Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BRS 2 > musculoskeletal > Flashcards

musculoskeletal Flashcards

1
Q

what is bone?

A

specialised form of connective tissue

unique histological
composition allows it to carry out numerous functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 5 functions of bone?

A

support

protection

locomotion

haematopoiesis

lipid and mineral storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the function of bone in terms of support?

A

framework and shape of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the function of bone in terms of protection?

A

surrounds major internal organs and vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the function of bone in terms of locomotion?

A

joints to allow flexibility and attachment site of muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the function of bone in terms of haematopoeisis?

A

reservoir of stem cells forming blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the function of bone in terms of lipid and mineral storage?

A

adipose tissue stored within bone marrow

calcium stored within hydroxyapatite crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 5 types of bone?

A

flat

long

short

irregular

sesamoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the function of flat bones?

A

protect internal

organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are some examples of flat bones?

A

skull

thoracic cage

sternum

scapula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the function of long bones?

A

support and facilitate

movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are some examples of long bones?

A

humerus

radius

ulna

metacarpals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the function of short bones?

A

provide stability and some movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how can a short bone be described?

A

no diaphysis, as wide

as they are long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are some examples of short bones?

A

carpals

tarsals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how can irregular bones be described?

A

vary in shape and

structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are some examples of irregular bones?

A

vertebrae

sacrum

pelvis – pubic, ilium
or ischium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

where are sesamoid bones found?

A

embedded within tendons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the function of sesamoid bones?

A

potentially protect tendons from stress or wear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are some examples of sesamoid bones?

A

patella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how can a long bone be divided up?

A

epiphysis

metaphysis -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the epiphysis?

A

rounded end of bone, found at joint with adjacent bone

area of long bone where bone growth takes place from

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does the epiphysis grow?

A

grow from the epiphyseal plate and push new bone outward

ossifies separately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the structure of the epiphysis?

A

spongy (cancellous) bone

layers of compact (cortical) bone around it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the metaphysis?

A

neck portion of a long bone between the epiphysis and the diaphysis

contains the growth plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the function of the metaphysis?

A

transfer loads from weight-bearing joint surfaces to the diaphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the epiphyseal line?

A

epiphyseal plate that has ossified

divides diaphysis and epiphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the periosteum?

A

membrane on outer surface of long bones

covers all except areas surrounded by cartilage and where tendons and ligaments attach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the structure of the periosteum?

A

outer fibrous layer - collagen and reticular fibres

inner proliferative cambial layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the medullary cavity?

A

central cavity of bone shafts where red bone marrow (in children) and/or yellow bone marrow (adipose tissue) is stored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the structure of bone in the diaphysis?

A

yellow bone marrow in medullary cavity (lined by endosteum)

surrounded by compact (cortical) bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how can bone ultrastructure be divided into 2 categories?

A

woven (primary) bone

lamellar (secondary) bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how can woven (primary) bone be described?

A

first type of bone to be formed – in embryonic development and fracture healing

consists of osteoid, randomly arranged collagen fibres

temporary structure replaced by mature lamellar bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how can lamellar (secondary) bone be described?

A

bone of the adult skeleton

highly organised sheets of mineralised osteoid, making it much stronger than woven bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how can lamellar (secondary) bone be categorised?

A

compact (cortical)

spongy (cancellous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how is cortical (compact) bone structured?

A

found in the diaphysis, forms the outer part of bone

organised in concentric circles around a vertical Haversian canal

Haversian canal are connected by Volkmann’s canals which contain small vessels that also supply periosteum

osteocytes located between lamellae, within small cavities called lacunae - these
are interconnected by a series of tunnels called canaliculi.

entire structure is known as an osteon, the functional unit of bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how is cancellous (spongy) bone structured?

A

found in the epiphysis

irregular crosslinking of trabeculae to form porous yet strong bone resistant against multidirectional lines of force

large spaces between trabeculae giving it a honeycombed appearance

contains red bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the purpose of the extracellular matrix in bone?

A

provides biomechanical and structural support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the components of extracellular matrix in bone?

A

collagen – Type I (90%) and type V

mineral salts – calcium hydroxyapatite (70% of bone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

when does calcification of bone occur?

A

mineral salts interpose between collagen fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

when is the extracellular matrix known as osteoid?

A

before calcification (before mineral salts interpose between collagen fibres)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the function of osteoblasts?

A

synthesis uncalcified extracellular matrix (osteoid)

i.e. build bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how are osteocytes formed?

A

as osteoid mineralizes, osteoblasts are entombed between lamellae, becoming osteocytes

lay down concentric lamellae to form osteons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the function of osteocytes?

A

regulate bone mass by monitoring mineral and protein

content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are osteoclasts derived from?

A

monocytes

are multinucleate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the functions of osteoclasts?

A

resorb bone, multinucleate cells

release H+ ions

release lysosomal enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are osteoprogenitor cells?

A

undifferentiated stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how does bone’s blood supply compare to that of cartilage?

A

good compared to cartilage

nutrient arteries supplying diaphysis and meta/epiphyseal vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what are the two ways in which bone can grow?

A

endochondral (appositional)

intramembranous (interstitial)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

how does the bone grow (endochondral)?

A

formation of bone onto a temporary cartilage scaffold (e.g. hyaline cartilage replaced by
osteoblasts secreting osteoid in femur)

provides length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how does the bone grow (intramembranous)?

A

formation of bone directly onto fibrous connective tissue (e.g. temporal bone or scapula)

provides width

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

how is bone removed?

A

via osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

why is bone removal as part of turnover important?

A

essential for body’s metabolism

removal of bone increases calcium in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how is bone produced?

A

via osteoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what allows osteoblasts to synthesise bone matrix?

A 
receptors from:
- PTH
- prostaglandins
- vitamin D
- cytokines 
are activated

allows synthesis of bone matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how can the co ordinated action of osteoblasts and osteoclasts be described?

A

cutting cones that essentially drill through old bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

how can osteoporosis be described?

A

decrease in bone density, reducing

structural integrity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

why does osteoporosis occur (referring to bone cells)?

A

osteoclast activity > osteoblast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are the three types of osteoporosis?

A

postmenopausal

senile

secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what causes rickets (children)?

A

vitamin D or calcium deficiency in childhood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what causes osteomalacia?

A

vitamin D or calcium deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what mechanism causes rickets and osteomalacia?

A

osteoid mineralizes poorly, remains pliable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

how does rickets affect epiphyseal growth plates?

A

can become distorted under body weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what are the negative consequences of osteomalacia?

A

increased fracture risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what causes osteogenesis imperfecta?

A

rare genetic autosomal dominant inheritance

causes abnormal collagen synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are the negative consequences of osteogenesis imperfecta?

A

increased fragility of bones

bone deformities

blue sclera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what can osteogenesis imperfecta be misdiagnosed as and why is this important?

A

can be mistaken as NAD (non-accidental damage?) in children

diagnosis important medicolegally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is a fracture?

A

discontinuity of bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what are the four ways of describing a fracture?

A

orientation

location

displacement

skin penetration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what are the four types of fracture orientation?

A

transverse

oblique

spiral

comminuted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

how can a transverse fracture be described?

A

straight through the width of the bone (90 degrees to bone direction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

how can an oblique fracture be described?

A

diagonal across bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

how can a spiral fracture be described?

A

winds around bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

how can a comminuted fracture be described?

A

break or splinter of the bone into more than two fragments

“spiderweb” appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what are the three types of fracture location?

A

proximal third (epiphysis, metaphysis, beginning of diaphysis)

middle third (middle portion of diaphysis)

distal third (lower portion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what are the two categories of displacement in a fracture?

A

undisplaced (fracture ends line up)

displaced (movement of bone, fracture end do not line up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what are the two categories of skin penetration in a fracture?

A

open (bone end has gone through skin)

closed (bone end remains within skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

why are fractures classified?

A

improve communication of fractures (standardised)

assist with prognosis or treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what are some different classification systems of a fracture?

A

descriptive classification (e.g. Garden, Schatzker, Neer, Wber)

associated soft tissue injury (e.g. Tscherne in closed, Gustilo-Anderson in open)

universal classification (e.g. OTA classification - AO/OTA classification considers the bone, where the fracture is, the type, group and subgroup)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

how does primary (direct) bone healing occur?

A

intramembranous healing, occurs via Haversian remodeling

little (<500mm) or no gap

slow process

cutter cone concept – like bone remodelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what are the four steps of secondary (indirect) bone healing occur?

A

haematoma formation

soft callus formation

hard callus formation

remodelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

how does secondary (indirect) bone healing occur?

A

endochondral healing, involves responses in the periosteum and external soft tissues

fast process resulting in callus formation (fibrocartilage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what occurs during haematoma formation in secondary (indirect bone healing)?

A

damaged blood vessels bleed forming a haematoma

neutrophils release cytokines signalling macrophage recruitment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what occurs during soft callus formation in secondary (indirect bone healing)?

A

collagen and

fibrocartilage bridge the fracture site and new blood vessels form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what occurs during hard callus formation in secondary (indirect bone healing)?

A

osteoblasts, brought in by new blood vessels, mineralise the
fibrocartilage to produce woven bone (calcified matrix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what occurs during remodelling in secondary (indirect bone healing)?

A

months to years after
injury osteoclasts remove woven bone and osteoblasts laid down as ordered lamellar bone

medullary canal re-established

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what are the prerequisites for fracture healing?

A

minimal fracture gap

no movement if direct (primary) bony healing, some movement if indirect
(secondary) bone healing

patient physiological state – nutrients, growth factors, age, diabetic, smoker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what are the usual timeframes for fracture healing?

A

usually pre-defined timeframe, around 6 months

lower limb fractures take twice as long as upper limb fractures to heal

paediatric fractures heal twice as quickly as adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what does Wolff’s law state?

A

bone adapts to forces placed upon it by remodelling and

growing in response to these external stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

how should Wolff’s law be applied if a child’s femur heals bent?

A

axial loading should be direct, with
remodelling occurring through axial loading

periosteum on the concave side will make more bone while on the convex
side, bone will be resorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what are the six types of fracture healing complication?

A

malunion

atrophic non-union

oligotrophic non-union

hypertrophic non-union (horse hoof)

hypertrophic non-union (elephant foot)

pseudoarthrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what is a fracture malunion?

A

bone healing occurs but outside of the normal parameters of

alignment (i.e. ends don’t line up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what is a fracture non-union?

A

failure of bone healing within an expected time frame

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what is an atrophic non-union in fracture healing?

A

healing completely
stopped with no XR changes, often physiological

caused by inadequate immobilization and inadequate blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is a hypertrophic non-union in fracture healing?

A

too much movement, causing callus healing

caused by inadequate stability with adequate blood supply and biology

abundant callous formation without bridging bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what are the four R’s in fracture management?

A

resuscitate - save the patients life, then worry about the fracture

reduce – bring the bone back together in an acceptable alignment

rest/restrict – maintain reduction to prevent distortion or movement, provide stability

rehabilitate - get function back and avoid stiffness (use, move, strengthen, weight bear)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what three things should be considered when assessing period of immobility in fracture healing?

