MSK Flashcards
1
Q
phalanges fracture healing time
A
3 weeks
2
Q
metacarpals healing time
A
4-6 weeks
3
Q
distal radius healing time
A
4-6 weeks
4
Q
forearm healing time
A
8-10 weeks
5
Q
tibia healing time
A
10 weeks
6
Q
femur healing time
A
12 weeks
7
Q
process of indirect fracture healing
A
haematoma formation
cytokine release
granulation tissue and blood vessel formation
soft callus formation (type 2 collagen - cartilage)
converted to hard callus (type 1 collagen - bone)
callus responds to activity, external forces, functional demands and growth
(wolffs law)
excess bone is removed
8
Q
List some specific and general fracture complications
A
General
- fat embolus
- local infection
- prolonged immobility
- DVT
Specific
- malunion / non union
- degenerative changes
- infection
- reflex sympathies hypertrophy aka complex regional pain syndrome
- neurovascular injury
- muscle / tendon injury
9
Q
How to prevent embolisms
A
Virchows traid:
Prevent stasis
Prevent coagulation
Fix vessel wall changes
10
Q
Why do intracapsular NOF fractures heal worse
A
Blood supply is more likely to be compromised, resulting in a vascular necrosis and non union
11
Q
Which line can you use to help you decide if there has been a hip fracture
A
Shentons line: goes from inside of femoral neck to superior pubic ramus
If unsure if there has been a hip fracture, look to see if she tons line has been disrupted
12
Q
what should you remember to do in the clinical examination of shoulder dislocation
A
assess neurological status: check if axillary nerve has become damaged
13
Q
how should you manage a dislocated shoulder
A
tract and counter traction with gentle internal rotation to dis-impact the humeral head
OR
if alone –> Stimson’s method
remember to maintain patient relaxation eg with benzodiazepines
14
Q
describe a Bankarts and Hill Sachs lesion
A
Bankarts lesion: humeral head moves forwards out of glenoid fossa and by doing so, tears away a price fo the labrum around the glenoid fossa
Hill sachs lesion: back of humeral head impacts with the front of the glenoid fossa, causing a dent in the bone of the head
15
Q
management of distal radius fracture
A
1) cast/splint:
as a temporary treatment and form of reduction whilst awaiting definitive fixation
or
as a definitive treatment if minimally displaced extra articular fracture
2) MUA (manipulation under anaesthetic) and K wires
for unstable extra articular fractures - esp in children
3) ORIF (open reduction internal fixation)
for displaced unstable fractures that are not suitable for MK wires
or
intra articular fractures
16
Q
what is lipohaemarthrosis
A
escape of fat and blood from bone marrow into the joint, as the result of an intra articular fracture
17
Q
what causes a tibial plateau fracture
A
Extreme valgus/varus force or axial loading causes impaction of the femoral condyles with tibial plateau
This causes the comparatively soft bone of tibial plates to depress or split.
18
Q
management of a tibial plateau fracture
A
non surgical: only of truly undisplaced and has good joint line congruency
surgical: restore articular surface using plates and screws. Use cement in bone graft to prevent further depression after fixation
19
Q
what is an avulsion fracture
A
An avulsion fracture occurs when a small chunk of bone attached to a tendon or ligament gets pulled away from the main part of the bone
20
Q
give 4 common causes of mechanical back pain
A
muscular tension
acute muscular sprain or spasm
degenerative disc disease
osteoarthritis of facet joints
21
Q
describe how a slipped disc causes sciatica
A
the intervertebral disc is made of nucleus pulposus in the middle and annulus fibrosus around the outside.
