)
4. Fracture passes Through epiphysis, physis, metaphysis
5. Crush injury to physis
326
which type of salter harris is most common
type 2
327
what are keys of fracture in growth arrest
location
timing
328
2 types of injuries to physis in growth arrest
Whole physis – limb length discrepancy
Partial physis – angulation as the non affected side keeps growing
329
treatment for growth arrest
1. limb length correction a9shorten long side or lengthen short side)
2, angular deformity (stop growth of unaffected side or reform bone via osteotomy)
330
main aim of growth arrest treatment
Minimise angular deformity
Minimise limb length difference
331
the 4 Rs in fracture management
1. resuscitate
2. reduce
3. restrict
4. rehabilitate
332
2 types of reducing fracture
open
closed
333
what is closed reduction in treat bone fracture
Reducing a fracture without making an incision
334
example of bone reduction
traction
manipulation
335
what is open reduction in healing bone fracture
Making an incision
The realignment of the fracture under direct visualisation
336
aim of reduction in treating bone fracture
Correct the deformity and displacement
Reduce secondary injury to soft tissue / NV structures
337
main goal of restriction in bone healing
Maintain the fracture reduction
Provides the stability for the fracture to heal
Children rarely have issues with bone not healing
Can have issues with too much healing!
338
2 types of restriction in bone healing
external and internal
339
examples of external restriction in bone healing
splints
plaster
340
examples of internal restriction in bone healing
plate and screws
intra-medullary device
341
benefits of fast remodelling and high healing potential in children using external restriction
operative internal fixation often can be avoided
342
internal restriction in bone healing drawbacks
Operative intervention may be required
need Consider the ongoing growth at the physis
Metalwork may need to be removed in the future
343
what is a great rehabilitator in children bone fracture treatment
playing
344
what is limping child
difficulty in walking
345
4 types of limping child
septic arthritis
transient synovitis
perthes
SUFE
346
is septic arthritis in child an orthpedic emergency
yes
347
treatment for septic arthritis in child
wash out of joint to clear infection
348
what classification to score probability of septic arthritis in child
Kocher’s classification
349
components of Kocher’s classification to score probability of septic arthritis
Non weight bearing
ESR >40
WBC >12,000
Temperature >38
350
key history of septic arthritis in child
Duration
Other recent illness
Associated joint pain
351
if there is no high temp/ increase WBC and ESR, what type of limping in child can we exclude and consider what
septic arthritis
can consider transient synovitis
352
what is transient synovitis
inflamed joint in response to a systemic illness
353
treatment for transient synovitis
Supportive treatment with antibiotics is the treatment
354
investigations for septic arthritis
USS
XRay
MRI
355
what is perthes disease
Idiopathic necrosis of the proximal femoral epiphysis
356
age of perthes disease in child
4-8yo
357
treatment for perthes disease
supportive treatment
358
what has to be excluded first before diagnosing perthes diseaase
septic arthritis
359
investigation for perthes disease
Xray
360
male or female more common in perthes disease
male
361
full name of SUFE in limping child
Slipped upper femoral epiphysis
362
what is SUFE
proximal epiphysis slips in relation to the metaphysis
363
age of SUFE common
12-13 yo during rapid growth
364
what has to be excluded first before diagnosing SUFE
septic arthriti
365
treatment for SUFE
operative fixation to prevent further slip and minimise long term growth problems
366
imaging for SUFE
xray
367
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