A

functional limitations and support needed

wider MDT

thromboembolism prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what are three forms of conservative fracture management?

A

rest, ice, elevation

plaster/fibreglass cast or splint

traction - skin/bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what are some forms of surgical fracture management?

A

external fixation

  • mono/biplanar
  • multiplanar - ring

arthroplasty

  • hemiarthroplasty
  • total joint replacement

ORIF (open reduction internal fixation) - open leg and move bone into optimal healing position using screws, rods etc.

intramedullary nail

MUA + K-wire (manipulation under anaesthetic and Kirschner wire) - bones moved into optimal healing position and (if unstable) wires are used to keep it in place (otherwise a cast is used)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

how is a fracture diagnosed?

A

history and examination – tenderness/limb
pain/swelling

obtain X-ray of affected region, ensure in at least two
planes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what is a six step approach to orthopaedic x-rays?

A

projection

patient details

technical adequacy

obvious abnormalities

systematically review the X-ray

summarise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

how is projection approached in orthopaedic x-rays?

A

any assessment of a bone or
joint generally requires at
least two views

for other sites where
fractures may be difficult to detect more than two views may be needed e.g. scaphoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

how are patient details approached in orthopaedic x-rays?

A

always check you are looking at the
correct X-ray for the correct patient

double check as often names can be
similar and correlate with DOB and
NHS/Hospital number

state the name, age, and date X-ray was
taken

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

how is technical adequacy approached in orthopaedic x-rays?

A

entire area in question should be included

is the exposure adequate to ensure differentiation of soft
tissues and bone?

is there rotation? does it complicate diagnosis?

do you need a full length X-ray or imaging of the joint
above and below?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

how are obvious abnormalities approached in orthopaedic x-rays?

A

is there anything obviously wrong that
stands out?

if there is an obvious abnormality,
comment on it before moving on

is there an obvious fracture, subluxation
or dislocation? can you see a bone lesion?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

how is a systematic review of x-ray approached in orthopaedic x-rays?

A

look around all edges of bones – should be smooth, any
disruption could represent a fracture

look at medulla for disruption to trabeculae or lines of lucency/sclerosis

assess for soft tissue swelling or joint effusions which
could be indirect evidence of fractures

look at joint surfaces for any evidence of subluxation or
dislocation

look at bone density and assess for degenerative changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

how is a summary approached in orthopaedic x-rays?

A

state key findings

describe fracture

suggest further investigations or management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what is the presentation of a shoulder dislocation?

A

variable history but often direct trauma

pain

restricted movement

loss of normal shoulder contour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

what clinical examination should be done for a shoulder dislocation?

A

assess neurovascular status – axillary nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

what investigations should be done for a shoulder dislocation?

A

X-ray prior to any manipulation – identify fracture e.g. humeral neck, greater tuberosity avulsion or glenoid

scapular-Y view/modified axillary in addition to AP (anterior-posterior)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what are the three types of shoulder dislocation?

A

anterior

posterior

inferior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

how is an anterior shoulder dislocation described?

A

commonest type (~90%)

bimodal distribution

humeral head not overlying glenoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

how is an posterior shoulder dislocation described?

A

rare (~6%)

associated with seizures/shocks

‘lightbulb sign’ on x-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

how is an inferior shoulder dislocation described?

A

rare (<2-4%)

arm held abducted above head

humeral head not articulating correctly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

how is a shoulder dislocation management undertaken?

A

( avoid vigorous or twisting manipulation
to avoid fractures)

safest method is to use traction-counter traction +/- gentle internal rotation to disimpact humeral head

ensure adequate patient relaxation – Entonox; benzodiazepines

if alone could use Stimson method

undertake in safe environment, especially in elderly e.g. resus, ask
for senior/anaesthetic support early on if necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

what are some complications of shoulder dislocation?

A

neurovascular

damage to labrum and/or glenoid

damage to humeral head

recurrent dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

how can neurovascular complications of shoulder dislocation occur?

A

at time of presentation due to trauma sustained e.g. axillary nerve injury

iatrogenic as a result of reduction manoeuvre

delayed onset due to an evolving haematoma post injury/manipulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

how can damage to the labrum and/or glenoid occur as a complication of shoulder dislocation?

A

Bankart lesion – soft or bony (inside of head)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

how can damage to the humeral head occur as a complication of shoulder dislocation?

A

Hill-Sachs lesion (outer edge of head)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

how can recurrent dislocations occur as a complication of shoulder dislocation?

A

lifetime risk increases i.e. younger the patient, the greater the risk of repeat dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what is the presentation of a proximal humerus fracture?

A

fall onto an outstretched hand

typically in the elderly or those with osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what investigations should be done for a proximal humerus fracture?

A

plain x-rays

CT if concern over articular involvement or high degrees of comminution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

how are proximal humerus fractures classified?

A

described by Neer

2 part - surgical neck fractures, avulsion fractures of greater tuberosity

comminuted fractures (>3 parts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

how is a 2 part proximal humerus fracture with minimal displacement managed?

A

collar and cuff

high surgical risk / comorbidities

compliant with post-operative care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

how is any proximal humerus fracture with displacement but not highly comminuted managed?

A

ORIF - plate and screws

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

how is a humeral head fracture with large displacement treated?

A

arthroplasty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

why is an arthroplasty used to manage a humeral head fracture with large displacement?

A

high risk of non-union

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

when is a reverse arthroplasty used (proximal humerus fracture) ?

A

unrepairable rotator cuff

previous unsuccessful shoulder replacement

complex fracture/chronic shoulder dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what is the presentation of a distal radius fracture?

A

very common, bimodal distribution

often present with clear mechanism of falling onto affected area, swelling and visible deformity

commonest presentation is dorsal displacement due to fall on outstretched hand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

what investigations are done for a distal radius fracture?

A

plain radiographs

PA/lateral views to assess fracture type

thorough clinical examination to avoid concomitant injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

what is an extra articular fracture?

A

break above wrist joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what are the two types of extra articular fracture?

A

dorsal angulation - Colles fracture

volar angulation - Smith fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what is an intra articular fracture?

A

break within wrist joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what are the two types of intra articular fracture?

A

dorsal angulation - Dorsal Barton

volar angulation - Volar/Reverse Barton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

how is a cast/splint used in management of distal radius fractures?

A

temporary treatment for any distal radius fracture – reduction of fracture and placement into cast until definitive fixation

definitive if minimally displaced, extra
articular fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

when is an MUA with K wires (manipulation under anaesthetic with Kirschner wires) used in management of distal radius fractures?

A

for fractures that are extra articular but have instability (particularly in children)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

how are K wires removed?

A

in clinic post-op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

when is an ORIF (open reduction internal fixation) used in management of distal radius fractures?

A

any displaced, unstable fractures
not suitable for K-wires

or with intra-articular involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what is the goal of operative management in distal radius fractures?

A

restore articular surface congruency

radial inclination 22º

radial height 11 mm

volar tilt 11º

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what are the eight carpal bones of the wrist?

A

first row (lateral to medial) - scaphoid, lunate, triquetrum, pisiform

second row (lateral to medial) - trapezium, trapezoid, capitate, hamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what is the presentation of scaphoid fractures?

A

commonest carpal bone injury, usually young patients

typically a fall backwards onto their hand, but think in any distal radius

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what clinical examinations should be done in scaphoid fractures?

A

anyone with FOOSH or with distal radius fracture should have scaphoid exam

palpation of anatomical snuffbox, scaphoid tubercle or telescoping of thumb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what investigations should be done in scaphoid fractures?

A

plain radiographs difficult to assess – request scaphoid views

delayed radiographs if normal but clinical suspicion

consider CT/MRI if still concerned

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

how is a displaced scaphoid fracture managed?

A

retrograde blood supply means high risk of non-union/avascular necrosis of proximal pole

most displaced fractures disrupt this and therefore ORIF usually undertaken

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

how is an undisplaced scaphoid fracture managed?

A

can be treated conservatively in a scaphoid cast

length of time to heal can be long, some surgeons opt for fixation as a result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what causes perilunate instability?

A

disruption to any of the ligament complexes

that surround the lunate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

what is the difference between perilunate and lunate dislocation?

A

perilunate - articulation with radius and surrounding carpal bones (scaphoid, triquetrum, capitate and hamate) is maintained

in lunate dislocation it is not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what group of injuries does perilunate dislocation belong to?

A

perilunate instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

how can a perilunate dislocation be seen on an x-ray?

A

normal: radius, lunate and capitate in straight line in lateral view

perilunate dislocation: radius and lunate in line with thumb, capitate in line with fingers in lateral view

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

how can a lunate dislocation be seen on an x-ray?

A

normal: radius, lunate and capitate in straight line in lateral view

lunate dislocation: radius and capitate in line with fingers in lateral view

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

what are the four stages of perilunate dislocation?

A

scapho-lunate dissociation

lunocapitate disruption

lunotriqeutral disruption

lunate dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what occurs in scapho-lunate dissociation (stage 1 of perilunate dislocation)?

A

widening of scaphoid and lunate due to scapholunate ligament

disruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what occurs in lunocapitate disruption (stage 2 of perilunate dislocation)?

A

lunate remains normally aligned with
distal radius, remaining carpal bones
dislocated

capitate and lunate widening

high association with scaphoid fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what occurs in lunotriqeutral disruption (stage 3 of perilunate dislocation)?

A

capitate and lunate are not aligned
with distal radius

lunate-triquestral ligament disrupted

high association with triquetral fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what occurs in lunate dislocation (stage 4 of perilunate dislocation)?

A

dislocation of lunate with a ‘tipped’
teacup’ sign

dorsal radiolunate ligament injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

how is perilunate instability managed non-operatively?

A

closed reduction and casting has no indication and often poor outcomes compared to non- operative management

high risk of recurrent dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

how is acute perilunate instability (< 8 weeks) managed operatively?

A

ORIF, ligament repair and fixation

good functional outcomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

how is non-acute perilunate instability (> 8 weeks) managed operatively?

A

proximal row carpectomy (converts wrist into simple hinge type)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

how are chronic injuries in perilunate instability managed operatively?

A

arthodesis of wrist

pain reduction especially if degenerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

what is the presentation of pelvic fractures?

A

usually a result of high energy trauma

patients can become very unstable – a lot of visceral organs and vasculature are adherent to the pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what examinations are done in pelvic fractures?

A

ABCDE approach -examine the perineam/urethral opening

digitate – vaginal or rectal examinations – check for visceral damage or bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

what investigations are done in pelvic fractures?

A

plain radiographs

urethrogram

CT +/- angiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

what are the three pelvic fracture classifications?

A

lateral compression

anterior-posterior compression

vertical shear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

how are pelvic fractures managed?

A

advanced trauma life support (ATLS) and ABCDE principles

address hypovolaemia (common)

definitive treatment via a specialist centre with pelvic surgeons

principle to restore integrity of pelvic ring and alignment of sacroiliac joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

how is the integrity of pelvic ring and alignment of sacroiliac joints restored in pelvic fractures?