when the disc slips, the annulus fibrosus tears and the central nucleus pulposus leaks out, impinging the lumbar nerve root
22
Q
urgent investigation for cauda equina
A
urgent Lumbar MRI spine
23
Q
causes of cauda equina
A
bony metastases, myeloma, TB, paraspinal abscess, large disc herniation
24
Q
serious causes of back pain
A
cancer
infection
- staphylococcus, streptococcus, TB, discitis, paraspinal abscess, vertebral osteomyelitis
inflammatory spondyloarthropathy
- ankylosing spondylitis, psoriatic arthritis, IBD related
fracture
referred pain
- kidneys, pancreas, abdominal aneurysm
large disc prolapse
25
if pt had back pain with a high PSA on blood test, what could the diagnosis be
prostate cancer with bony metastases
26
if pt had back pain and blood test showed high alkaline phosphate, what could the diagnosis be
bony metastases
27
if pt had back pain and blood test showed high calcium, what could diagnosis be
myeloma, bony metastases
28
best imaging for soft tissue structures eg tendons, ligaments
MRI
29
best imaging for spinal cord
MRI
30
treatment for herniated disc
NSAIDs
nerve root injection/block
- mixture of analgesia and steroids injected around the swollen or compressed spinal nerve to relieve the pain and inflammation
the disc itself tends to regress back to its original position over time
31
list the main connective tissue disorders
systemic lupus erythematosus
Sjogren's syndrome
autoimmune musclar inflammatory disease - polymyositis, dermatomyositis
systemic sclerosis (scleroderma) - diffuse or limited cutaneous involvement
overlap syndrome
32
where do the autoantibodies in rheumatoid arthritis usually attack
synovium
33
what are the autoantibodies in rheumatoid arthritis
rheumatoid factor
anti cyclic citrullinated peptide antibody (anti CCP antibody) --> aka ACPA (antibody for citrullinated peptide antigen)
34
what is ankylosing spondylitis and where is the usual site of inflammation
chronic spinal inflammation resulting in spinal fusion and deformity
enthesis
seronegative inflammation
35
what are the main seronegative spondyloarthropathies
ankylosing spondylitis
psoriatic arthiritis
reactive arthritis
enteropathic synovitis
36
in which group does Lupus usually present
females
15-45 yrs old
37
what is SLE
systemic lupus erythematosus - autoimmune inflammation against mostly kidneys, skin, joints
38
symptoms of SLE
malar rash
photosensitive rash
mouth ulcers
alopecia
raynauds
arthralgia and arthiritis
serositis (pericarditis, pleuritis, peritonitis)
cerebral problems
glomerular nephritis
39
investigations for SLE
clinical signs eg malar rash
bloods: anaemia, lymphopenia, thrombocytopenia, high ESR but low CRP
check for presence of autoantibodies - should have high autoantibodies and low complement
thrombosis - due to anti phospholipid AB
proteinuria (urine protein: creatinine ratio)
40
key points to look for when considering a connective tissue disorder diagnosis
arthralgia and arthiritis are non erosive
auto antibodies - may aid with diagnosis and level may correlate with disease severity
raynauds phenomenon (can also be benign)
41
what is raynauds phenomenon
intermittent vasospasms in fingers in cold
1) white --> vasospasm
2) blue --> cyanosis
3) red --> reactive hyperaemia
42
antibodies in SLE
anti nuclear antibody
anti dsDNA antibody
anti phospholipid antibody
43
antibodies in reactive arthritis
none - seronegative
44
antibodies in systemic vasculitis
anti neutrophilic peptide
45
2 common patterns to look out for with lupus
high anti ds DNA antibody with low complement components (C3+4)
high ESR with low CRP
46
which complement proteins do you test for in lupus
C3 and C4
47
which antibodies do you test for in lupus
ANA first - very sensitive but not specific
then dsDNA and anti phospholipid - more specific but less sensitive
48
most commonly affected joint in gout