A

internal fixation with plate and screws

external fixation if patient unstable and not suitable for invasive surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

how is hypovolaemia addressed (in pelvic fractures)?

A

IV access and resuscitate the patient, think of major haemorrhage protocols early

pelvic binders are use as a tamponade device but need to be placed accurately (over greater trochanters)

ongoing instability should suggest laparotomy or angiographic embolisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

what is the usual cause of a proximal femur/neck of femur fracture in young people?

A

high energy major trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

how are proximal femur/neck of femur fractures pathological?

A

result of osteoporosis and minimal trauma in elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

what are the general features of a proximal femur/neck of femur fracture history?

A

often a fairly inconspicuous history of a minor fall

may report groin, thigh or buttock pain

ask about preceding symptoms, always think of pathological causes for a fall (e.g. MI, TIA/stroke, seizure)

ask about comorbidity

pre-injury mobility

social history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

what examinations are done for a proximal femur/neck of femur fracture?

A

MSK – look, feel, move

thorough secondary survey and top-to-toe examination to look for other injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

what investigations are done for a proximal femur/neck of femur fracture?

A

plain radiographs

CT if not identified but high suspicion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

what is the initial emergency department management for proximal femur/neck of femur fractures?

A

rule out any other injury/pathology causing fall

involvement of orthogeriatricians/medical team early

pain relief – consider fascia iliaca block in ED if necessary

catheterise – limited mobility

blood tests

ECG/Chest X-ray if >55

pre-operative optimisation – fluids, transfusion?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

what is the general guidance for management of patients with suspected proximal femur/neck of femur fractures?

A

ambulance

  • Entonox PRN via mask/mouthpiece
  • gain IV access if possible

A&E

  • paracetamol +- NSAID
  • morphine orally or IV (avoid IM if possible)
  • ensure IV route available: start IV fluids 1l NaCl in 10 hrs
  • take history
  • x-ray
  • hourly pain scores (further analgesia if needed)
  • if fracture confirmed consider fascia iliaca block, admit to ward give oxygen)

arrival at ward

  • pain score, analgesia if needed
  • check IV fluids

until surgery and post-op

  • 4 hourly pain scores (further analgesia if needed)
  • if pain unresolved in 4 hours call pain team
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

what are the three types of intracapsular fracture?

A

subcapital (femoral head and neck)

transcervical (midportion of femoral neck)

basicervical (base of femoral neck)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

what are the three types of extracapsular fracture?

A

intertrochanteric (between greater and lesser trochanter)

subtrochanteric (between the lesser trochanter and the femoral isthmus, proximal part of the femoral shaft)

reverse oblique (from lesser trochanteric to lateral edge of femur, parallel to neck)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

what are the three types of intracapsular treatment?

A

total hip arthroplasty

hemiarthroplasty

cannulated screws

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

what are the two types of extracapsular treatment?

A

dynamic hip screw

intramedullary nail

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

what factors are prerequisites for a total hip arthroplasty?

A

mobile with <1 walking
stick outdoors

no cognitive
impairment

medically suitable for
procedure and
anaesthetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

what factors are prerequisites for a hemiarthroplasty?

A

mobile with >1
walking stick
outdoors

reduced AMTS (abbreviated mental test score)

comorbidities or
reduced baseline not
benefiting from THR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

what factors are prerequisites for cannulated screws?

A

undisplaced fractures
where vessels unlikely
to be disrupted

young patients

compliant with nonweightbearing while
fracture heals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

when is a dynamic hip screw used?

A

for 2-4 part intertrochanteric fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

what is the benefit of a dynamic hip screw?

A 
provides
compression as
prosthesis is
perpendicular to
fracture line
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

why are intramedullary nails used?

A

subtrochanteric
fractures are unstable
due to pull of hip girdle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

why are reverse oblique fractures not amenable to dynamic hip screws?

A

fracture line not perpendicular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

what healthcare professionals need to be present for a post-op proximal femur/neck of femur fracture MDT?

A

geriatrician

physiotherapy

occupational therapy/social worker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

what is the role of a geriatrician post-op for proximal femur/neck of femur fracture?

A

bone health

medical optimisation

secondary fall prevention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

what is the role of a physiotherapist post-op for proximal femur/neck of femur fracture?

A

prevent leading causes of death (HAI, deep vein thrombosis, pulmonary embolism) by early mobilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

what is the role of an occupational therapist/social worker post-op for proximal femur/neck of femur fracture?

A

help with post-operative care needs, package of care and assistance or aids at home

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

why is a femoral shaft fracture concerning?

A

significant force required to fracture it (largest bone)

high incidence of concomitant life threatening injuries can exist

(assess using ABCDE and advanced trauma life support (ATLS))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

what should a clinical examination include in a femoral shaft fracture?

A

assessment of neurovascular status of affected limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

what x-rays should be taken of a femoral shaft fracture (and any diaphyseal injury)?

A

x-ray joints above and below to look for fractures or dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

what steps are taken for management of a femoral shaft fracture?

A

resuscitate patients as necessary (hypovolaemia is common as long
bone fractures can bleed a lot)

traction is useful in the first instance as a way of temporarily reducing both pain and bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

what are the two operative options for a femoral shaft fracture?

A

intramedullary nail

ORIF (open reduction and internal fixation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

how is intramedullary nailing used in treatment of a femoral shaft fracture?

A

can be either antegrade (from the hip) or retrograde (from the knee)

depends on:

  • surgeon preference
  • injury pattern
  • existing prostheses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

when is ORIF (open reduction and internal fixation) used in treatment of a femoral shaft fracture?

A

used if nailing unsuitable (e.g. a segmental

fracture, knee or hip replacements)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

why is the proximal tibia important?

A

key weightbearing surface as part of knee joint, articulating with the distal femur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

how can the tibial joint surface be described?

A

relatively flat

comprises both medial and lateral
plateaus

central tibial spine acting as an insertion point for ligaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

how is a tibial plateau fracture caused?

A

extreme valgus/varus force or axial loading across the knee

impaction of the femoral condyles causes the
comparatively soft bone of the tibial plateau to depress or split

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

what injuries are not uncommon with a tibial plateau fracture?

A

concomitant ligamentous or meniscal injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

what are the three types of lateral tibial plateau fracture?

A

type 1 - split

type 2 - split and depression

type 3 - depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

what is the one type of medial tibial plateau fracture?

A

type 4 - medial plateau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

what are the two types of medial and lateral tibial plateau fracture?

A

type 5 - bicondylar

type 6 - metaphyseal-diaphyseal dissociation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

what kind of tibial plateau fractures can be managed non-operatively?

A

only truly undisplaced fractures with good joint line congruency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

how can a tibial plateau fracture be assessed for non-operative management?

A

assessed on CT or

high fidelity imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

how is a tibial plateau fracture managed operatively?

A

restoration of articular surface using combination of plate and screws

bone graft or cement may be necessary to prevent further depression after fixation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

what is the ankle joint comprised of?

A

talus articulating with tibia and fibia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

what two things provide joint stability necessary for function in the ankle joint?

A

ligaments

bone projections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

which ligaments provide joint stability necessary for function in the ankle joint?

A

medially: talofibular and calcaneofibular ligaments
laterally: deltoid ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

which bone projections provide joint stability necessary for function in the ankle joint?

A

medially: medial malleolus of tibia
laterally: lateral malleolus of fibula
posteriorly: posterior malleolus of tibia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

how can an ankle fracture occur?

A

with twisting or axial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

what are two common presenting features of an ankle fracture?

A

extensive soft tissue swelling

inability to weightbear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

what does a clinical examination assess in an ankle fracture?

A

identify tenderness over ligament complexes

for assessing stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

what does an x-ray assess in an ankle fracture?

A

to ascertain talar shift

for assessing stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

how are ankle fractures classified?

A

Weber A-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

what are the features of a Weber A fracture?

A

occur below the level of the syndesmosis

ligament disruption and joint stability unlikely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

what are the features of a Weber B fracture?

A

occur at the level of
the syndesmosis

ligament
disruption and joint stability possible (stress testing or weightbearing
assessment for talar shift necessary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

what are the features of a Weber C fracture?

A

occur above the level of the syndesmosis

ligament disruption and
joint instability likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

how is an ankle fracture managed non-operatively?

A

non-weightbearing below knee cast for 6-8 weeks

can transfer into walking boot

physiotherapy to improve range of motion/stiffness from joint isolation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

when is an ankle fracture managed non-operatively?

A

Weber A (i.e. below syndesmosis and therefore thought to be stable)

Weber B - if no evidence of instability (no medial/posterior malleolus fracture and no talar shift)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

when is an ankle fracture managed operatively?

A

Weber B (unstable fractures – talar shift/medial or posterior malleoli fractures)

Weber C i.e. fibular fracture above the level of the syndesmosis therefore unstable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

what does an operative procedure in ankle fracture management require?

A

soft tissue dependent – patients need strict elevation as injuries often swell considerably

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

how is an ankle fracture managed operatively?

A

ORIF (open reduction internal fixation)

with or without syndesmosis repair (using screw or tightrope technique)

syndesmosis screws can be left in situ but may break after some time so therefore can be removed at a later date if necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

what is a Maisonneuve fracture?

A

spiral fracture of the proximal third of the fibula

associated with a tear of the distal tibiofibular syndesmosis and the interosseous membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

what causes a Maisonneuve fracture?

A

twisting injury disrupts syndesmosis

causes a high fibula fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

what should be checked for in ankle fractures during clinical examination?

A

proximal tenderness (Maisonneuve fracture)

patients may have distracting pain of ankle fracture and be unaware

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

what should be checked if there is widening of the syndesmosis on radiographs but no obvious fibula
fracture?

A

Maisonneuve fracture – energy has to dissipate

somewhere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

what kind of x-rays should be taken for a Maisonneuve fracture?

A

long length x-rays to visualise the full fibula and ensure no missed fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

what are the key differences between a child and adult skeleton?

A

child - 270 bones, continuously changing

physis - one on proximal and distal end of long bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

what are the physis?

A

growth plates

areas from which long bone growth occurs post-natally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

what 2 pathways can bone development be broadly differentiated into?

A

intramembranous to produce flat bones (cranial bones, clavicle) (mesenchymal cells>bone)

endochondral for long bones (mesenchymal cells > cartilage > bone)

231
Q

what is the process of intramembranous ossification (flat bones)?

A

condensation of mesenchymal cells which differentiate into osteoblasts – ossification centre forms

secreted osteoid traps osteoblasts which become osteocytes

trabecular matrix and periosteum form

compact bone develops superficial to cancellous bone - crowded blood vessels condense into red bone marrow

232
Q

what are primary ossification centres?

A

sites of pre-natal bone growth through endochondral ossification from the central part of the bone

233
Q

what are secondary ossification centres?

A

occurs post-natal after the primary ossification centre

long bones often have several (the physis)

234
Q

what are the 2 parts of endochondral ossification?