1st MTP - big toe - podagra
49
most commonly affected joint in pseudogout
knee joint
50
what is the best test for small joints suspected of gout
serum urate
- fine needle aspirate is difficult to do from small joints
51
what are white opacities in the joint space and what condition do they suggest
chonedrocalcinosis --> calcification of cartilage
this finding suggests pseudogout
52
if an elderly pt is actually unwell with another illness and comes in with painful warm and swollen wrist, what are the most likely diagnoses
septic arthritis - infection spread in blood to joint
pseudo gout - commonly affects elderly who are acutely unwell with another illness
reactive arthritis - usually a bit later, 1-4 weeks after the infection
53
middle aged woman with joint pain in fingers and hands, and swollen finger joints. what are the main differential diagnoses
rheumatoid arthritis
lupus - If symmetrical
psoriatic arthritis - more commonly asymmetrical
pseudo gout
54
investigations if suspect psoriasitoc arthritis
check for red scaly skin patch on extensor surfaces
do tests to rule out other causes of join pain
- bloods to check for rheumatoid factor
- fine needle aspiration and synovial fluid analysis to check for gout
55
best treatment for recurrent psoriatic arthritis
DMARDs: methotrexate
56
what are bridging syndesmophytes and which condition do they suggest
ossification of ligaments
- ankylosing spondylitis
57
what does HLA-B27 positive indicate
makes you more susceptible to autoimmune conditions
- reactive arthritis, psoriatic arthritis, ankylosing spondylitis
58
most commonly affected joints in osteoarthiritis
CMC (joint of thumb to hand)
PIP- bouchards
DIP - heberdens
59
most commonly affected joints in rheumatoid arthiritis
MCP
MTP
PIP
wrists, knees, ankles
60
What are the components of a synovial joint and describe each of them?
Synovium - 1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte). Type I collage also present.
Synovial fluid - Hyaluronic acid-rich viscous fluid.
Articular cartilage - Type II collagen + Proteoglycan (aggrecan)
61
what are the primary inflammation and secondary inflammation causes of arthiritis
primary inflammation
- autoiumme (lupus, psoriatic, reactive, rheumatoid)
secondary inflammation
- infection (TB, septic)
- crystal arthritis (gout, pseudogout)
62
what are the sterile and non sterile inflammatory causes of arthiritis
sterile
- autoimmune
- crystal arthiritis
non sterile
- infectious
63
why are children bones more elastic
increased density of Haversian canals
64
increased elasticity of children's bones lead to which 3 types of bone deformities
plastic deformity (bone bends)
torus/buckle fracture
greenstick fracture
65
name of fracture where piece of bone is pulled off by ligament/tendon
avulsion fracture
66
describe intramembranous ossification
- condensation of mesenchymal cells which differentiate into osteoblasts
- leads to formation of ossification centre
- osteoid is secreted which traps oestoblasts, causing them to convert into osteocytes
- trabecular matrix and periosteum formation
- compact bone develops superficial to the cancellous bone
- crowded blood vessels condense to form red bone marrow
67
where does intramembranous ossification happen
cranial bones, clavicle, mandible
68
what are primary ossification centres
sites of prenatal bone growth - endochondral ossification
in central part of bone
69
where does endochondral ossification happen
all long bones at primary and secondary ossification centres
70
what are secondary ossification centres
sites of post natal bone growth
in physis, long bones have several of them
71
in which type of fractures does direct fracture healing often occur
intra-articular fractures - so doesn't cause post traumatic arthiritis
72
what scan is done to see a paediatric joint below the age of secondary ossification