A

primary ossification - central part of diaphysis (prenatal bone growth)

secondary ossification - physis grow to form long bones (post natal)

235
Q

what is the process of primary ossification in endochondral bone?

A

mesenchymal differentiation at primary centre

cartilage model of the future bony skeleton forms

capillaries penetrate cartilage, calcification at the primary ossification centre – spongy bone forms, perichondrium transforms into periosteum

cartilage and chondrocytes continue to grow at ends of the bone

secondary ossification centres develop with own blood

236
Q

what is the main difference between endochondral and intramembranous ossification?

A

endochondral involves cartilage before bone

237
Q

what do the physis contain?

A

cartilage

238
Q

how does the epiphyseal side of the physis allow bone elongation?

A

hyaline cartilage active and dividing to form hyaline cartilage matrix

239
Q

how does the diaphyseal side of the physis allow bone elongation?

A

cartilage calcifies and dies, then replaced by bone

240
Q

what kind of events may impact the growth of a child?

A

damage to physis

traumatic, infective etc.

241
Q

what are the 4 main ways in which children’s skeleton differs to that of adults?

A

more elasticity

physis (i.e. bone growth)

speed of healing (due to continued growth)

remodelling (greater remodelling potential due to growth, can tolerate lots of deformity and angulation)

242
Q

why are children’s bones more elastic than adults?

A

increased density of Haversian canals

243
Q

why do children have increased density of Haversian canals?

A

bones more metabolically active (continuously growing)

244
Q

how do children’s bones break differently?

A

plastic deformity (bends before breaking)

245
Q

how is a buckle fracture caused?

A

child may fall onto outstretched hand

instead of the bone fracturing it buckles in on itself

creates Tarus like structure (roman column)

246
Q

what is a greenstick injury?

A

(in children)

one side buckles and bends, the other snaps

247
Q

when does growth stop in children?

A

growth occurs at varying rates at varying sites

growth stops as the physis closes

248
Q

what factors affect the closure of the physis?

A

puberty

menarche in girls

parental height (other genetic factors)

249
Q

when do the physis close?

A

girls - 15-16 years

boys - 18-19 years

250
Q

what can physeal injuries lead to?

A

growth arrest

growth arrest can lead to deformity (e.g. if only part of the physis cannot grow)

251
Q

what do the speed of healing and remodelling potential depend on?

A

location of injury

age of patient (younger child heals quicker as growing more rapidly)

252
Q

how does the rate of growth vary from physis to physis?

A

upper limb - around the shoulder and the wrist have faster growth rates

lower limb - knee has faster growth rates (distal femur, proximal tibia)

253
Q

what are 4 common children’s congenital conditions?

A

developmental dysplasia of the hip

club foot

achondroplasia

osteogenesis imperfecta

254
Q

what is developmental dysplasia of the hip (DDH)?

A

disorder of the neonatal hip

head of the femur is unstable or incongruous in relation to the acetabulum

255
Q

what causes developmental dysplasia of the hip (DDH)?

A

occurs when child is in the mother’s womb (“packaging disorder”), usually due to the way that the child sits

affects hip positioning in acetabulum and normal hip development

256
Q

how does developmental dysplasia of the hip (DDH) affect development of the acetabulum and hip?

A

acetabulum relies on concentric reduction and balance forces

hip needs to sit within the acetabulum and have the normal forces going through the joint

neither hip nor acetabulum develop properly

257
Q

what is the spectrum of developmental dysplasia of the hip (DDH) conditions?

A

dysplasia (most common, 2:100)

subluxation

dislocation (least common, 2:1000)

258
Q

what is dysplasia in developmental dysplasia of the hip (DDH)?

A

hip may be within the socket, but not centrally placed

socket does not develop into cup

259
Q

what is subluxation in developmental dysplasia of the hip (DDH)?

A

hip is in socket

however due to the shallow nature of the socket hip will pop in and out

260
Q

what is dislocation in developmental dysplasia of the hip (DDH)?

A

packaging disorder been so severe that the hip has never been inside the socket (develops outside)

therefore socket has very shallow cup

261
Q

what are the risk factors for developmental dysplasia of the hip (DDH)?

A

female 6:1

first born

breech

FHx

oligohydramnios (not enough fluid within the amniotic sac)

262
Q

in which populations is developmental dysplasia of the hip (DDH) more common?

A

Native American populations and Laplanders

due to the habit of swaddling of the hip

263
Q

how is developmental dysplasia of the hip (DDH) examined for?

A

usually picked up on newborn baby check – screening

range of motion in the hip examined

  • usually limitation in hip abduction
  • leg length (Galeazzi test)

3 months or older -Barlow and Ortalani tests are non-sensitive

264
Q

how is developmental dysplasia of the hip (DDH) investigated?

A

ultrasound – birth to 4 months

after 4 months - x-ray

prior to 6 weeks -needs to be age adjusted (abnormal examinations in premature children)

measures acetabular dysplasia and the position of hip

265
Q

why is an x-ray only used after 4 months of age?

A

no benefit prior to this

secondary ossification centres of the hip have not yet ossified

266
Q

how is developmental dysplasia of the hip (DDH) usually treated?

A

Pavlik harness

holds leg flexed and abducted to hold femoral head within the acetabulum (concentric pressures through the hip joint for normal development)

267
Q

when is a Pavlik harness used to treat developmental dysplasia of the hip (DDH)?

A

reducible hip

<6 months old

268
Q

what treatment is used if a Pavlik harness fails/abnormality is picked up late?

A

MUA (manipulation under anaesthetic) + closed reduction and Spica

269
Q

when is surgery used to treat developmental dysplasia of the hip (DDH)?

A

failed Pavlik harness

6-18 months (secondary changes to capsule + soft tissue)

270
Q

what is congenital Talipes Equinovarus?

A

congenital deformity of the foot (“club foot”)

271
Q

who is most likely to suffer from congenital Talipes Equinovarus?

A

1:1000

highest in Hawaiians

M2:1F

50% are bilateral

272
Q

how does genetics affect congenital Talipes Equinovarus?

A

genetic link (PITX1 gene)

approx. 5% likely of future siblings

familial in 25%

273
Q

what are the 4 aspects of a congenital Talipes Equinovarus deformity?

A

cavus – high arch: tight intrinsic flexor halluxes longus and flexor digitorum longus

adductus of foot: tight tibia posterior and anterior

varus: tight tendoachilles, tibia posterior and anterior
equinous: tight tendoachilles

274
Q

what is the ideal method of treatment to correct congenital Talipes Equinovarus?

A

Ponseti Method

1 - series of casts to correct deformity

2- many require operative treatment (usually just soft tissue releases)

3 - foot orthosis brace

4 - some will require further operative intervention to correct final deformity (e.g. further soft tissue releases, significant operative interventions such as tendon transfers)

275
Q

what is achondroplasia?

A

abnormality in the proliferation zone of the physis (inhibition of chondrocyte proliferation )

defective endochondral bone formation (secondary endochondral ossification)

276
Q

what causes achondroplasia?

A

autosomal dominant

G380 mutation of the FGFR3

277
Q

what is the usual deformity that is seen in achondroplasia?

A

Rhizomelic dwarfism

  • humerus shorter than forearm
  • femur shorter than tibia
  • normal trunk
  • adult height -approx. 125cm
  • usually causes significant spinal issues
278
Q

what is osteogenesis imperfecta?

A

brittle bone disease

279
Q

what causes osteogenesis imperfecta?

A

hereditary – autosomal dominant or recessive

decreased Type I collagen due to:

  • decreased secretion
  • production of abnormal collagen

insufficient osteoid production

280
Q

what are the orthopaedic effects of osteogenesis imperfecta?

A

fragility fractures
- prone to multiple fractures

short stature

scoliosis (other spinal manifestions)

281
Q

what are the non-orthopaedic effects of osteogenesis imperfecta?

A

cardiac issues

blue sclera

dentinogenesis imperfecta – brown soft teeth

Wormian skull (abnormal fusion of cranial sutures)

hypermetabolism (typically affects parathyroid pathway)

282
Q

how can fractures be described?

A

pattern

anatomy

intra/extra articular

displacement

283
Q

what is Salter-Harris classification?

A

classification of physis fracture in children

284
Q

what is an avulsion fracture?

A

bone has been pulled off by its ligamentous attachment

285
Q

what are the 4 types of displacement?

A

displaced (ends move away from each other)

angulated (both parts at an angle to each other)

shortened (ends move towards each other)

rotated

286
Q

why is primary bone healing preferred in intra articular fracture?

A

minimises risk of post traumatic arthritis

287
Q

what is important to consider when describing a fracture in children?

A

both proximal and distal bone have secondary ossification centres (physis) - location

different fracture patterns (plastic deformity)

faster healing potential and remodelling potential (more allowance in displacement, shortening, angulation)

288
Q

what is type 1 Salter-Harris physeal injury?

A

physeal separation (injury goes straight through physis)

289
Q

what is type 2 Salter-Harris physeal injury (most common)?

A

fracture transverses through physis

exits above physis or through metaphysis

290
Q

what is type 3 Salter-Harris physeal injury?

A

fracture traverses physis

exits epiphysis

291
Q

what is type 4 Salter-Harris physeal injury?

A

fracture passes through epiphysis, physis, metaphysis

292
Q

what is type 5 Salter-Harris physeal injury?

A

crush injury to physis

293
Q

how does risk increase by Salter-Harris classification?

A

risk of growth arrest increases from 1 -5

294
Q

how can the effects of physeal injury vary between younger and older children?

A

closer to physeal closure (older) - only small amount of potential growth left (growth arrest less concerning)

potential for growth arrest in young children is greater

295
Q

what does injury to the whole physis cause in terms of growth arrest?

A

limb length discrepancy

296
Q

what does partial injury to the physis cause in terms of growth arrest?

A

angulation

non affected side keeps growing

297
Q

what are the aims of treatment of growth arrest?

A

correct deformity

minimise limb length discrepancy or angulation

298
Q

what are the 2 methods of limb length correction?

A

shorten the long side

lengthen the short side

299
Q

how does shortening the long side correct limb length?

A

prematurely stop growth of unaffected side to balance limb length

300
Q

how can the long side be shortened in limb length correction?

A

prematurely fused physis of bone using crossed screws

301
Q

how can the short side be lengthened in limb length correction?

A

intra-medullary device that is a limb lengthening device

302
Q

what are the 2 methods of correcting angular deformity?

A

stop the growth of the unaffected side

reform the bone (osteotomy)

303
Q

what must be considered in paediatric reduction of bone?

A

plastic deformity/increased elasticity of bone

consider soft tissue injuries and neurovascular structures that might be affected by energy dissipation during fracture

304
Q

why are closed reduction techniques (traction, manipulation in A&E) more common in children?

A

greater remodelling potential

305
Q

what is the principle behind gallows traction?

A

skin traction applied to femur with a weight

hold the long bones of the lower limb whilst the fracture heals

306
Q

what is an issue with healing in younger children?

A

overgrowth, too much healing

307
Q

what are the external methods of restricting a fracture?

A

e.g. splints, plaster

308
Q

what are the internal methods of restricting a fracture?

A

e.g. plate and screws, intramedullary nail

309
Q

what methods of restriction are more common in paediatric orthopaedics?

A

external (more remodelling capacity - operations can be avoided)

310
Q

what is a Spica cast?

A

used in very young children

holds lower limbs in place

311
Q

when are operative interventions more likely to be required in paediatric orthopaedics?

A

fracture affects the physis

correct potential deformity

(metalwork will likely need to be removed later due to growth)

312
Q

what is the principle of using flexible titanium nails to treat fractures?

A

slightly elastic, help tension through intraosseous membrane to hold reduction in place

allow primary bone healing

313
Q

what are 4 differentials for a limp in children?

A

septic arthritis

transient synovitis

perthes

SUFE

314
Q

what is septic arthritis?

A

bacterial infection in intra articular space of the joint

can cause irreversible long term damage to a joint

315
Q

how does septic arthritis cause irreversible long term damage to a joint?

A

necrosing effect of proteases that are created within the joint itself

pressure effect from chondrocytes and cartilage due to oedema within closed space

316
Q

how is septic arthritis managed?

A

surgical wash out (lavage) of the joint to clear the infection

antibiotics

(immobilise joint in acute phase, physiotherapy if necessary)

317
Q

why is septic arthritis so problematic?

A

sometimes challenging and difficult to diagnose

318
Q

how is probability of septic arthritis classified?

A

Kocher’s classification

319
Q

what aspects of a history are important in diagnosis of septic arthritis?

A

duration (chronic vs acute?)

other recent illness

associated joint pain

any other symptoms e.g. rashes, vomiting, diarrhoea

320
Q

what is a typical septic arthritis history?

A

child previously fit and well

gone off food and drink over the last 24-48 hours

does not want to move knee and hip

321
Q

what are the 4 criteria in Kocher’s classification for septic arthritis?

A

non weight bearing

ESR > 40

WBC > 12,000

temperature > 38

(more categories = increased likelihood)

322
Q

what is a key differential for septic arthritis (or a diagnosis once septic arthritis is excluded)?

A

transient synovitis

323
Q

what is transient synovitis?

A

inflamed joint in response to a systemic illness (usually coryzal)

324
Q

how is transient synovitis treated?

A

supportive measures e.g. fluids, observation and antibiotics

325
Q

what is Perthes disease?

A

idiopathic necrosis of proximal femoral epiphysis

326
Q

in which populations is Perthes disease more likely?

A

usually in those 4-8 years old

male 4:1 female

327
Q

what are the key differences between Perthes disease and septic arthritis?

A

Perthes more chronic than septic arthritis (and transient synovitis)

no temperature or inflammatory markers

(must exclude septic arthritis first)

328
Q

what is the key diagnostic test for Perthes disease?

A

plain film radiograph

epiphysis is not as symmetrical and well-formed as the other side

329
Q

how is Perthes disease managed/treated?

A

supportive

referral for continued observation and management

330
Q

what is SUFE (slipped upper femoral epiphysis)?

A

proximal epiphysis slips in relation to the metaphysis

331
Q

in which populations is SUFE (slipped upper femoral epiphysis) more likely?

A

usually obese adolescent male

12-13 years old during rapid growth

332
Q

what are risk factors for SUFE (slipped upper femoral epiphysis)?

A

FHx

underlying endocrine disorder (hypothyroidism, hypopituitarism)

333
Q

how is SUFE (slipped upper femoral epiphysis) differentiated from septic arthritis?

A

no temperature or raised biochemical markers

334
Q

how can the presentation of SUFE be broadly differentiated?

A

chronic vs acute

(can be both -episodes of pain and limping in the past, now worsened)

classification to assess weight bearing

335
Q

what is non-specific low back pain?

A

pain not due to anyspecificor underlying disease that can be found

(investigations must be done to try and find underlying cause)

336
Q

what is mechanical low back pain?

A

painafter abnormal stress and strain on the vertebral column

337
Q

what is sciatica/nerve root pain?

A

painradiating to the lower limbs with or without neuralgic symptoms

338
Q

what kind of pain is associated with sciatica/nerve root pain?

A

burning, aching

maybe associated pins and needles

sometimes sensory loss

339
Q

what are the main mechanical causes of lower back pain? (accounts for most low back pain cases)

A

disc degeneration

disc herniation

annular tears

facet joint osteoarthritis

instability

340
Q

how can disc herniation cause lower back pain?

A

disc has slipped from vertebral body

may compress a nerve and cause nerve symptoms

341
Q

what are annular tears?

A

rips within the disc that allow inner material (nucleus pulposus) to leak out

342
Q

how can annular tears cause lower back pain?

A

nucleus pulposus leakage into outer margins of disk

irritation due to prostaglandins, interleukins, tumour necrosis factor etc.

343
Q

how can facet joint osteoarthritis cause lower back pain?

A

cartilage breakdown between facet joints

lack of cartilage causes pain, loss of motion, stiffness

344
Q

what are the facet joints?

A

2 joints at the back of the vertebrae that join vertebrae at each level

345
Q

how can instability cause lower back pain?

A

intense wear and tear causes bones to move out of position (causes pain in itself)

damage to surrounding tissue

346
Q

what are some non-mechanical causes of low back pain?

A

tumour - multiple myeloma (important to treat)

infection (e.g. tuberculosis of the spine)

spondyloarthropathy

pars interarticularis injury

compression fracture

visceral

347
Q

what is spondyloarthropathy?

A

inflammatory joint disease (e.g. ankylosing spondylitis, psoriatic arthritis - usually rheumatological intervention)

348
Q

what kind of people are likely to suffer from spondyloarthropathy?

A

middle age to younger years

349
Q

why is it important to treat spondyloarthropathic conditions quickly?

A

causes disability

350
Q

what is the pars interarticularis?

A

part of the vertebra between inferior and superior articular processes of the facet joint

351
Q

what causes pars interarticularis injuries?

A

stress fractures usually occurring in adolescence due to strenuous activities such as dance, gymnastics etc.

352
Q

why is it important to catch pars interarticularis injuries quickly?

A

stopping strenuous activity allows spontaneous healing

otherwise fractures worsen, instability occurs

353
Q

what can cause compression fractures?

A

if osteoporotic, everyday activities

otherwise, trauma radiating through spinal column (e.g. jumping off a building and landing on feet)

354
Q

how can visceral pain cause low back pain?

A

referred pain from another area

e.g. aortic dissection, pancreatitis etc.

355
Q

what are indicators of sciatica?

A

unilateral leg pain greater than low back pain

pain radiating to foot or toes (may just be to knees depending on nerve affected)

numbness and paraesthesia in the same distribution (variable - depends if sensory nerves are affected)

straight leg raising test induces more leg pain (moves nerves - if trapped, causes pain)

localised neurology i.e. symptoms limited to one nerve root (combine with history and imaging)

356
Q

what are the NICE guidelines for imaging in low back pain?

A

do not routinely offer imaging in a non-specialist setting for people with low back pain with or without sciatica

explain to people with low back pain with or without sciatica that if they are being referred for specialist opinion, they may not need imaging

consider imaging in specialist settings of care (for example, a musculoskeletal interface clinic or hospital) for people with low back pain with or without sciatica only if the result is likely to change management

357
Q

what are some treatments for low back pain (according to NICE guidelines)?

A

injections

exercise

corsets

traction

manipulation

acupuncture

ultrasound therapy

transcutaneous nerve stimulation

psychological therapy

NSAIDS

paracetamol

weak opioids

opioids

radiofrequency denervation

epidural

spinal fusion

disc replacement

358
Q

how can low back pain be treated conservatively?

A

analgesia (paracetamol) - (morphine rarely effective, risk of addiction)

anti-inflammatory drugs (ibuprofen)

manipulation to attempt realignment etc. (chiropractors, osteopaths, physiotherapists)

acupuncture

massage to loosen muscle spasm

allow some time to pass - most heal spontaneously

359
Q

why does bed rest not result in faster recovery for low back pain?

A

muscle atrophy makes movement more difficult

360
Q

what are the red flag symptoms for low back pain?

A

weight loss

fever

night pain

under 19 years

361
Q

what may weight loss indicate as a red flag symptom for low back pain?

A

cancer

infection

362
Q

what may night pain indicate as a red flag symptom for low back pain?

A

malignancy involving bones

may just be from turning over etc.

363
Q

what is the problem with the red flag symptoms for low back pain?

A

insufficient evidence (e.g. no research suggesting weight loss percentage association with serious disease)

364
Q

what are the symptoms of cauda equina syndrome/red flag symptoms for leg pain?

A

bladder or bowel dysfunction

saddle anaesthesia

neurological deficit in legs

365
Q

what should be done if cauda equina syndrome is suspected?

A

imaging and treatment immediately

366
Q

what are 2 common metastatic malignancies that are involved with low back pain?

A

breast cancer

prostate cancer

367
Q

why is it important not to wait too long when dealing with malignancies associated with low back pain?

A

risk of weak bones collapsing

may cause severe fracture, compression of the spinal cord and paralysis

368
Q

why is it important not to wait too long when dealing with inflammatory arthropathy associated with low back pain?

A

early diagnosis for effective treatment with biologics

369
Q

what does a malignancy (low back pain) look like on an MRI?

A

areas of disease show up white within spinal column (water oedematous)

CSF shows up as white

370
Q

what does a inflammatory arthropathy (low back pain) look like on an MRI?

A

shiny corner on vertebra

oedema due to inflammatory process

371
Q

what MRI scans are done when checking for inflammatory arthropathy (low back pain) ?

A

whole spine

sacrum

leg joints

372
Q

why is it important not to wait too long when dealing with myeloma associated with low back pain?

A

early diagnosis catches disease at more treatable stage

373
Q

why is it important not to wait too long when dealing with tuberculosis associated with low back pain?

A

early diagnosis catches disease at more treatable stage

prevents spinal collapse, compression, paralysis

374
Q

what are primary investigations in imaging for low back pain?

A

MRI

375
Q

what are primary investigations in imaging for low back pain?

A

radiographs, CT

376
Q

why is an MRI the most effective investigation for low back pain imaging?

A

shows destruction, oedema and swelling in bone marrow

377
Q

what are the benefits of x-rays?

A

cheap

readily available

traditional

378
Q

what are the disadvantages of x-rays compared to MRIs?

A

radiation (moderate, not high risk)

overlook details of many important diseases (e.g. sarcoma related to Paget’s disease)

379
Q

what are the disadvantages of radiographs compared to MRIs?

A

miss lesions

380
Q

what is an osteoid osteoma?

A

benign tumour of bone

displaces bone around

381
Q

how does an osteoid osteoma present on a CT?

A

small hole

large area of white (lateral view may look like inflammatory arthropathy)

382
Q

how is an osteoid osteoma treated?

A

ablation

needle inserted using CT control, heated

383
Q

what are the clinical signs of a fracture?