arthrogram - allows you to see cartilage
73
describe briefly how long bones are lengthened
at the physis: endochondral secondary ossification (endochonral bone growth at secondary ossification centres)
epiphyseal side: hyaline cartilage is active and dividing to form hyaline matrix
diaphyseal side: cartilage calcifies and dies and is replaced by bone
74
main differences in structure of bones in children vs adults
children:
- have physis
- more elastic
- thicker periosteum
- immature bone - less dense + greater porosity
- greater speed of healing
75
what are the two different types of growth arrest
whole physis --> limb length discrepancy
partial --> angular deformity
76
how to fix limb length discrepancy vs angular deformity
limb length discrepancy: shorten unaffected bone or lengthen affected bone
angular deformity: stop growth in the unaffected side of the bone or reform the bone (osteotomy)
77
what are the main forms of external and internal restriction
external: splinter, plaster
internal: plates + screws, intra medullary device
78
what is developmental dysplasia of the hip and in which group is it most common
femoral head not congruent with acetabulum
can be sublaxation (they still touch but not congruent) or dislocation (don't even touch)
most common in
- females
- first born
- breech
- family history
- oligohydramnios
79
investigations for developmental dysplasia of the hip, and what is the most indicative clinical sign
check range of motion: most indicative clinical sign = limited abduction
check limb length discrepancy: Galeazzi's sign
for <3 months: can do Barlow and Ortalani manoeuvre (checks if femoral head can be dislocated out of acetabulum (Barlow) and then pushed back in (ortolani))
after this need to do imaging
<4 months = USS
>4 months = x ray
80
treatments for developmental dysplasia of the hip
for reducible hip and <6months
- palvik harness
if palvik harness doesn't work/ >6months:
- MAU (closed reduction)
- spica
81
what is congenital talipes equinovarus and what are the main features
club foot
CAVE
Cavus - high arch of foot
Adductus - front of foot/toes pointed medially
Varus - whole foot twisted from outside inwards
Equinous - limited flexibility of ankle and ability to dorsiflex
82
which group is congenital talipes equinovarus most common in
males and Hawaiian
83
treatment for congenital talipes equinovarus
ponseti method (series of casts)
may need surgery
Foot orthosis brace
84
genetic cause of congenital talipes equinovarus
PITX1 Gene
85
what is the genetic hereditary pattern of achondroplasia
autosomal dominant
86
genetic cause of achondroplasia
G380 mutation in FGFR3 gene
87
what is achondroplasia
inhibited chondrocyte proliferation in the proliferative zone of the physis
results in defects of endochondral bone growth
causes Rhizomelic dwarfism
88
describe the dwarfism of achondroplasia
rhizomelic dwarfism
- humerus shorter than forearm
- femur shorter than tibia
- trunk size normal
89
what is the genetic hereditary pattern of osteogenesis imperfecta
autosomal dominant or recessive
90
cause of osteogenesis imperfecta
decreased type 1 collagen (cartilage) due to either
- reduced secretion
or
- abnormal production
--> lead to decreased osteoid secretion
91
orthopaedic manifestations of osteogenesis imperfecta
brittle bones (fragility fractures)
scoliosis
short stature
92
non orthopaedic manifestations of osteogenesis imperfecta
heart issues
blue sclera
dentinogenesis imperfecta (soft brown teeth)
wormian skull
hyper metabolism
93
what is kochers classification for septic arthritis
non weight bearing
temp > 38
WBC >12 000
ESR > 40
94
what is it more likely to be if it doesn't fulfil kochers classification
transient synovitis
95
main 3 dangerous causes of limping child, and which should you rule out first
septic arthritis (1st!!)
perthes disease
SUFE
96
what is perthes disease, which group is it most common in and how do you treat
idiopathic necrosis of proximal femoral epiphysis
males, 4-8yrs old
supportive therapy, will grow back
97
what is SUFE, which group is it most common in and how do you treat
Slipped upper femoral epiphysis (proximal epiphysis slips in relation to metaphysis)
obese adolescent males
operative fixation using screw
98
what are osteocytes
mature bone cells embedded in matrix
formed when osteoblasts get trapped in their secretions and mature
99
where are osteogenic cells found
deep layers of periosteum
100
what is in the medullary cartilage
nutrient artery
101
what are volkmans canals
transverse canals which allow communication of periosteum with bone and between Haversian canals
102
structure of osteon
central Haversian canal (vein, artery, nerve, lymphatic)
surrounded by concentric lamellae
lacunae seen between lamellae - contain osteocytes
canaliculi radiate from lacunae and connect them with each other
volkmans canals - transverse - connect haversions canals
103
3 types of fracture
trauma - high/low energy
stress
pathological
104
4 scans for fracture
radiograph
MRI
CT
bone scan
105
management for extracaspular NoF fracture
internal fixation
106
management for undisplaced intracaspular NoF fracture
fixation with screws
107
management for displaced intracaspular NoF fracture
if <50: reduce and fixate with screws
if >50 and fit: full hip replacement
if >50 and unfit: hemiarthoplasty
108
what is cartilage made of
Specialised cells → Chondrocytes
ECM: Water, collagen and proteoglycans (mainly aggrecan)
109
what is aggrecan and what is it characterised by
Proteoglycan possessing many chondroitan sulphate and keratin sulphate chains
Characterised by ability to interact with hyaluronan (HA) to form large proteoglycan aggregates
110
what are the main radiographic features seen in OA
LOSS
Loss of joint space
Osteophytes
Sclerosis
Subchondral cysts
111
what is infection of the bone called and how is out treated
osteomyelitis
surgical drainage and IV antibiotics
in severe cases - amputation
112
conservative OA management
physiotherapy
walking aid
analgesia
steroid injection
113
what is joint impingement
painful condition caused by friction of joint tissues
114
list some red flags for back pain
worse in morning/when supine
thoracic pain
bladder or bowel disturbances
altered sensation
fever
weight loss
night sweats
pain is getting progressively worse
older age or younger age
previous malignancy
currently immunosuppressed
115
which blood tests do you do for back pain
ESR - myeloma, chronic inflammation, TB
CRP - infection, inflammation
FBC - check for anaemia (myeloma, chronic inflammation) or raised WCC (infection
ALK (alkaline phosphate) - bony mets, myeloma
PSA - prostate cancer mets
116
3 main types of inflammatory spondyloarthiritis
ankylosing spondylitis
psoriatic arthiritis
IBD
117
4 main extra articular manifestations of inflammatory SpA
4 A's:
anterior uveitis
aortitis /aortic regurgitation
apical lung fibrosis
amyloidosis
118
what happens if you leave ankylosing spondylitis untreated
spinal enthesitis --> bridging syndesmophytes --> spinal fusion
119
main articular features of akylsoing spondylitis
spondylitis
sacroilitis
ethesitis
120
treatment for ankylosing spondylitis
pshyiotherapy
1st line: NSAIDs
2nd line: Biologics
121
what can you take with NSAIDs to reduce risk of GI ulcer
selective COX2 inhibitors eg celecoxib
122
important cytokines in ankylosing spondylitis
IL17
IL23
TNF alpha
123
important genetic component in ankylosing spondylitis
HLA-B27
124
describe Types A,B,C of webers classification
A: fibula is fractured below the tibial plafond: syndesmosis not affected
B: fibula is fractured at level of the tibial plafond: syndesmosis affected in 50% off cases
C: fibula is fractured above the tibial plafond: syndesmosis always affected
125
What causes septic arthritis?
Bacterial infection of a joint (usually caused by haematogenous spread)
126
septic arthritis risk factors
Immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)
127
What bacteria are commonly responsible for septic arthritis?
Staphylococcus aureus, Streptococci, Gonococcus
128
How many joints are usually affected in septic arthritis? And what is the main exception?
1 (mono-arthritis)
Gonococcal septic arthritis - often affects multiple joints (polyarthritis); it is less likely to cause joint destruction.
129
septic arthritis treatment
surgical lavage and IV antibiotics
130
what is gout caused by and what is a risk factor for gout?
uric acid crystals deposited in joints causing inflammation
Hyperuricaemia: High uric acid levels in blood → Risk factor for gout (not everyone who has high levels will have develop attacks of gout)
131
What are the causes of hyperuricaemia?
Genetic tendency
Increased uptake of purine rich foods (Purine gets broken down into uric acid → Beer drinkers particularly vulnerable).