A

pain

swelling

crepitus

deformity

adjacent structural injury (nerves, vessels, tendons, ligaments)

384
Q

what are some general fracture complications?

A

fat embolus (hours)

deep vein thrombosis (days-weeks)

pulmonary embolism

infection/sepsis

prolonged immobility (UTI, chest infections, sores)

385
Q

what are some urgent local complications of fractures?

A

local visceral injury

vascular injury

nerve injury

compartment syndrome

haemarthrosis

infection

gas gangrene

386
Q

what is compartment syndrome?

A

pressure within a compartment increases, restricting blood flow and damaging structures

387
Q

what are some less urgent local complications of fractures?

A

fracture blisters

plaster sores

pressure sores

nerve entrapment

myositis ossificans

ligament injury

tendon lesions

joint stiffness

algodystrophy

388
Q

what are the 3 types of joint classified by structure?

A

fibrous

cartilaginous

synovial

389
Q

what are the 3 types of fibrous joint?

A

sutures

syndesmosis

interosseous membrane

390
Q

what are the 2 types of cartilaginous joint?

A

synchondroses (e.g. spine)

symphyses (e.g. pubic)

391
Q

what are the 6 types of synovial joint?

A

plane (e.g. between tarsal bones)

hinge (e.g. elbow)

condyloid (e.g. between radius and carpal bones in wrist)

pivot (e.g. between C1 and C2 vertebrae)

saddle (e.g. between trapezium carpal bone and first metacarpal bone)

ball and socket (e.g. hip)

392
Q

how are synovial joints stabilised?

A

muscles/tendons

ligaments

bone surface congruity

393
Q

what is the structure of a synovial joint?

A

joint cavity filled with synovial fluid between bone

lined with articular cartilage

394
Q

what is the structure of the synovium?

A

1-3 cell deep lining

contains type A synoviocyte - macrophage-like phagocytic cells

contains type B synoviocyte - fibroblast-like cells that produce hyaluronic acid

type I collagen

395
Q

what is synovial fluid?

A

hyaluronic acid-rich viscous fluid

396
Q

what is the structure of articular cartilage?

A

type II collagen

proteoglycan (aggrecan)

397
Q

what 2 things is cartilage composed of?

A

specialized cells (chondrocytes)

extracellular matrix - water, collagen and proteoglycans
mainly aggrecan

398
Q

what is aggrecan?

A

proteoglycan

possesses many chondroitin sulfate and keratin sulfate chains

399
Q

what is aggrecan characterised by?

A

ability to interact with hyaluronan to form large proteoglycan aggregates

400
Q

what are the 2 major divisions of arthritis?

A

osteoarthritis

inflammatory arthritis (main type - rheumatoid arthritis)

401
Q

how do radiographic changes differ in rheumatoid arthritis and osteoarthritis?

A

joint space narrowing - both

subchondral sclerosis - rheumatoid arthritis

osteophytes - osteoarthritis

osteopenia - rheumatoid arthritis

bony erosion - rheumatoid arthritis

402
Q

what is the pathophysiology of osteoarthritis?

A

degradation of chondral cartilage

inflammation occurs late compared to rheumatoid arthritis

inflammatory mediators include proteinases, inflammatory cytokines (enhance synthesis of proteinases and other catabolic factors to degrade articular cartilage membrane)

403
Q

what are the main risk factors for osteoarthritis?

A

age

excess weight

mechanical constraints (e.g. extreme sports)

heredity

female gender, menopause

osteonecrosis

leg bone malalignment

oestrogen deficiency

metabolic syndorme

advanced hip osteoarthritis (spondyarthritis or rheumatoid)

404
Q

what are the non-major risk factors for osteoarthritis?

A

injury (cruciate ligament rupture, menisectomy)

metabolic disease (chondrocalcinosis, genetic haemochromatosis)

infectious diseases involving bone

rheumatoid arthritis sequellae

405
Q

what should be assessed in osteoarthritis?

A

pain (exertional/rest/night)

disability (walking distance/stairs/giving way)

deformity

previous history (trauma/infection)

treatments given (physio/injections/operations)

other joints affected

406
Q

how is osteoarthritis assessed?

A

look

feel

move

special tests

407
Q

what are some signs of ACL injury?

A

valgus alignment, walk with antalgic gait

small effusion on palpation

knee flexion is 70 degrees compared with healthy knee

positive anterior drawer consistent with ACL

408
Q

what are the 4 radiographic changes of osteoarthritis?

A

osteophyte

loss of joint space

subchondral cysts

sclerosis

409
Q

what are some conservative methods of osteoarthritis management?

A

analgesics

physiotherapy

walking aids

avoidance of exacerbating activity

injections (steroid/viscosupplementation)

410
Q

what are some operative methods of osteoarthritis management?

A

replace (knee/hip)

realign (knee/big toe)

excise (toe)

fuse (big toe)

synovectomy (rheumatoid)

denervate (wrist)

411
Q

what are the risk factors for septic arthritis?

A

immunosuppressed

pre-existing joint damage

intravenous drug use

412
Q

how is septic arthritis diagnosed?

A

joint aspiration

gram stain and culture of sample

413
Q

how is osteomyelitis treated?

A

IV antibiotics

surgical drainage, especially collections/sequestrum

chronic - antibiotic suppression/dressings

(amputation)

414
Q

what are the most common shoulder conditions in 15-45 year olds?

A

dislocation

fractures

415
Q

what are the most common shoulder conditions in 45-60 year olds?

A

dislocation

fractures

impingement

acromioclavicular joint osteoarthritis

rotator cuff tears

416
Q

what are the most common shoulder conditions in 60+ year olds?

A

fractures

impingement

rotator cuff tears

glenohumeral osteoarthritis

417
Q

what are the most common hip conditions in 15-45 year olds?

A

developmental dysplasia

leg length discrepancy

impingement

418
Q

what are the most common hip conditions in 45-60 year olds?

A

impingement

osteoarthritis

avascular necrosis

419
Q

what are the most common hip conditions in 60+ year olds?

A

osteoarthritis

post total hip replacement

420
Q

what are the most common knee conditions in 15-45 year olds?

A

patellofemoral maltracking

ACL/PCL

meniscal tears

fractures

421
Q

what are the most common knee conditions in 45-60 year olds?

A

osteoarthritis

patellofemoral maltracking

ACL/PCL

meniscal tears

fractures

422
Q

what are the most common knee conditions in 60+ year olds?

A

osteoarthritis

423
Q

what radiology investigations are done for bone or joint infection?

A

plain films

MRI scans: bony architecture/collections (CT if MRI not available)

bone scans: multifocal disease

labelled white cell scans

424
Q

what blood tests are done for bone or joint infection?

A

CRP: acute marker

ESR (slower response)

WCC

TB culture/PCR

425
Q

how can stress cause a fracture?

A

overuse - stress exerted overcomes remodelling capacity

bone weakens, causes stress fracture

426
Q

what are the weight bearing bones?

A

femur

tibia

metatarsals

navicular

427
Q

what some activity related stressors that can cause fractures?

A

athletes

military

female athletes (female athlete triad)

428
Q

what are 3 factors contributing to secondary osteoporosis?

A

hypogonadism

glucocorticoid excess

alcoholism

429
Q

what is Paget’s disease?

A

excessive bone break down and disorganized remodelling

causes deformity, pain, fracture or arthritis

may become malignant

430
Q

what are the 4 stages of Paget’s disease?

A

osteoclastic Activity

mixed osteoclastic-osteoblastic activity

osteoblastic activity

malignant degeneration

431
Q

what are the 4 primary bone cancers?

A

osteosarcoma

chondrosarcoma

Ewing sarcoma

lymphoma

432
Q

what are the 4 malignancies that cause lytic bone damage?

A

kidney

thyroid

lung

breast

433
Q

what are the 2 malignancies that cause blastic bone damage?

A

prostate

breast

434
Q

what are the 3 forms of tendinopathy?

A

tendinosis (abnormal thickening)

tendinitis (inflammation)

rupture

435
Q

how are ligament injuries classified?

A

grade 1 to 3

436
Q

what are the features of a grade 1 ligament injury?

A

slight incomplete tear, stretching

no notable joint instability

437
Q

what are the features of a grade 2 ligament injury?

A

moderate/severe incomplete tear

some joint instability.

1 ligament may be completely torn

438
Q

what are the features of a grade 3 ligament injury?

A

complete tearing of 1 or more ligaments

obvious instability

surgery usually required

439
Q

how can tendon or ligament tears be managed conservatively?

A

immobilise (plaster, boot or brace)

440
Q

how can tendon or ligament tears be managed surgically/operatively?

A

suture

441
Q

what are the benefits of immobilisation on injured ligamentous tissue?

A

less ligament laxity

442
Q

what are the benefits of mobilisation on injured ligamentous tissue?

A

ligament scars are wider, stronger, more elastic

better alignment/quality of collagen

443
Q

what are the disadvantages of immobilisation on injured ligamentous tissue?

A

less overall strength of ligament repair scar

protein degradation exceeds protein synthesis (decreased collagen quantity)

production of inferior tissue by blast cells

resorption of bone at site of ligament insertion

decreased tissue tensile strength

444
Q

how do ligaments heal?

A

inflammatory phase - tissue damage

proliferative phase - growth factors/cytokines

tissue remodelling -collagenase, enzymes, macrophages to form structure

445
Q

what is the purpose of the inflammatory phase in ligamentous healing?

A

debris clearance

446
Q

what cells are involved in the inflammatory phase in ligamentous healing?

A

platelets, macrophages activate mast cells, neutrophils and phagocytes

447
Q

what is the purpose of the proliferative phase in ligamentous healing?

A

new collagen

angiogenesis

neovascularisation

448
Q

what cells are involved in the proliferative phase in ligamentous healing?

A

fibroblasts

endothelial cells

myofibroblasts

449
Q

how can the healing environment be divided?

A

mechanical environment

biological environment

450
Q

what 2 things make up the mechanical environment for healing?

A

movement

forces

451
Q

what 4 things make up the mechanical environment for healing?

A

blood supply

immune function

infection

nutrition

452
Q

what are the 2 components of bone matrix?

A

organic

inorganic

453
Q

what 2 things make up the organic component of bone?

A

type 1 collagen (90%)

ground substance

454
Q

what 2 things make up the inorganic component of bone?

A

calcium hydroxyapatite

osteocalcium phosphate

455
Q

what 3 things make up the ground substance in the organic component of bone?

A

proteoglycans

glycoproteins

cytokines and growth factors

456
Q

what is appositional growth?

A

deposition of bone beneath the periosteum to increase thickness

457
Q

what are the 4 stages of appositional growth?

A

ridges in periosteum create groove for periosteal blood vessel

periosteal ridges fuse, forming endosteum-lined tunnel

osteoblasts in endosteum build new concentric lamellae inward toward centre of tunnel, forming new osteon

bone grows outwards as osteoblasts in periosteum build new circumferential lamellae

(osteon formation repeats as new periosteal ridges fold over blood vessel)

458
Q

what are the 3 types of joint classified by function?