Reduced excretion (kidney failure) of uric acid
132
what is pseudo gout caused by and what are the risk factors
Syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals → Crystals lead to inflammation.
Background osteoarthritis, elderly patients, intercurrent infection.
133
clinical features of gout and most commonly affected joints
Typically presents with an acute mono-arthritis. First MTP joint is the most commonly affected joint (Podagra = gout of the foot, esp the big toe)
Other joints affected → joints in foot, ankle, knee, wrist, finger and elbow are most frequently affected.
Crystal deposits (tophi) developing around hands, feet, elbows and ears. → Yellowish appearance
134
The diagnosis of crystal arthritis is made by aspirating fluid from affected joint and examining under a microscope using polarised light. What would you see for gout and pseudo-gout?
Gout - needle-shaped crystals with -ve birefringence.
Pseudo-gout - rhomboid shaped crystals with +ve birefringence.
(Birefringence is the optical property of a material having a refractive index that depends on the polarization and propagation direction of light)
- p for pseudo gout, p for positive
- rhomboid is tilted so its the one that is refracted
135
The primary site of pathology for rheumatoid arthritis is in the synovium (inflammation occurs here). What 3 things does this include?
Synovial joints
Tenosynovium surrounding tendons
Bursa (fluid-filled sacs that provide lubrication to allow easy movement)
136
The presence of which extra articular feature confirms diagnosis of RA?
subcutaneous/rheumatoid nodule: is invariably associated with the rheumatoid factor
137
What is the pattern of joint involvement in rheumatoid arthritis?
Symmetrical
Affects small and large joints, but particularly hands and feet.
Commonest affected joints:
MCP
MTP
PIP
Wrists
Knees
138
What is Felty’s syndrome?
triad of splenomegaly (enlarged spleen), leukopenia (low WBC count) and RA
139
What are the common and uncommon extra-articular features of rheumatoid arthritis?
Common
Fever, weight loss
Subcutaneous nodules
Uncommon
Vasculitis
Ocular inflammation - episcleritis
Neuropathies (damage to nerves)
Amyloidosis (**a group of rare, serious conditions caused by a build-up of an abnormal protein called amyloid in organs and tissues throughout the body**. The build-up of amyloid proteins (deposits) can make it difficult for the organs and tissues to work properly)
Lung disease - nodules, fibrosis, pleuritis (inflammation of pleura which are the lining of the lungs)
Felty's Syndrome - triad of splenomegaly, leukopenia and RA
140
causes (genetic and environmental) of RA
HLA- DR
other genes: PTPN22, IL6R
environmental:
smoking
microbiome
porphyromonas gingivalis
poor oral health
141
describe the composition of the subcutaneous nodules in RA
centre of fibroid necrosis
surrounded by histiocytes + connective tissue
142
describe the formation of a pannus in RA
Neovascularisation
Lymphangiogenesis
Inflammatory cells → activated B and T cells, plasma cells, mast cells and activated macrophages.
There is an excess of pro-inflammatory (IL1, TNF alpha) vs. anti-inflammatory (soluble tNF receptor, IL10, TNF receptor agonist) cytokines
143
whta is the main inflammatory cytokine in RA and describe how it affects the joint/causes the diseases
stimulates
- chondrocytes: cartilage degradation -->joint space narrowing
- osteoclasts: bone erosion
- synoviocytes: joint inflammation and pain
144
describe how researchers found TNF alpha to be the main inflammatory cytokine in RA
they inhibited it using monoclonal antibodies (inflixumab and adalimumab) and soluble TNF receptor fusion proteins (etanercept)
as a results the other inflammatory cytokines IL 1,6,8, GMCSF were blocked
145
what is rheumatoid factor
IgM anti IgG antibody
146
what are anti cyclic citrullinated peptide antibodies and which reaction do they target
arginine -- (PADs: peptide arginine deiminases) --> citrulline