A

synarthosis (no movement allowed)

amphiarthroses (limited movement allowed)

diarthroses (free movement - synovial only)

459
Q

what signs and symptoms is osteoarthritis associated with?

A

joint pain (worse with activity)

joint crepitus

joint instability (‘giving way’)

joint enlargement
e.g. Heberden’s nodes

joint stiffness after immobility (‘gelling’)

limitation of range of motion

460
Q

how does inflammation manifest clinically?

A

rubor (redness)

dolor (pain)

calor (heat)

tumor (swelling)

loss of function

461
Q

what are the 3 causes of joint inflammation?

A

infection (e.g. septic arthritis, tuberculosis)

crystal arthritis (e.g. gout, pseudogout)

immune-mediated (“autoimmune”) (e.g. rheumatoid, psoriatic, reactive arthritis, systemic lupus erythematosus (SLE))

462
Q

what is gout?

A

form of crystal arthritis

syndrome caused by deposition of monosodium urate (uric acid) crystals leading to inflammation

causes gouty arthritis, tophi

463
Q

what is the main risk factor for gout?

A

hyperuricaemia

464
Q

what are 3 causes of hyperuricaemia?

A

genetic tendency

increased intake of purine rich foods

reduced excretion (kidney failure)

465
Q

what is pseudogout?

A

form of crystal arthritis

syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) leading to inflammation

466
Q

what are the main risk factors for psuedogout?

A

background osteoarthritis

elderly patients

intercurrent infection

467
Q

where does gout usually present?

A

first metatarsophalangeal joint most common (podagra)

foot, ankle, knee, wrist, finger, and elbow joints most frequently affected

468
Q

how is crystal arthritis diagnosed?

A

aspirating fluid from affected joint - synovial fluid analysis

examining it under a microscope using polarized light

gram stain - culture, antibiotic sensitivity assays

469
Q

how can gout be diagnosed from a synovial fluid analysis?

A

needle shaped crystals

negative birefringence

470
Q

how can pseudogout be diagnosed from a synovial fluid analysis?

A

rhomboid/brick shaped crystals

positive birefringence

471
Q

what are the 3 key features of rheumatoid arthritis?

A

chronic arthritis

extra articular disease (rheumatoid nodules, rarely vasculitis, episcleritis)

rheumatoid factor may be detected in blood

472
Q

how can the pattern of joint involvement in rheumatoid arthritis be described?

A

symmetrical

affects multiple joints (polyarthritis)

affects small and large joints, but particularly hands and feet

473
Q

what is the primary site of pathology in rheumatoid arthritis?

A

synovium

includes

  • synovial joints
  • tenosynovium surrounding tendons
  • bursa
474
Q

what are the common extra articular features in rheumatoid arthritis?

A

fever

weight loss

subcutaneous nodules

475
Q

what are the uncommon extra articular features in rheumatoid arthritis?

A

vasculitis

ocular inflammation (e.g. episcleritis)

neuropathies

amyloidosis

lung disease – nodules, fibrosis, pleuritis

Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis

476
Q

what are subcutaneous nodules in rheumatoid arthritis?

A

central area of fibrinoid necrosis

surrounded by histiocytes and peripheral layer of connective tissue

477
Q

the synovial membrane is abnormal in rheumatoid arthritis - why does the synovium become a proliferated mass of tissue?

A

neovascularisation

lymphangiogenesis

inflammatory cells:

  • activated B and T cells
  • plasma cells
  • mast cells
  • activated macrophages

excess of pro-inflammatory cytokines promotes excessive recruitment, activation and effector functions

478
Q

what is is the dominant pro-inflammatory cytokine in the rheumatoid synovium for the pathogenesis of rheumatoid arthritis?

A

tumour necrosis factor alpha (TNFα)

479
Q

how can tumour necrosis factor alpha (TNFα) be inhibited in treatment of rheumatoid arthritis?

A

antibodies or fusion proteins

parenteral administration (most commonly subcutaneous injection)

480
Q

what are the 2 types of autoantibody generally found in rheumatoid arthritis patients?

A

rheumatoid factor

antibodies to citrullinated protein antigens (e.g. anti-cyclic citrullinated peptide antibody or ‘anti-CCP antibody’)- highly specific for rheumatoid arthritis, associated with worse prognosis

481
Q

what is rheumatoid factor?

A

anti-IgG (Fc portion) and IgM

i.e. IgM anti-IgG antibody

482
Q

what does effective management of rheumatoid arthritis require?

A

early recognition of symptoms, referral and diagnosis

prompt initiation of treatment: joint destruction = inflammation x time

aggressive treatment to suppress inflammation

483
Q

what drugs are used to treat rheumatoid arthritis?

A

disease modifying anti-rheumatic drugs (DMARD) to control disease process

1st line treatment:
methotrexate with hydroxychloroquine or sulfasalazine

484
Q

how are biological therapies used to treat rheumatoid arthritis (2nd line)?

A

proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine

485
Q

what are 4 biological therapies used to treat rheumatoid arthritis (2nd line)?

A

inhibition of tumour necrosis factor-alpha (‘anti-TNF’)

  • antibodies
  • fusion proteins

B cell depletion
– antibody against B cell antigens

modulation of T cell co-stimulation

inhibition of interleukin-6 signalling
– antibody against interleukin-6 receptor

486
Q

what is psoriatic arthritis?

A

psoriasis - autoimmune disease affecting the skin (scaly red plaques on extensor surfaces)

some patients also have joint inflammation

487
Q

how does psoriatic arthritis present?

A

classically asymmetrical arthritis affecting interphalangeal joints

can also manifest as:

  • symmetrical involvement of small joints (rheumatoid pattern)
  • spinal and sacroiliac joint inflammation
  • oligoarthritis of large joints
  • arthritis mutilans
488
Q

what is reactive arthritis?

A

sterile inflammation in joints following infection

especially urogenital and gastrointestinal infections (may be mild)

may be first manifestation of HIV or Hep C infection

489
Q

what are 3 important extra articular manifestations of reactive arthritis?

A

skin inflammation

eye inflammation

enthesitis (tendon inflammation)

490
Q

who is most likely to suffer from reactive arthritis?

A

commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (i.e. infection

symptoms follow 1-4 weeks after infection

491
Q

what are the key differences between septic and reactive arthritis?

A

synovial fluid culture - positive in septic, sterile in reactive

antibiotic therapy and joint lavage (in large joints) for septic arthritis

492
Q

what are tophi?

A

aggregated deposits of monosodium urate (uric acid) crystals in tissue

493
Q

how does gout present?

A

abrupt onset

extremely painful

joint red, warm, swollen and tender

resolves spontaneously over 3-10 days

494
Q

how can gout be seen on an x-ray?

A

juxta-articular ‘rat bite’ erosions

495
Q

how is an acute attack of gout managed?

A

colchicine

NSAIDs

steroids

496
Q

how is chronic gout managed?

A

allopurinol (lowers levels of uric acid)

497
Q

what is ankylosing spondylitis?

A

seronegative spondyloarthropathy (no positive autoantibodies)

chronic sacroiliitis (inflammation of sacroiliac joints)

results in spinal fusion – ankylosis

498
Q

what demographic is most likely to suffer from ankylosing spondylitis?

A

20-30 year old

male

(back pain > 3 month in < 45 year olds - suggestive)

499
Q

what gene is ankylosing spondylitis associated with?

A

HLA B27

500
Q

how does ankylosing spondylitis present clinically?

A

lower back pain + stiffness (early morning, improves with exercise)

reduced spinal movements

peripheral arthritis

plantar fasciitis, Achilles tendonitis

fatigue

altered posture - hyperextended neck, loss of lumbar lordosis, flexed hips and knees

501
Q

what blood test results are seen in ankylosing spondylitis?

A

normocytic anaemia

raised CRP, ESR

HLA-B27

502
Q

what imaging results are seen in ankylosing spondylitis?

A

x-ray

MRI
- squaring vertebral bodies, Romanus lesion

  • erosion, sclerosis, narrowing sacroiliac joint
  • bamboo spine
  • bone marrow oedema
503
Q

how is ankylosing spondylitis managed?

A

physiotherapy

exercise regimes

NSAIDs

peripheral joint disease - DMARDs

504
Q

what investigations are done for psoriatic arthritis?

A

x-rays of affected joints – pencil in cup abnormality

MRI – sacroiliitis and enthesitis

bloods – no antibodies as seronegative

505
Q

how is psoriatic arthritis managed?

A

DMARDs – methotrexate

506
Q

why are oral steroids avoided in management of psoriatic arthritis?

A

risk of pustular psoriasis due to skin lesions

507
Q

what is systemic lupus erythematous (SLE)?

A

multi-system autoimmune disease

multi-site inflammation (often joints, skin, kidneys, haematology - involves lungs and CNS)

autoantibodies for components of cell nucleus (nucleic acids and proteins)

508
Q

how can autoantibodies be used diagnostically in systemic lupus erythematous (SLE)?

A

antinuclear antibodies (ANA):

  • high sensitivity for SLE but not specific
  • negative test rules out SLE, but a positive test does not mean SLE

anti-double stranded DNA antibodies (anti-dsDNA Abs):
- high specificity for SLE in the context of the appropriate clinical signs

(anti-phospholipid antibodies)

509
Q

which demographic is systemic lupus erythematous (SLE) most common in?

A

9F:1M

15 - 40 yrs

increased prevalence in African and Asian ancestry populations

510
Q

what are the 3 types of diagnostic test done in rheumatology?

A

blood test

synovial fluid analysis

imaging

  • x-ray
  • ultrasound
  • CT
  • MRI
511
Q

what are the basic rheumatology blood tests?

A

full blood count (FBC)

urea and electrolytes (U&E) - urea, sodium, potassium, creatinine

liver function tests (LFT) - bilirubin, ALT, ALP, albumin

bone profile - ALP, calcium, phosphate

erythrocyte sedimentation rate (ESR)

C-reactive protein (CRP)

512
Q

how do haemoglobin levels vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?

A

inflammatory arthritis - low Hb (anaemia) or normal

osteoarthritis - normal

septic arthritis - usually normal

513
Q

how does MCV vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?

A

inflammatory arthritis - normal

osteoarthritis - normal

septic arthritis - normal

514
Q

how does WCC vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?

A

inflammatory arthritis - usually normal

osteoarthritis - normal

septic arthritis - raised WCC (leucocytosis)

515
Q

how does PLT (platelet count) vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?

A

inflammatory arthritis - normal or raised

osteoarthritis - normal

septic arthritis - normal or raised

516
Q

what does a high creatinine indicate as part of rheumatological diagnostics?

A

worse renal clearance (indicating kidney problem)

517
Q

what are some examples of rheumatological diseases affecting the kidneys?

A

systemic lupus erythematous (SLE) causes lupus nephritis

vasculitis leads to nephritis

chronic inflammation in poorly controlled inflammatory disease leads to high levels of serum amyloid A protein, deposits in organs (AA amyloidosis)

(NSAIDs used in treatment may cause kidney impairment)

518
Q

why are LFTs important in rheumatological diagnostics?

A

DMARDs can cause liver damage - patients need regular tests

519
Q

what can low albumin as a result in LFTs indicate? (rheumatological diagnostics)

A

problem of synthesis (in liver)

problem of leak from kidney (e.g. in lupus nephritis)

520
Q

what are the results of a bone profile in Paget’s disease?

A

raised ALP

521
Q

what are the results of a bone profile in osteomalacia?

A

ALP - normal or raised

Ca and PO4 - normal or low

522
Q

what are the results of a bone profile in osteoporosis?

A

ALP, PO4, Ca - usually normal

523
Q

what are some other (non-inflammatory) reasons for raised ESR?

A

elevated immunoglobulin level

paraprotein (myeloma)

anaemia

tends to rise with age

524
Q

how are ESR and CRP used in diagnosis of systemic lupus erythematosus (SLE)?

A

usually - ESR high, CRP normal

(CRP high if synovitis or inflammatory pleural/pericardial effusion)

should have low index of suspicion for infection if CRP raised

525
Q

what are some non-specific causes for the presence of anti-nuclear antibodies (ANA)?

A

relatively common in general healthy population at low titre (level)

prevalence generally increases with age

sometimes transiently positive following infection

526
Q

what may a high titre of anti-nuclear antibodies (ANA) indicate?

A

autoimmune connective tissue disease (SLE, scleroderma, Sjogren’s syndrome)

stronger test is more likely to be clinically significant

must be in combination with correct clinical features

527
Q

how is an ANA (anti-nuclear antibody) test interpreted?

A

strength reported as maximal dilution at which it is still detectable
e.g. 1:80 (weak), 1:320, 1:640, 1:1280 (strong)

negative test rules out SLE

positive test does not necessarily mean SLE, but suggestive IF there are other clinical and lab features to support the diagnosis

528
Q

what other tests are ordered if an ANA test is positive?

A

ENA (extractable nuclear antigens):

  • Ro - lupus or Sjogren’s syndrome
  • La - lupus or Sjogren’s syndrome
  • RNP - lupus or mixed connective tissue disease
  • Smith - lupus
  • Jo-1 - polymyositis

complement C3 and C4 - may be low in active lupus

dsDNA (double stranded DNA) antibodies - highly specific for lupus, associated with renal involvement, useful for tracking lupus activity over time

529
Q

what are the benefits of x-rays in rheumatology?

A

first line

cheap

widely available

530
Q

what are the benefits of CT scans in rheumatology?

A

more detailed bony imaging

531
Q

what are the benefits of MRIs in rheumatology?

A

best visualization of soft tissue structures like tendons and ligaments

best for spinal imaging: can see spinal cord and exiting nerve roots

532
Q

what are the disadvantages of MRIs in rheumatology?

A

expensive

time-consuming

533
Q

what are the benefits of an ultrasound in rheumatology?

A

visualise soft tissue structures

534
Q

what are the disadvantages of ultrasounds in rheumatology?

A

good for smaller joints - less good for deep/large joints (knee or hip)

535
Q

what are the radiographic features of rheumatoid arthritis?

A

soft tissue swelling

peri-articular osteopenia

bony erosions (only in established disease, aim to treat before this)

536
Q

what are the ultrasound features of rheumatoid arthritis?

A

(better for detecting synovitis)

synovial hypertrophy (thickening)

increased blood flow (seen as doppler signal)

may detect erosions not seen on plain X-ray

537
Q

what are the main connective tissue diseases?

A

systemic Lupus Erythematosus (SLE)

Sjögren’s syndrome

autoimmune inflammatory muscle disease

systemic sclerosis (scleroderma)

overlap syndromes

538
Q

what are the 2 types of autoimmune inflammatory muscle disease?

A

polymyositis

dermatomyositis

539
Q

what are the 2 types of systemic sclerosis (scleroderma)?

A

diffuse cutaneous

limited cutaneous

540
Q

what are the seronegative spondyloarthropathies?

A

ankylosing spondylitis

reactive arthritis (Reiters syndrome)

psoriatic arthritis

enteropathic synovitis (arthritis associated with GI inflammation)

541
Q

what phenomenon is common in connective tissue disorders?

A

Raynaud’s phenomenon

542
Q

what is Raynaud’s phenomenon?

A

intermittent vasospasm of digits on exposure to cold

typical colour changes – white to blue to red

  • vasospasm leads to blanching of digit
  • cyanosis as static venous blood deoxygenates
  • reactive hyperaemia

(usually isolated and benign)

543
Q

what is the significance of serum autoantibodies in connective tissue disorders?

A

may aid diagnosis

correlate with disease activity

may be directly pathogenic

544
Q

what are the typical clinical manifestations of systemic lupus erythematosus (SLE)?

A

malar rash (erythema that spares the nasolabial fold)

photosensitive rash

mouth ulcers

hair loss

Raynaud’s phenomenon

arthralgia and sometimes arthritis (non-erosive)

serositis (pericarditis, pleuritis, less commonly peritonitis)

renal disease – glomerulonephritis (‘lupus nephritis’)

cerebral disease – ‘cerebral lupus’ e.g. psychosis

545
Q

what is the pathogenesis of systemic lupus erythematosus (SLE)?

A

apoptosis leads to translocation of nuclear antigens to membrane surface

impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells

B cell autoimmunity

tissue damage by antibody effector mechanisms (e.g. complement activation and Fc receptor engagement)

546
Q

what are anti-phospholipid antibodies associated with in systemic lupus erythematosus (SLE)?

A

risk of arterial and venous thrombosis

may also occur in absence of SLE in what is termed the ‘primary anti-phospholipid antibody syndrome

547
Q

what autoantibodies are associated with systemic vasculitis?

A

antinuclear cytoplasmic antibodies (ANCA)

548
Q

if an ANA test is positive, what other antibodies are screended for?

A

anti-Ro

anti-La

anti-centromere

anti-Sm

anti-RNP

anti-ds-DNA antibodies

anti-Scl-70

cytoplasmic antibodies

  • anti-tRNA synthetase antibodies
  • anti-ribosomal P antibodies
549
Q

what is the significance of anti-Sm antibodies in systemic lupus erythematosus (SLE)?

A

specific for SLE

serum level of antibody does NOT correlate with disease activity

550
Q

what is the significance of anti-Ro and anti-La antibodies in systemic lupus erythematosus (SLE)?

A

secondary Sjögren’s syndrome

neonatal lupus syndrome (transient rash in neonate, permanent heart block)

551
Q

what is the significance of anti-ribosomal P antibodies in systemic lupus erythematosus (SLE)?

A

cerebral lupus

552
Q

what autoantibodies are associated with diffuse systemic sclerosis?

A

anti-Scl-70 antibody

553
Q

what autoantibodies are associated with limited systemic sclerosis?

A

anti-centromere antibodies

554
Q

what autoantibodies are associated with dermatomyositis/polymyositis?

A

anti-tRNA transferase antibodies

e.g. histidyl transferase, also termed anti-Jo-1 antibodies

555
Q

what autoantibodies are associated with Sjögren’s syndrome?

A

no unique antibodies but typically see:

  • anti-Ro and anti-La antibodies
  • rheumatoid factor
556
Q

what autoantibodies are associated with mixed connective tissue disease?

A

anti-U1-RNP antibodies

557
Q

how can disease activity be assessed in systemic lupus erythematosus (SLE)?

A

low complement C3 and C4

high anti-dsDNA antibodies

low platelet (PLT)

558
Q

how is systemic lupus erythematosus (SLE) managed?

A

treatment aims at remission or low activity and prevention of flares

hydroxychloroquine is recommended in all lupus patients

maintenance treatment glucocorticoids minimised or withdrawn if possible

(appropriate initiation of immunomodulatory agents (methotrexate, azathioprine, mycophenolate) can expedite the tapering/discontinuation of glucocorticoids)

cyclophosphamide and B cell targeted therapies (rituximab and belimumab) for persistently active or severe disease

assess antiphospholipid antibody status, infectious and CVD risk profile

pregnancy planning

559
Q

what is Sjögren’s syndrome?

A

autoimmune exocrinopathy

mainly lymphocytic infiltration of exocrine glands, sometimes of other organs (extra-glandular involvement)

(‘secondary’ Sjögren’s syndrome if in context of another connective tissue disorder e.g. SLE)

560
Q

what does the exocrine gland pathology of Sjögren’s syndrome result in?

A

dry eyes (xerophthalmia)

dry mouth (xerostomia)

parotid gland enlargement

561
Q

what are the most common extra-glandular manifestations of Sjögren’s syndrome?

A

non-erosive arthritis

Raynaud’s phenomenon

562
Q

what tests can be done for Sjögren’s syndrome?

A

salivary gland biopsy

Schirmer’s test

563
Q

how does a salivary gland biopsy test for Sjögren’s syndrome?

A

show lymphocytic infiltration

mostly CD4 helper T cells, B lymphocytes to lesser extent

564
Q

how does a Schirmer’s test test for Sjögren’s syndrome?

A

assess tear production

filter paper placed under lower eyelid, extent of wetness measured after 5 minutes

abnormal result: <5mm

565
Q

what is inflammatory muscle disease?

A

proximal muscle weakness due to autoimmune-mediated inflammation

with a rash - dermatomyositis

without a rash -polymyositis

566
Q

what skin changes take place in dermatomyositis (inflammatory muscle disease)?

A

lilac-coloured (heliotrope) rash on eyelids, malar region and naso-labial folds

red or purple flat or raised lesions on knuckles (Gottron’s papules)

subcutaneous calcinosis

mechanic’s hands (fissuring and cracking of skin over finger pads)

567
Q

what conditions is inflammatory muscle disease associated with?

A

malignancy

pulmonary fibrosis

568
Q

how is inflammatory muscle disease diagnosed?

A

elevated creatinine phosphokinase

abnormal electromyography

abnormal muscle biopsy

polymyositis = CD8 T cells
dermatomyositis = CD4 T cells in addition to B cells
569
Q

what are the features of systemic sclerosis/scleroderma?

A

thickened skin with Raynaud’s phenomenon

dermal fibrosis, cutaneous calcinosis, telangiectasia

570
Q

what are the features of diffuse systemic sclerosis?

A

fibrotic skin proximal to elbows or knees (excluding face and neck)

anti-topoisomerase-1 (anti-Scl-70) antibodies

pulmonary fibrosis, renal (thrombotic microangiopathy) involvement

short history of Raynaud’s phenomenon

571
Q

what are the features of limited systemic sclerosis?

A

fibrotic skin hands, forearms, feet, neck and face

anti-centromere antibodies

pulmonary hypertension

long history of Raynaud’s phenomenon

572
Q

what is overlap syndrome?

A

features of more than 1 connective tissue disorder are present

573
Q

what is undifferentiated connective tissue disease?

A

incomplete features of a connective tissue disease are present

574
Q

what is mixed connective tissue disease?

A

features of multiple connective tissue disorders

identified by presence of anti-U1-RNP antibody

BRS 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions