MSK Flashcards
(239 cards)
1
Q
What are some examples of perinatal disorders?
A
Congenital scoliosis - abnormal curvature of the spine, usually in the coronal plane.
The most common type of scoliosis is idiopathic but a known cause of scoliosis is congenital malformation of the spine. This can occur when the vertebrae fail to separate or form properly during foetal growth (around the 4th to 6th week gestation), and is often part of a more widespread foetal develpment disorder, that includes the heart, gastrointestinal and genitourinary systems.
Congenital deficiencies - a collection of disorders that result from the failure of formation of a bony part of the body, like fibular hemimelia, which is a congenital absence of the fibula, leading to a shortened, bowed tibia on the affected side.
Hand deformities - radial club hand (radius failed to form, incomplete formation of thumb), syndactyly (fingers failed to separate properly), polydactyly (duplicated finger), central deficiency (no middle/ring finger).
DDH - developmental dysplasia of the hip - acetabulae fail to form properly and as a result of this, the femoral heads fail to form properly as the child ages.
2
Q
What are some examples of growth disorders?
A
Achondroplasia - a skeletal dysplasia caused by a pathology in the physes of long bones causing disproportionate dwarfism (trunk/limb imbalance).
Endocrine causes - too much or too little of a hormone, like the thyroid hormones or human growth hormone, really tall due to an overproduction of human growth hormone from a pituitary tumour resulting in acromegaly. Really short due to primordial dwarfism, which in itself is a term used to refer to 1 of 5 genetic, rather than endocrine, disorders.
Nutritional causes - rickets due to lack of Vitamin D.
Physeal arrest - trauma.
3
Q
What are some examples of soft tissue degeneration?
A
Slipped/herniated disc - due to repeated microtraumas to the intervertebral discs over a patient’s lifetime, happens when the nucleus pulposus (inner part of the disk) bursts through the worn annulus fibrosis (outer part) causing severe back pain and occasionally pressing on a nerve or the spinal cord itself.
Meniscus tear from degeneration - makes more likely to tear.
Shoulder impingement - rotator cuff tears, ACJ arthritis from wear and tear, making the tissues fibrilated and more likely to tear.
4
Q
What are the metabolic skeletal functions?
A
Blood cell production, metabolic storage and homeostasis.
5
Q
What is the function of red bone marrow?
Where does it exist?
A
Red bone marrow is where the production of blood cells takes place, a process known as hematopoiesis, hemato- =“blood”, -poiesis = “to make”.
Red blood cells, white blood cells, and platelets are allproduced in red bone marrow.
It exists mainly in non-long bones of the body.
6
Q
How to bones serve as a site for blood cell production?
A
Via the unique connective tissue that fills the interior of most bones, the bone marrow.
There are two types of bone marrow: yellow bone marrow and red bone marrow. Red is where blood cell production occurs.
7
Q
What is the function of yellow bone marrow?
Where does it exist?
A
Yellow bone marrow contains adipose tissue, and the triglycerides stored in the adipocytes of this tissue can be released to serve as a source of energy for other tissues of the body.
Mainly in the medullary cavity of long bones’ shaft.
8
Q
What is the metabolic function of bone?
A
Storage:
Fat in yellow bone marrow,
A number of minerals important to the functioning of the body, especially calcium, and phosphorus in the actual bone.
These minerals, incorporated into bone tissue, can be released back into the bloodstream to maintain levels needed to support physiological processes.
Calcium ions, for example, are essential for muscle contractions and are involved in the transmission of nerve impulses.
9
Q
What are the main drives of bone metabolism?
A
Bone metabolism is driven by the cycle of deposition by osteoblasts and resorption byosteoclasts, sequestering and releasing calcium and phosphate to and from thecirculation.
10
Q
What is the mechanical function of bone?
A
Structure,
Motion (anchor point for soft tissue - muscles of movement and organs),
Protection (skull protects head organs, spine the spinal cord, ribs the lungs/mediastinum, pelvis; notice these are all flat bones),
Hearing (specialised bones - auditory ossicles - malleus, incus, stapes),
Breathing (diaphram attached to bones - xiphoid process, costal margin, ribs, thoracolumbar spine - creates vaccum for air into lungs, creates pressure to vomit, urine, feces, prevent acid reflux; intercostal muscles also help forced ins/ex-piration during activity)
11
Q
What are some adaptations for bipedalism?
A
Spinal curves - lumbar/cervical lordosis and a thoracic kyphosis which prevents vertibral column from leaning forward, keeping everything directly above the centre of balance; means less energy to stand upright. These also act like compressive springs - allow hight changes and mobility of upper body.
Intervertebral discs - shock absorbers which, combined with the compressive spring arrangement of spinal curvatures, dampens the heavy impacts that come with the whole body weight landing on single limb during walking, running or jumping.
Weight bearing axis of hip and knees - enalarged hip and knee joints to cope with increased forces, shorter and broader shaped pelvis to decrease lever length so muscles of hip abduction don’t need towork as hard to stand on one leg. Longer legs improves the lever effect for muscles and also improves the pendulum swing of the leg, preserving moreenergy during walking. Human femur angle medially, keeping the knees and ankles directly underneath body at all points during walking, increases power and allows locking kneea to use minimal power to stand for extended periods. Gluteus maximus prevents body pitching forwards and extends hip, propelling forward when running.
Tripod arrangement of foot - enlarges ankle bones, especially calcaneus and calcaneus, great toe and small toe MTP joints make arch which absorbs energy when stretched and propels forwards when released, reducing overall energy expenditure while moving.
Soleus - ‘slow’ muscle maintains standing posture, stopping dorsifelxion.
12
Q
What are osteogenic(osteoprogenitor) cells?
A
Mesenchymal stem cells (derived from foetal mesencyme) that differentiate into various different specialised bone cells. Precursors to adipocytes, myocytes, chondrocytes and osteoblasts.
Depends on the mechanical environment they exist in and chemical signalling:
Minimal movement (strain) - become osteoblasts, signalled by RunX2 and osterix, released by osteocytes that sense movement via mechanotransduction
More movement - become chondrocytes
They can be present within the bone marrow, the endosteum and the cellular layer of the periosteum.
13
Q
What are octeoblasts function?
A
Two functions:
1. Formbonebyproducingnon‐mineralisedmatrix - have more endoplasmic reticulum, golgi apparatus, mitochondria, allowing synthesis and secretion of bone matrix.
When stimulatedbyPTH,theyproducetype1collagenandalkalinephosphatase (enzymethatdephosphorylatesmanyorganicmolecules)initiatingthecalcificationofthematrixbylayingdowndepositsofcalciumphosphate.
TheyalsohaveavitDreceptorandwhenstimulated,OBsproducematrix,alkalinephosphataseandspecificboneproteinslikeosteocalcinandosteonectin.
- RegulatingosteoclastfunctionviatheRANK/OPGaxis - inresponsetoPTH,osteoblastsreleaseRANK‐Ligandwhichisasignallingmoleculethatbindstothecorrespondingreceptor,RANK,stimulatingosteoclastprecursorstobecomeactiveosteoclasts,thusstimulatingboneresorption.
Theyalsosecreteosteoprotegrin,whichisadecoyreceptorthatirreversiblybindstofreeRANKligand,preventingitfromattachingtoRANKontheosteoclastprecursors.Osteoprotegrinthereforeinhibitsthedifferentiation,fusionand activationofosteoclastsandthereforepreventsboneresorption.
14
Q
What are osteoclasts?
A
Multinucleatedgiantcells,formed fromthefusionofmultiple myeloidhaematopoieticcellsfromthemonocyte/macrophagelineage.
They reabsorb bone by firstdissolvingtheinorganichydroxyapatiteandthentheorganicmatrixbyproteolyticdigestion.
Theyhavereceptorsontheirsurfaceforcalcitonin,whichinhibitstheiractivityandareactivatedbyRANK‐Ligand.
RANK-L causes osteoclast progenitor cells to fuse together and migrate to site of bone resorption, attach to bone surface and become active.
Forms a ruffled border at bone surfacethenreleasesvarioussubstancesincludingtartrateresistantacidphosphate,knowasTRAP,whichhelpsdissolvetheinorganichydroxyappetite,andproteolyticenzymes likecathepsinK,whichbreakdowntheorganiccomponents.
Resorptionofboneformsasmallpit,knownasHowship’s lacunae.
Theruffledborderthenresorbstheorganicandinorganicproductsofdegradationfromthe Howship’s lacunae,transportingthemacrossthecellforexcretionviathesecretorydomain.
15
Q
What are osteocytes?
A
Former osteoblasts trapped in matrix, account for 90% cells in mature skeleton. They maintaintheboneandcellularmatrix,regulatingtheconcentrationsofcalciumandphosphorusinbone.
Long cellular processes for communication through smallchannelsinthebonecalledcanaliculi (part of haversian system).
Sense via mechanotransduction movement of fluid that happens when tissue is placed under compressive load, then can signal over long distances via their cellular processes.
Regulate bone remodelling in response to local mechanical or systemic (PTH) signals.
16
Q
How are octeoblasts formed?
What is osteoblasts fate?
A
Mono-nucleated, form from osteoprogenitor cells, that differentiate intoPre‐OBtoOB under theinfluenceofsignallingfactors RunX2andosterix.
Lifespan of about 6 months, then;
1. 10-15% becomeentombedinthematrixtheyhaveproducedandbecomeosteocytes.
2. Die by apoptosis
3. Differentiateintoliningcells,thatsitonthesurfaceofquiescentbone - these areflattened,inactiveosteoblaststhathavethepotentialtobecomematureosteoblastsforfutureremodelling.
17
Q
How do osteocytes respond to signals?
A
They regulate bone remodelling in response to local mechanical or systemic (PTH) signals.
Increase osteoclast formation by increasing RANK-L, leading to bone resorption.
Inhibits osteoblast formation by producing sclerostin, decreasing bone formation.
PTH and mechanical loading inhibits sclerostin production, increasing bone formation.
Inducesrapidcalcium release (osteocytic osteolysis) in response to PTH levels increasing.
18
Q
What are the zones in active osteoclasts?
What is the area of the bone underneath it called?
A
Sealing zone - one side of cell seals to bone surface
Secretory domain - cell surface away from bone where products of degradationarereleasedintotheinterstitialfluid
Ruffled border - at bone surface, this increases the surface area, aiding secretionandabsorptionofenzymesandproductsofdegradation
Resorptionofboneformsasmallpit,knownasHowship’s lacunae.
19
Q
What is bone?
A
Arigidorganwithavarietyoffunctionsincludingstructural,endocrineandmetabolic.
20
Q
What is bone tissue?
A
Dense connective tissue with;
High compressive strength (pushed together), low tensile and shear strength (pull apart), rigid but significant elasticity
It is ananisotropicmaterial as strengthisdependantonhowaloadisapplied.
21
Q
How do you classify bone anatomically?
A
Flat - thin,flatorcurvedbonesthatsandwichathinlayerofcancellousbonebetween2layersofcortex (majority of skull, sternum)
Short - roughly cube-shaped (carpals, tarsals)
Sesamoid - exist in tendons, improvethepowertheattachedmusclebyholdingthetendonfurtherfromthecenter ofthejoint,therebyincreasingitsleverage (patella, pairofsesamoidsunderthegreattoemeta‐tarsophalangeal joint)
Irregular - unique shape for individual purpose (vertebrae)
Long - havethreeanatomicregions; epiphysis,metaphysis andthediaphysis (femur, phalanges)
22
Q
Describe the structure of long bones.
A
Threeanatomicregions;
Epiphysis - end forming articular surface, covered by articular cartilage with physis and subchondral region underneath
Metaphysis - thin cortical bone surrounding loose trabecular
Diaphysis - thick cortiical bone surrounding central canal of bone marrow, outer region covered by the periosteum which is whichisdense,irregularconnectivetissuethat provides blood supply to the bone and provides fibroblasts and progenitor cells that can develop into osteoblasts/chondroblasts. Inside the medullary cavity there’s an endosteum which helps bone turnover and remodelling.
23
Q
What is the physis?
A
The growth plate - aspecialised zoneofcartilagelocatedattheendsoflongbonesthatisresponsibleforlongitudinalgrowth. Fuses as a child becomes an adult
24
Q
How do you classify bone by it’s macroscopic structure?
A
Cancellous (trabecular/spongy) - most in epiphysis and then metaphysis, less bending force so don’t need thick cortices to withstand them; mainly experience commpressive forces (especially sudden shock as weight is applied to joint) so supports articular surface, resists impact and transfers weight evenly
Cortical (hard) - diaphysis of long bones is mainly cortical, strong and rigid, good for big lever for multiplying great force over long distances, resists bending forces of muscles; slow turn-over rate
In diaphysis and mid-bone (metaphysis) mainly cortical woth a little cancellous.
At isthmus, in long bones diaphysis, thickest cortices and narrowest medullary canal.
25
How is cortical bone organised?
Main structural unit is an osteon - 2-3mm long cylinder with 8-15 concentric rings of bone called lamellae, each 0.2mm wide.
Their axis is parallel to the long axis of the bone.
Has channels containing neurovascular sytuctures called Haversian canals, if parallel to axis of bone; called Volksman's canals if perpendicular to long axis of bone. Together these form neurovascular network throughout the bone, connecting individual osteons.
26
How is cancellous bone organised?
A loose network of struts - makes it less rigid, more elasic than cortical.
Has a high surface area for metabolic functions so important for Ca homeostasis since high turnover compared to cortical, and can remodel quickly according to stress.
Trabeculae are organised along lines of maximum mechanical stress which act like struts and arcs of a bridge - gives a lot of strength wihtout weight of solid bone, allowing for effective transmission of loads, supporting areas of maximum stress.
27
How is bone organised microscopically?
Two types:
Woven bone - immature bone formed rapidly (foetal growth, fracture); collagen fibres organised haphazardly, not stress orientated so mechanically weak
Lamellar bone - highly organised, stress orientated, made by remodelling woven bone; collagen fibres in parallel sheets/lamellae so structurally strong as organised, stress orientated pattern
28
Describe the composistion of bone.
40% organic bone matrix (osteoid)
60% inorganic (calcium hydroxyapatite)
29
Describe the organic part of the bone matrix (the osteoid).
Makes up 40% of the bone.
90% of it is type one collagen, providing bone with tensile strength.
Rest is non-collagenous proteins;
proteoglycans (contribute to compressive strength) and matrix proteins (osteocalcin, osteonectin, osteopontin).
Most abundant non-collagenous protein is osteocalcin, produced by mature osteoblasts, promotoes mineralisation and formation of bone and attracts osteoclasts - clinical marker of bone turnover (serum/urine).
Cytokines and growth factors in matrix too - aids cell differntiation, activation, growth, turnover. Includes interleukins 1 and 6, insulin‐like growth factor and bone morphogenetic proteins.
30
Describe the inorganic part of the bone matrix.
Makes up 60% bone.
Calcium hydroxyapatite - suuports and gives bone compressive strength (so do proteoglycans in organic); main form Ca is stored in the body.
31
What are the functions of Calcium?
Structural - hard component of bone, without Ca salt hydroxyapatite, bones less dense and strong
Muscle - Ca ions vital for contraction cycle; action potential reaches motor endplate and triggers the depolarisation of the muscles sarcoplasmic reticulum and begins excitation‐contraction coupling
Ion channels - nerve action potential depends on voltage-gated ion channels sensitive to [Ca2+] in plasma, decreases in serum Ca cause ion channels to leak Na, making them hyperexcitable, increase means more Ca binds to these channels preventing depolarisation. So [Ca2+] levels off interfere with muscle and nerve function, causing cardia arryuthmias, muscle tetany, weakness.
Protein binding - like in the clotting cascade
Cell signalling - neurotransmitter release
32
What is the Calcium concentration in serum?
Total plasma concentration: 2.2 - 2.6 mmol/L
35-50% bound to protein, 5-10% in complexes with organic acids/phosphates. The remaining 50-60% is ionised and what is measured. It's clinically relevant in identifying ionised/total Ca imbalance like when serum proteins like albumin levels are low.
33
What is the differnce between serum and intracellular concentrations?
Why is this important?
Intracellular concentration 7000x lower than blood plasma.
Means cell sugnalling is very powerful as tiny amounts of Ca entering cell can be detected.
34
How does the body respond to hypercalcaemia?
1. Ca concentration risen above normal detected by thyroid
2. Thyroid releases calcitonin
3. Calcitonin acts on kidneys to reduce renal uptake of Ca so more lost in urine.
3. Calcitonin also inhibits osteoclasts so less Ca released into circulation from bone.
4. Serum Ca levels drop back to normal levels.
35
How does the body respond to hypocalcaemia?
1. Parathyroid gland detects serum Ca concentration drops below normal
2. It releases parathyroid hormone (PTH)
3. PTH stimulates osteoblasts, which have PTH receptor on surface, increases interleukins and macrophage colony stimulating factor and RANKL, these all stimulate osteoclast activity, reabsorbing bone
3. PTH also stimulates vitamin D hydroxylation to calcitriol in kidneys, PTH and calcitriol together increase RANKL from osteoblasts, and increases Ca uptake in kidneys and intestine.
4. Osteoclast activation slow, intestinal uptake intermediate, renal uptake fast, all increase Ca levels to normal homeostasis.
36
How do the intestines influence intake and excretion of calcium to affect concentration?
Normally 20mmol Ca absorbed by intestines per day by binding to calbindin as it brushes intestinal epithelial cells, which is a vitamin D dependent protein, absorption of Ca is reglated by calcitriol (active vit D).
Intestines get 15mmol Ca from excreted bile which combines with the 25mmol we get from diet, so about 40mmol passes through.
Intestines also excrete Ca via bile so net gain is about 5mmol.
37
How do the kidneys influence intake and excretion of calcium to affect concentration?
They filter about 250mmol Ca per day and reabsorb about 245mmol, so net loss of 5mmol.
Calcitonin - increases renal excretion (inhibits reabsorbtion).
PTH - major affer is stimulating process of vitamin D to calcitriol, minor affect reducing renal excretion.
38
How do bones influence calcium concentration?
10mmol exchanged everyday.
Calcitonin from thyroid directly inhibits osteoclasts.
Osteoblasts indirectly stimulate osteoclasts by releasinf RANK-L under influence of PTH.
39
What controls serum calcium concentration?
Chief cells within the four parathyroid glands (located on the back of neck thyroid gland) release PTH (parathyroid hormone) which is most importnat regulatory hormone of [Ca].
Fall in [Ca] detected by PTH receptors which then synthesise and release PTH into blood. This acts on kidneys, intestines, osteoblasts and, indirectly, osteoclasts.
Also releases calcitonin from parafollicular cells, opposing PTH action, directly inhibiting osteoclasts.
Oestrogen also inhibits RANKL release from osteoblasts, reducing osteoclast activity and bone resoption (lost in menopause - lower bone density).
40
How is vitamin D acticated?
What does it do?
Must undergo two hydroxylations, first in liver, making 25hydroxyvitaminD; then in kidney, making calcitriol (1‐25dihydroxyvitaminD).
Conversion in kidneys is stimulated by PTH or low serum calcium.
Calcitriol has 3 main actions:
Stimulate osteoblasts to release RANK-L to stimulate osteoclasts and increase absorption and reabsorption in GI tract and kidneys.
41
What is bone remodelling?
The cycle by which small increments of bone are removed and then replaced by new bone.
42
Why is bone remodelling necesary?
Micro-trauma from everyday life results in micro-damage/micro-fractures which would weaken the bone leading to further damage of bone around them, eventually resulting in mechanical failure (fractures) if not repaired.
It is needed to repair macro-damages (fractures).
Allows bones to change in response to changing loads.
It is needed for calcium homeostasis.
43
How frequently are bones remodelled?
5-15% of the surface of adult bones are normally undergoing remodelling.
In a year, about 18% of an adult skeleton is replaced - 20% of cancellous bone and 2% of cortical bone is replaced.
44
What are the six stages in the bone remodelling cycle?
Six stages:
1. Quiescence - dormancy
2. Activation - RANKL, PTH, M-CSF, vit D
3. Resorption - osteoclasts migrate to bone and break it down
4. Reversal - osteoblasts activated by osteoclasts
5. Formation - osteoblasts lay down osteoid
6. Mineralisation - hydroxyapatite deposited
45
What happens during the quiescence stage of the bone remodelling cycle?
90% bone in state of inactivity/dormance.
Osteoblasts are flattened inactive cells lining bone surface, osteocytes maintain and monitor bone for local changes and produce sclerostin - protein that inhibits osteoblastic activity to keep in resting state.
46
What happens during the activation stage of the bone remodelling cycle?
Local/systemic signallers bring it out of quincience stage.
Local - osteocytes detect stress/micro-damage and signal to osteoblasts to release RANK-ligand and macrophage colony stimulating factor (M-CSF).
Systemic - PTH and vit D, as well as some endocrine hormones like thyroid and growth hormones (oestrogen and calcitonin are antagonistic to this, inhibiting bone resoption)
These begin the recruitment, differentiation and activation of osteoclasts.
47
What happens during the resorption stage of the bone remodelling cycle?
RANKL/M-CSF activated osteoclasts begin resorption process:
1. attach to bone with tight seal around edge
2. polarose themselves, forming ruffled border near the bone, and functional secretory domain on far side
3. release hydrochloric acid from ruffled border, dissolving inorganic bone (hydroxyapatite), forming resorption pit
4. release protease to dissolve organic matrix
5. transport degredation products to be secreted through the functional secretory domain
48
What happens during the reversal stage of the bone remodelling cycle?
Osteoblasts migrate to resorption pit because of signals while osteoclasts are regressing to their inactivate state.
They differentiate and activate due to direct osteoclast to osteoblast signalling molecules.
49
What happens during the formation stage of the bone remodelling cycle?
Activated osteoblasts lay down organic bone matrix - osteoid.
Osteoid is made of type one collagen with various bone proteins like osteocalcin and proteoglycans. It fills the resorption pit.
The osteoblasts then control the mineralisation of the osteoid.
50
What happens during the mineralisation stage of the bone remodelling cycle?
This happens concurrently to formation stage producing osteoid. 75% happens in first week or two, then the rest in weeks-months.
Hydroxyapatite crystals are deposisted, forming the inorganic matrix (made of calcium and inorganic phosphate).
This turns the unmineralised osteoid from soft to hard mineralised bone.
51
What regulates bone mineralisation?
Local - presence of inorganic pyrophosphate (PPi) act as a inhibitor to mineralisation, so in fluid like synovial fluid where Ca and PO4 present but mineralisation would be bad, acts as a feedback loop;
Osteoblast-derived proteins (osteocalcin promotes but osteopontin inhibits mineral binding).
Systemic - PTH, vit D, fibroblast growth factor 23 (FGF23 - increases PPi, decreases PTH/vitD).
52
What are the two mechanisms of bone formation?
Intramembranous ossification - osteoblasts lay down osteoid within loose fibroconnective tissue of a fibrous membrane, no prior structure.
Endochondral ossification - osteoid is deposited on an existing cartilage scaffold, most bones in developing feotus produced this way.
53
When does intramembranous ossification occur?
In foetus, flat bones of face, most cranial bones, clavicles formed this way.
In primary healing of fractures (when treated with solid metal plate forcing the ends together with no movement).
When bones grow in width (appositional growth), intramembranous ossification occurs at the periosteum or perichondrium at the physis. This relys on matching resorption of bone on inner surface of diaphysis by cells on endosteum.
54
What is intramembranous ossification?
How is it formed?
Bone develops directly from sheets of undifferentiated mesencymal cells without a cartilage model.
Mesenchymal cells in embryonic skeleton proliferate in fibrous tissue, some differnetiating into osteogenic cells which become osteoblasts.
Osteoblasts cluster to form the ossification centre, which produces osteoid (random arrangement of woven bone), in which hydroxyapatite is deposisted within a few days.
Osteoblasts become trapped and transition into osteocytes, mesenchymal cells surrounding ossification centre replenish osteoblast supply.
As the bone matures, trabecular network of calcified matrix develops around the blood vessels, periosteum forms from surface osteoblasts and mesenchyme.
Then compact cortical bone forms below periosteum and blood vessels in the trabecular bone condense into red marrow.
55
How are primary centres of endochondral ossification formed?
Osteoid is deposited and mineralised ontop of preformed diaphyseal cartilage scafold while the cartilage is being removed.
In early foetal development mesenchymal cells differntiate into chondrocytes, forming cartilaginous skeletal precursor. The perichondrium forms on the surface.
Perichondrium becomes the periosteum, producing thin layer of bone on surface of the diaphyseal cartilage (periosteal collar).
As more cartilage matrix is produced, chondrocytes at the centre of the scaffold enlarge and begin to calcify the matrix which prevents nutrients from reaching the chondrocytes, so they die and surrounding cartilage disintegrates.
Blood vessels invade spaces left by disintegrated cartilage, carrying osteogenic cells, so primary ossification centre forms in middle of cartilage scaffold (ossification begins).
More cartilage forms at ends of bones, increasing length, diaphyseal cartilage being replaced with bone.
56
When does endochondral ossification form?
Osteoid is deposited on preformed cartilage.
Most of skeleton developed this way, how the physis facilitate longitutinal growth and involved in 'secondary healing' of fractures, when not fully immobilised (forms soft callus cartilage then replaced by hard woven bone and remodelled into lamellar bone).
57
What is endochondral ossification?
Osteoid is deposited and mineralised ontop of preformed cartilage scafold while the cartilage is being removed.
58
How are secondary centres of endochondral ossification formed?
Osteoid is deposited and mineralised ontop of preformed cartilage scafold of epiphysis while the cartilage is being removed.
Chondrocytes die in the calcified matrix, blood vessels infiltrate along with osteogenic cells and ossification occurs.
Secondary ossification centres form at birth in predictable way - can age child from skeleton.
59
What are traction epiphyses?
Secondary ossification centres formed in non-weight bearing part of bone (like greater trochanter of femur), at ligament/tendon attachment sites.
60
What contributes to cessation of growth?
Epiphyseal growth plates close, when depends on sex and physis location. But generally 14 in females, 16 in males.
It is genetically determined - average both partents, subtract 6cm for female, add 6cm for males.
Ostrogens/Androgens initially increase growth hormone secretion in early puberty and increase bone growth but later induce closure of growth plates.
Premature growth plate closure leads to shortened bones.
Caused by systemic disease (leukemia), poor nutrition, endocrine deficiencies (growth hormone), thyroid problems, infection, osteomyelitis, trauma...
61
What are the physis?
What are they responsible for?
Hyaline cartilage plates at ends of long bones.
Bone longitudinal growth at actual physis (endochondral ossification), circumferential growth at the perichondrium (ntramembranous).
62
Describe the macroscopic structure of the physis.
Secondary ossification centre - forms new bone.
Physis - zone of provisional calcification (ZPC) and primary groeth plate.
Perichondrium - encircles outer edge of physis, perichondral ring (at ossification groove) is continuous with the metaphyseal periosteum, increasing strength of attachement of bone and physis.
63
How is blood supplied to the physis?
Why is blood supply important?
Three main routes:
1. Perichondral artery - main blood supply to the physis
2. Epiphyseal artery - supplies resting zone
3. Metaphyseal arteries - supplies metaphyseal spongiosa
Bone growth highly vascular as needs constant energy and building blocks. Any interuption is very bad (like in Perthe's disease of the hip).
64
What are the microscopic zones of the physis?
How do chondrocytes differ at each zone?
Resting zone (at the epiphyseal end)
Proliferation zone
Hypertrophic zone (zones of maturation, degeneration, provisional calcification)
Metaphyseal bone (primary/secondary spngiosa)
Chondrocytes sparsely packed at ephiseal end in resting zone, as move towards metaphysis, cells multiply and line up in columns longitudinally and increase in size.
As the cells go through changes they remain stationary and the actual physis itself migrates.
65
What happens at the resting zone of the physis?
At the epiphyseal end, contains sparsely packed chondrocytes, not curently changing size/producing matrix.
They contain large lipid stores, glycogen, and proteoglycans for future growth/matrix production.
Epiphyseal arteries supply blood.
66
What happens at the proliferation zone of the physis?
Stimulated choondrocytes stack up in columns and multiply at increased rate.
They begin to produce cartilaginous ECM (similar structure to bone without Ca to make rigid) and will continue to do this throughout transition (but highest rate here).
67
What conditions occur from defects at the proliferative zone of the physis?
Defects alter rate cells multiply, causing decreased/increased bone length as in achondroplasia and gigantism.
68
What happens at the hypertrophic zone of the physis?
After cells multiplied many times in proliferation zone, proceed to increase size many times in three hypertrophic sub-zones (maturation, degenration, provisional calcification).
As they increase size, chondrocytes collect and store Ca to release when they die.
69
What can go wrong in the hypertrophic zone in the physis?
It is a relatively weak point in physis so site of slipped upper femoral epiphysis (SUFE) and Salter-Harris fractures.
70
What happens at the zone of maturation in the physis?
First of hypertrophic zones, cells differentiate, mature, and slowly increasing size until double.
71
What happens at the zone of degredation in the physis?
Second of hypertrophic zones, chondrocyes have a 5-fold increase in size, becoming almost too big too survive so must undergo apoptosis (in third zone -of calcification).
72
What happens at the zone of provisional calcification in the physis?
Third (and last) of the hypertrophic zones, now massive chondrocytes die by apoptosis and release Ca they have stored up to calcify surrounding matrix.
73
What happens at the metaphyseal bone during growth at the physis?
Next to the dying chondrocytes, osteoprogenitor cells and blood vessels infiltrate the calcified matrix, rapidly lay down immature, woven bone (primary spongiosa).
This immature bone is then remodelled in the secondary spongiosa to make the highly organised structure of lamellar bone (takes much longer than rapid production of woven bone, months).
74
What is Achondroplasia?
A disease of the physis, most common skeletal dysplasia.
From defect in Fibroblast Growth Factor Receptor 3 (FGFR3) gene.
Causes increased inhibition of chondrocyte proliferation in proliferation zone. Autosomal dominant inheritance but 80% new mutations.
'Disproportionate dwarfism' as affects different body parts differently and doesn't affect trunk. Follows 'rhizomelic' pattern as proximal limbs affected more than distal.
75
What is Gigantism?
Disease of the physis causing hight well above average (>2.1m).
Excess growth hormone leads to increased proliferation of cells in proliferation zone.
Normally caused by a pituitary adenoma.
Causes gigantism in children but in adults, because physis are closed, causes acromegaly (hands, feet, forehead, jaw, nose increase in size).
76
What is the normal immature gait?
When does the gait mature?
Early walking: short Stride length, fast cadence, low Velocity, widened base of support (until 30-36 months), can't stand on one leg.
Mature gait develops around age 7.
77
What causes an abnormal gait in children?
Often atraumatic, incidence of 180/100,000 so common.
Limp caused by pain (legs, pelvis, lower back), mechanical problem (dysplasia), neuromuscular problems.
78
What is the common MSK conditions causing limping in children ages:
0-2
2-8
4-8
13-16
0-16?
0-2: DDH
2-8: Transient Synovitis
4-8: Perthes'
13-16: SUFE
0-16: Tumour/septic arthritis/neuromuscular
79
What does acute, contant, morning/after inactivity, night pain suggest in a limping child?
Acute - trauma, infection
Constant - malignancy, chronic infection
Morning pain/pain after inactivity - Inflammatory joint disorders
Night Pain - malignancy, osteoid osteoma, benign “growing pains”
80
What do you have to check during exaination of a limping child?
Gait
Spine
Asymmetry
Deformity
Swelling
Tenderness
Examine all joints
Rotational profile
81
What is Transient Synovitis?
What are the clinical investigations and treatments?
Irritable hip, very common in ages 2-5.
Non-specific, short term inflammatory synovitis with synovial effusion of the hip joint.
Clinical features:
Painful hip/thigh/knee
Often associated with viral infection
Synovial fluid effusion
Hip held in flexion, lateral rotation and abduction
Exclusion of other conditions (mainly infection/sepsis)
Investigations:
Full blood count
ESR, CRP
X rays (AP & frog lateral)
Ultrasound (look for effusion, should be small or none)
MRI, bone scan... (not routine)
Paracetamol and ibuprofen, but self limiting.
82
What is developmental dysplasia of the hip?
What are the risk factors?
DDH is when accetabelum is less rounded so hip is more prone to dilsocation.
Risk factors are genetic, breach after 32 weeks or Caesarian, 1st Born, Oligohydramnios in womb, females 5x more likely.
Identification of risk factor will lead to formal examination.
83
What are the examinations for checking for DDH?
Barlows - test if hip is dislocated, (B for brutal), legs to 90 degrees flexion and then push knees, trying to dislocate, should feel clunk as easily dislocate in DDH
Ortolani - test if hip is dislocated, (O for out), hip already dislocted, bring hip out to abduction and feel clunk back in
Other things to look for:
Deepening skin crease/asymetry
Leg length discrepancy (especially in older infants after 6-8 weeks) by the Gally-atsy test
Reduced abduction (especially in older infants after 6-8 weeks), should be able to get to frog position
Also x-ray, checks if hip is in socket...
Ultra-sound confirms
Try pick up <6weeks.
84
What is treatment for DDH?
Infants - Harness to hold hips adducted and flexed, regular checks.
If treated early, 95% success.
Older infants (3 months) - surgery
85
What is Perthes' Disease?
What are the risk factors?
Osteonecrosis (avascular necrosis) of femoral epiphysis caused by poorly understood non-genetic factors, flattened, fragmented femoral head on x-ray but socket normal.
Normally ages 4-8, 4x as likely in boys, more common in lower social class, likely due to smoking.
86
What is the treatment of Perthes' disease?
Principles are prevention of stiffness, contain femoral head in acetabulum (containment, sometimes need surgery), keep moving - needs a good physio for 2-3 years. Normally blood supply will return on its own.
Surgical treatment required in certain circumstances (tip head down into socket), outcome depends on how well femoral head remodels.
87
What is Slipped Upper Femoral Epiphysis?
What are the risk factors?
SUFE is metaphysis slipping off of epiphysis.
Normally in ages 13-16, males 3x more likely, younger in females (not after menarche), obese/tall and slender, rapid growth, genetic - 7% risk 2nd family member involved.
Overweight big factor so increasing incidence.
Bilateral in 42% so often treat both sides.
88
What are the clinical features and treatment for SUFE?
Acute/chronic/acute on chronic pain in groin, thigh, knee. Often boy, slightly overweight with knee pain due to referred pain.
Limp, antalgic gait, externally rotated and adducted limb.
Frog lateral x-ray good to see.
Treatment is surgery to pin in situe to remodel in good position, epiphysis to diaphysis. High rate of bilateral and stops leg length discrepancy so do both sides.
89
What are red flags for paediatric MSK?
Neonate with painful paralysedlooking arm or leg, even without fever/other signs (septic arthritis/infection)
Asymmetry of spine or limbs (scoliosis (forward bend test)/DDH)
School age child with limp (Perthes' disease)
Knee pain in adolescent (SUFE/tumour)
Back pain (discitis)
NAI (especially <1year)
90
What infections can cause limping child?
What emergency protocol needs done?
Cellulitis (skin infection)
Osteomyelitis (bone infection)
Septic arthritis (joint infection)
Usually requires emergent referral for investigation +/- aspiration.
91
What is discitis?
Inflammation of the vertebral discs.
Presentation can be subtle so usually MRI required.
Normally inflammatory but hard to get sample so treat with antibiotics.
Epidural abscess (if bacterial) is surgical emergency.
92
What could painless atraumatic swelling be?
Tumours:
Ewings tumours in infants
Osteosarcomas in adolescents (especially around knee)
Get x-ray, early diagnosis is key.
93
What should raise suspicion for NAIs?
Pre-existing disability, vague history, inconsistent history with injury, delay in presentation, multiple bruises of varying age, multiple fractures, burns.
94
How are children’s bones different from adult bones?
More numerous as some fuse in adulthood like ilium/ischium/pubis in pelvis, open physis (dark lines on radiograph), ossification centres (lighter circular areas). These are predictable.
The bones are less rigid and brittle, much more elasticity (bend and spring back) and plasticity (bone changes permanently).
Periosteum covering diaphysis surface is much thicker (like leather) which makes fractures easier to reduce as periosteum remains intact so bones don’t displace as much.
95
What fracture patterns in bones are typically seen in children?
Greenstick fracture - on tension side (where force is applied) as bone pulled apart but crack only part way across bone.
Buckle/torus fracture - on compression side (opposite tension side), force too great so buckles under pressure and bulges out the side.
96
When is the remodelling potential of fractured bones greatest?
At young age, deformity corrects as bone grows, so greater time before physis fuse means more time for correction.
Closer to joint and deformity in same plane as joint as greater potential for remodelling.
In children periosteum covering diaphysis surface is much thicker (like leather) which makes fractures easier to reduce as periosteum remains intact so bones don’t displace as much and go back to anatomical position.
Wolf’s law also important as bone deposited on compression side (more load here) and absorbed on tension side (less load), healing residual angular deformity. However this means no potential for remodelling rotational deformities, as rotational movement doesn’t put much force through bone.
97
Why are fractures at the physis important?
They allow longitudinal growth so before fusion (14-16) can cause growth problems.
Also right next to joint surface so intra-articular fractures can lead to step in articular surface, which if unaddressed can quickly damage cartilage on other side of joint, leading to post-traumatic arthritis.
98
What is the Salter-Harris classification system?
How should bone be orientated when considering mnemonic?
Used to describe fractures based on pattern around physis, good for determining management plan. Types:
1. Straight
2. Above
3. Lower
4. Through
5. Ruined
Orient bone with articulation surface at the bottom so can use SALTR mnemonic, describing fracture as above/below.
99
Describe type 1 Salter-Harris fractures.
Straight. Fracture line straight across the physis. Doesn’t involve bone, only cartilage.
Difficult to diagnose (especially if completely undisplaced as only evidence is soft tissue swelling around it) but least likelihood of growth abnormality.
Treatment is reduce (closed normally) and immobilise (cast normally enough, sometimes wires).
100
Describe type 2 Salter-Harris fractures.
Above. Fracture line exists above the physis, exiting above physis into metaphysis so metaphyseal wedge attached to the epiphysis.
Most common SH fracture (70%), low chance of growth deformity.
Treat with reduction (normally closed) and immobilisation (cast). Sometimes if unstable/difficult to reduce, need open reduction and a worse across fracture for stability.
101
Describe type 3 Salter-Harris fractures.
Lower. Fracture line below the physis, exits into the joint (so need to be worried about step at fracture line) or fracture line exits below the physis, epiphyseal fragment.
First of the intra-articular type, chance of growth deformity.
Treat with anatomic reduction surgery and monitor after for growth deformity. Physis above epiphyseal fragment can become confused and close if not reduced properly/severe injury, causing asymmetrical growth.
102
Describe type 4 Salter-Harris fractures.
Through. Fracture passes through the physis itself, creating combined metaphyseal/epiphyseal fragment.
Second intra-articular SH type, chance of growth deformity reasonably common.
Treat by anatomically reducing in surgery and monitor growth deformity (happens where physis is damaged at fragment only), asymmetrical as bone growth can continue on other side of physis.
103
Describe type 5 Salter-Harris fractures.
Ruined. Crush injury to physis, with worst prognosis and growth arrest.
Treat to monitor growth arrest and plan epiphysiodesis (physis fusion) on contralateral limb to prevent significant leg length discrepancy.
104
What are some common fractures in children?
How do you reduce the fracture?
Forearm and wrist fractures
Femoral fractures
Supracondylar elbow fractures (can be type 1 - nondisplaced, type 2 - angulated with intact posterior cortex, type 3 - completely displaced)
Treat wrist/femoral by manipulating under anaesthetic:
Apply force to bend bone back and counter-force as a fulcrum (to push against).
Can use K-wires and flexible nails to support if needed.
Treat femoral by bed traction, flexible nails.
105
What are risk factors of children of non-accidental injuries?
First-borns, unplanned, premature, disabilities, step-children, younger (immobile).
106
What are risk factors of adults of non-accidental injuries?
Single parent, unemployed, substance abuse, personal history of abuse, lower SE status.
107
What are common soft tissue injuries of non-accidental and accidental?
Accidental is normally bruising of hands/feet/lower legs.
Non-accidental often:
Head/face injuries <18 months
Lumbar injuries <5 years
Bite marks (human characteristically painful, dimensions used to estimate size of biter, higher infection rate than animals)
Burns (cigarette, lighter, held to hot buggy heated by sun, neglect causing bad sunburn)
Bruising (grip marks from force feeding on face - intraoral often finds torn frenulum, bridge between top lip and gum)
Petechial bruising (burst blood vessels after slap around white finger/belt marks)
Abdominal bruising (after repetitive punching, indicates significant injury like liver laceration)
108
What are common fractures caused by NAIs?
Metaphyseal corner fracture (most specific for NAI - in around 50% cases) almost all <2y/o, small enough to be shaken and muscle tone doesn't protect limbs, shear force causes whiplash of limbs, results in multiple microfractures across metaphysis perpendicular to long axis of bone.
Rib fractures (especially posterior) in 50% cases, often diagnosed from skeletal survey, from crushing while shaking.
Femoral fractures <3y/o (non-ambulatory) can be accidental but treated as NAI until proven.
109
What are characteristics of osteogenesis imperfecta?
Group of genetic disorders caused by defect in type 1 collagen, causing extreme bone fragility.
May cause several fractures by 1st birthday, misattributed to abuse until diagnosis. Careful consideration as also more vulnerable to abuse due to disability.
Also causes blue sclera, hearing loss, short stature.
110
What are some acute traumatic sport injuries?
Cutaneous - bruising, cuts, abrasions
Head injuries - contact sports, long-lasting neurological damage
Cartilage/meniscal injuries
Muscle/tendon/ligament injuries - ankle ligaments, hamstring muscles, complete ruptures of ligaments (ACL)
Dislocations - contact sport, shoulders, ankles, fingers
Fractures - high energy movement
111
What are some chronic overuse sport injuries?
Tendonitis - tendon repeatedly loaded above ability, causing inflammation, swelling, degeneration, restrict movements, weak/painful movements; fibrous scar tissue can form on tendon, bulking and weakening it. Must rest and correct form.
Stress fractures - repetitive stress above normal causes microfractures and periosteum inflammation (foot and tibia common). Must rest and correct form.
Back pain - lower spine, worsened existing pathology, repeated microtrauma, most likely in people with poor core muscle power. Treatment/prevention focuses on improving core, avoid worsening it.
Instability after injury like shoulder dislocation. Physio can help to improve muscle tone and proprioception.
112
How can we prevent sport injuries?
Conditioning - minimal fitness (cardiovascular, balance, muscle strength, flexibility) reached so can perform and endure exercise, building up gradually with new sports (frequency, duration, intensity)
Warm up/Cool down - stretched and light at start to prep CV by increase HR, SV, BP; MSK by increasing blood flow to muscles, raise temperature, reduce stiffness, improving range of motion; ventilation (rate and volume) increase; neural pathways primed, metabolic hormone levels change (like glucagon increase to provide glucose-rich blood)
Technique - good form and take safety measures
Equipment - well maintained, correct
Avoid overstressing - don't push body past threshold, rest if needed
Anatomy - like females ACL
113
What is an acute apophyseal avulsion (paediatric MSK)?
At the apophysis (secondary ossification centre where tendon inserts into bone), this is only connected by cartilage so weak point, forceful contraction of muscle can pull (avulse) apophysis from rest of bone. Sudden snap/pop sensation at site of avulsion, pain and weakness in muscle.
Diagnose with a radiograph, MRI if unclear. Generally treat with rest, protected weight bearing, early ROM, passive stretching; rarely surgery (>3cm displacement).
114
What is chronic apophysitis (paediatric MSK)?
What are common locations and their corresponding names?
Caused by repeated microtrauma to an apophysis, causing range from inflammation to fragmentation of apophysis.
Radiographs to diagnose (MRI if unclear), local tenderness and pain on resisted muscle contraction.
Conservative management of rest, NSAIDs, stretches, modified activity.
Osgood-Schlatter’s disease - tibial tuberosity
Sinding-Larsen-Johansen disease - inferior pole of the patella
Sever’s disease - calcaneus.
115
What are common sites of apophyseal injuries?
At the apophysis - secondary ossification centres, where tendons insert into bone. In children this hasn't fused so only joined by cartilage and weaker.
Greater trochanter - abductor muscles attach
Lesser trochanter - iliopsoas
Iliac crest - abdominal muscles
Anterior superior iliac spine - sartorius
Anterior inferior iliac spine - rectus femoris
Ischial tuberosity - hamstrings
116
What are the three types of shoulder dislocations?
Anterior (most common) - humeral head anteriorly, slightly inferiorly
Posterior (extreme muscle contractions like seizures/electrocution) - humeral head posteriorly rotates; can be hard to diagnose on radiograph
Luxatio Erecta (high energy trauma, rarest) - humeral head levered out with hyperabduction and trapped inferior to glenoid
117
What nerve is commonly injured in anterior shoulder dislocations?
How do you test for this?
Axillary nerve.
Sensation of it tested over lateral shoulder.
118
How are anterior shoulder dislocations diagnosed?
Squared off shoulder, arm held in adduction and internal rotation.
Plane radiograph of 2 views, like scapular Y view/axilliary shoot through.
119
What damage can occur during anterior dislocations to humeral head/glenoid/soft tissue?
Hill-Sachs lesion - compression fracture to posterolateral humeral head as it's crushed by anterior glenoid rim; surface of bone impacted but intact due to overlying cartilage.
Bankart lesion - humeral head fractures edge of glenoid rim or rips through anterior labrum, meaning it cannot hold the humerus in place properly anymore
120
What is the 3 step treatment of an acute shoulder dislocation?
1. Reduce - methods include longitudinal traction +/- lateral force to humeral head, use sedation/muscle relaxants
2. Restrict - short period of time in shoulder immobiliser (<2 weeks) to settle pain and recover soft tissue
3. Rehabilitate - early ROM exercises with physio, return strength of dynamic stabilisers
121
What is elbow epicondylitis?
What is the investigation?
Chronic overuse injury to medial/lateral elbow epicondyle.
On medial side, flexor-pronator mass. On extensor side, extensors originate. All bunched around epicondyle prominences, so a lot of strain.
Clinical diagnosis, radiographs may ay show calcification of the affected tendons. Ultrasound good as it's a dynamic test which high accuracy but is user dependent. MRI useful to evaluate out other pathologies like ulnar collateral ligament injuries, pronator origin ruptures.
122
What is the treatment of elbow epicondylitis?
Conservative first (90% success).
Rest/avoid exacerbating 3-6 months, activity modifications (assess racquet set-up/swing technique), physio, ice, bracing, NSAIDs.
Possibly extra-corporeal shockwave therapy - ultrasound energy through skin to promote angiogenesis, tendon healing, short-term analgesia.
Corticosteroids injections can reduce inflammation but significant side-effects like tendon weakening, nerve injury, skin pigmentation.
Surgical if conservative fails - debridement of inflamed tendon tissue, reattachment of muscles, release nerves (if trapped). 80-90% good outcome but lower in lateral or if neural involvement.
123
What is lateral epicondylitis?
Tennis elbow. From overuse of common extensor origin (often ECRB - extensor carpi radialis brevis), repeated microtrauma causes inflammation.
Activities using wrist extension, gripping, heavy lifting often cause - half professional tennis players develop due to backhand swing (risks: poor swing technique, heavy racquet, incorrect grip size, high string tension), repetitive hammer using.
Pain over ECRB origin/lateral epicondyle, actions that stretch common extensor origin - resisted wrist/finger extension, passive wrist flexion in pronation.
Can have radial tunnel syndrome - deep aching pain in dorsoradial forearm due to posterior interosseous nerve compression.
124
What is medial epicondylitis?
Golfers elbow less common than lateral (tennis). Can have both.
From overuse of flexor-pronator mass: repetitive wrist flexion/pronation in golf, baseball racquet sports, jobs requiring force grip and heavy lifting - plumber, carpenter, construction.
Pain 1cm distal and anterior to medial epicondyle, worsened by resisted wrist flexion/pronation.
Can have ulnar neuritis - paraesthesia in ring/small fingers.
125
What are sprains?
What are strains?
What are common locations?
What is the treatment?
Sprains are sudden stretching of ligaments past their elastic limit, deforming or tearing them.
Strains are over-stretched/used muscle causing tears in the muscle fibers/tendons.
Common sites - the groin (hip adductors), the hamstrings and the ankle.
Treated with rest, ice, activity modification and early RoM exercises; severe ankle ligament injuries can cause instability that might need surgery.
126
What are common soft-tissue knee injuries?
Very common in high impact sports - contact and noncontact.
Meniscal, PCL, ACL, collaterals.
Combination is quite common (like ACL+meniscal), can happen all at once with knee dislocation.
127
What is a common history and presentation of meniscal tears?
How do you examine this?
Twisting injury with delayed swelling (after 30 mins), sometimes can play on, immediate may indicate ACL/PCL. Localised pain to one side of knee with mechanical symptoms: locking (block to fully extending knee, not muscle spasm), giving way, ‘Clicking’ - indicates displaced meniscal tear trapped between the joint surfaces.
Localised joint-line tenderness over affected side (most sensitive test); most have some effusion, picked up by patellar tap/sweep test; check for other knee injuries using radiograph.
MRI used to diagnose.
128
What is management of meniscal tears?
Conservative - rehabilitation with NSAIDs, physio to strengthen knee muscles/return proprioception.
Surgery (arthroscopically) -
Removal: minimise amount of tissue removed, only remove if irreparable/failed repair, poor outcome if completely removed (arthritis 100%) so cadaver transplant considered if young but 8-12 month healing time.
Repair: return fragment to anatomical position to heal with fibrocartilaginous scar, reliant on blood supply so best in red-red zone.
129
What is a common history and presentation of an anterior cruciate ligament tear?
Common, from non-contact twisting (especially studded boot), 4.5x in females.
Likely with a meniscal tear.
Acute 'pop' sensation, immediate extensive swelling/haemarthrosis as own blood supply (since intracapsular ligament), inability to play on.
130
What is best test for ACL tear?
Lachman's test.
131
What is a common history and presentation for posterior cruciate ligament tear?
Less common than ACL, from direct blow to flexed knee, not normally isolated - usually occurs with other injuries like posteolateral corner injury.
Acute 'pop' sensation, immediate extensive swelling/haemarthrosis as own blood supply (since intracapsular ligament), inability to play on.
132
What is examination for PCL tear?
Posterior sag - tibia sags backwards with gravity.
Use dial and quads active tests.
133
What is common history and presentation of medial collateral ligament tear?
Caused by valgus stress, often by direct blow/contact to lateral knee.
No hemarthrosis and late swelling as don't have significant blood supply so often play on.
Medial knee pain and valgus instability, tenderness over MCL/it's origin or insertion.
Combined ACL/MCL most common multi-ligamentous injury, rule out other pathologies.
134
What is common history and presentation of lateral collateral ligament tear?
Rarely injured in it's own - often with PCL.
Caused by varus stress, often by direct blow to medial knee.
No hemarthrosis and late swelling on it's own as no significant blood supply.
Lateral knee pain and varus instability, tenderness over LCL/it's origin or insertion.
Dial test is performed to examine posterolateral corner injury.
135
What is the investigation for most knee ligamentous injuries?
Plain radiograph first - detects effusion, haemarthrosis, rules out fractures/dislocations. Stress views to visualise varus/valgus openings of collateral injury.
MRI is gold standard to determine severity/grade and look for other injuries like meniscal and bone bruising.
136
How can you prevent ligamentous injuries of the knee?
Plyometrics (jump training - land properly, strengthen and condition)
Neuromuscular training
Female athlete focus on landing in less valgus, more flexion to protect ACL
Hamstring strength
Skiers fall correctly
Knee bracing (some evidence for MCL in contact sports but not others)
137
How do we treat ACL injuries?
3 categories of patients: copers (compensate and play on), adapters (change sporting level, minimise knee stability need), and non-copers (unsatisfied and so opt for surgery).
Rehab involves: cryotherapy (ice), early passive extension, closed-chain exercises for hamstring/quads strength, 9-month physio program, some unhappy with results.
Surgery - arthroscopic reconstruction with the patients own hamstrings or patellar tendon, or with an allograft from a donor. Post-op rehab similar but emphasis on graft protection.
137
How do we treat PCL ruptures?
Mostly non-operative, protected weight-bearing, immobilise in extension (if grade 3).
Quad strength and early RoM exercises.
Surgical reconstruction if multi-ligamentous, bony avulsions, and tried conservative but too unstable.
138
How do we treat collateral ligament injuries?
Mainly conservatively - NSAIDs, rest, physio for quads strength, resistance exercises.
Aim to return to sport at 6-8 weeks.
Repair if multi-ligamentous or unstable grade 3.
138
How do we treat multi-ligamentous knee injuries?
Normally surgery - emergent reduction then neurovascular assessment, external fixator as very unstable knee may re-dislocate, also allows vascular repair if needed.
Then delayed repair of up to 3 weeks.
139
What are the three pathologies of shin splints?
Tibial stress syndrome
Tibial stress fracture
Exertional compartment syndrome
140
What is tibial stress syndrome?
Shin splints - a traction periosteitis of the origins of the tibialis anterior/posterior muscle.
Common in runners (insufficient shock-absorption from footwear/hard or uneven surfaces).
Can progress to stress fractures.
Often diffuse pain over mid-tibia, improving with running but worse after.
May have tight achilles/pes planus (flat feet), pain provoked by resisted plantarflexion.
Radiograph/bone scan to exclude stress fractures, MRI identifies other soft-tissue pathologies.
Most treated conservatively - NSAIDs, activity modification.
Surgery rare - fasciotomies to decompress deep posterior leg compartment.
141
What is exertional compartment syndrome?
Reversible muscle ischaemia in lower leg compartments (normally anterior).
Common in runners and soldiers (differentiate from tibial stress syndrome).
Burning/aching leg pain related to exercise, relieved with rest.
Paraesthesia in 1st dorsal web space of foot (deep peroneal nerve).
Diagnose by directly measuring compartment pressures with cannula deep into muscle belly at rest and after a brisk run/exercise. Significant differences noted.
Treat by modifying activity.
Surgical decompression with fasciotomies sometimes (allows continuation of sport/job).
142
What are signs of Genu Varum/Valgum?
How do you treat it in infants?
Asymmetric legs, resistant, short stature, varus >11 ̊, trauma/systemic cause.
Treat surgically with an eight plate while they grow.
143
What is Rotational – In/Out-toeing?
What can this cause?
Present as clumsy, tripping/limping/"deformed".
Causes:
Femur (femoral anteversion)
Tibia (external tibial torsion)
Foot
Many resolve with growth or remain asymptomatic.
Can cause miserable malalignment - combination of PFA and ext tib torsion results in patellar instability.
144
What are some foot deformities seen in children?
Metatarsus Adductus
Club foot (CTEV) - treat with cast series
Flat foot (planovalgus) - only treat if symptomatic; with subtalar implant
145
What is a:
Fracture
Dislocation
Subluxation
Comminution
Intra-articular
Fracture dislocation
Open fracture?
Fracture: A disruption in bone continuity
Dislocation: Complete loss of continuity of 2 bones forming a joint
Subluxation: Partial loss of continuity of 2 bones forming a joint
Comminution: Multiple fragments
Intra-articular: Fracture extend into a joint
Fracture dislocation: A dislocated joint with associated fracture
Open fracture: A direct communication between the fracture and the external environment
146
What 3 mechanisms cause a fracture?
1. Normal bone, abnormal force - injury mechanism that exceeds maximum force the bone can withstand
2. Abnormal bone, normal force - co-morbidity that increases risk of fracture after injury; congenital (osteogenesis imperfecta) or acquired - metabolic (rickets/osteomalacia), degenerative (osteoporosis), tumour (primary, secondary, haematogenous)
3. Normal bone, abnormal force, increased risk of trauma - co-morbidity that increases risk of injury (visual impairment, alcohol/drug use, neuropathy, balance disorder, epilepsy)
147
What are the fracture patterns in adults?
Complete - fracture all the way through the bone
Incomplete - the whole cortex is not broken
148
How can you further describe complete fractures?
Simple - Transverse (across bone), Oblique (across bone at angle), Spiral (helix around bone - zig zag)
Complex/Comminuted - more than 2 main fragments
Compression - wedge compression of vertebrae
Articular involvement - intra (into joint)/extra (no joint involvement
149
How do you describe where a fracture is on a bone?
Epiphysis: ‘Epi’ = next to; often intra-articular
Metaphysis: ‘Meta’ = changing
Diaphysis: ‘Dia’ = between; split into thirds (describe as proximal/middle/distal) and junctions
150
How should you request a radiograph?
Ask for specific area - XR of joint, not whole limb as beam divergence (XR comes from point source)
At least 2 views - AP/lateral, special views: mortise, scaphoid
151
How should you describe a fracture on a radiograph?
1. There is a...
displaced/undisplaced
2. ...Fracture of the...
proximal/midshaft/distal
3. ....Bone – humerus, femur, etc
4. Add in qualifiers: Comminution,
Articular involvement,
Oblique/spiral/transverse,
Type/degree of displacement
152
What is primary fracture healing?
Direct healing without fracture callus, requires edges to be touching exactly with no movement - absolute stability. Also called Haversian healing as lamellar bone is formed.
Does not occur naturally (only happens with surgery - plate and screws), important for certain fractures.
Relies on the coordinated, organised activity of osteoblasts and osteoclasts in units called cutting cones, with blood vessel in the centre.
Cutting cone moves through the bone with the osteoclasts resorbing bone at the front and the osteoblasts forming new organised bone behind.
Once healed this cutting cone becomes an osteon.
It is also the process that converts immature woven bone to lamellar bone.
153
What is secondary fracture healing?
Occurs when there is relative stability of the fracture - but still a tiny bit of movement (plaster cast, intramedullary (IM) nail).
Endochondral ossification as new bone forms ontop of cartilage model.
Stem cells crucial - come from periosteum and endosteum.
Follows stages of inflammation, repair and remodelling.
154
Describe the stages of secondary healing.
1. Inflammation (as soon as fracture occurs) - haematoma forms with hematopoietic (for growth factor) and inflammatory cells; osteoblasts and fibroblasts proliferate; granulation tissue forms by FBs around bone edges, reducing motion
2. Repair phase 1 (<2 weeks) - chondroblasts make primary soft callus (internal and external cartilage); wider than bone for strength and reduced movement
3. Repair phase 2 - soft callus replaced by bone (hard callus) in endochondral ossification; rapidly produced woven bone disorganised and not stress-orientated
4. Remodelling (years) - begins in middle of repair, turning woven to lamellar bone using cutting cones and trabecula remodelling, via Wolf's Law (according to stress)
155
What influences osteoprogenitor cells differentiation during fracture healing?
Strain (movement at fracture site)
More movement (>10%) = chondroblasts
Less movement (<10%) = osteoblasts
Soft callus by osteoclasts stabilises fracture, reducing movement so more osteoblasts.
Big issue if not immobilised enough so movement stays above 10% as no osteoblasts, leading to non-union.
156
What are some complications with fracture healing?
Mal-union - heals in a sub-optimal position, giving reduced function (angulation)
Delayed union - bone heals but in a longer than expected timeframe
Non-union - fracture fragments remain separate (too much movement)
Infection - open fractures/surgery; can cause non-union and/or osteomyelitis
157
What affects the time frame of fracture healing?
1. Patient related factors - healing very vascular and energy intensive so smoking (causes vasoconstriction), alcohol, malnutrition, NSAID use, co-morbidity (diabetes, vascular insufficiency)
2. Fracture related factors - energy transfer of the injury, associated soft tissue injury, morphology of fracture (bone loss), blood supply injured (scaphoid, talus, femoral and humeral head - can develop vascular necrosis)
3. Fixation related factors - adequate stability of cast/brace; surgery - adequate fixation, infection, too much soft tissue dissection (strips the bone of periosteal and hence of its blood and stem cell supply); patient compliance
158
What are the goals of fracture care?
In the least intrusive way (taking into account the risks/benefits to the patient):
1. Prevent pain - stabilise quickly
2. Preserve function
3. Avoid complications - (untreated trauma) infection, deformity, non-union, post-traumatic arthritis
159
What are the 4 ‘R’s of fracture management?
1. Resuscitate - save life
2. Reduce - put bone fragments back
3. Restrict - keep bone fragments in right place until it heals
4. Rehabilitate - joint stiffness, muscle power, RoM, coordination so many weeks rehab
160
What bone fractures need reduced?
Bone ends not adequately apposed
Intra-articular displacement
Neurovascular structures at risk
Special considerations - Salter-Harris...
161
How do you tell if fracture is stable?
Stable fractures (ongoing assessment):
Remain in place under minimum physiological load,
Bone ends well aligned,
Minimal comminution,
Good soft tissue support
Unstable fractures (need surgery):
Will lose position under minimum physiological load,
Comminution or bone loss,
Known unstable patterns: Ankle - Talar shift, Wrist - Volar (anterior) displacement
162
When is it risky to not operate for a fracture?
If fracture is unstable, or,
Elderly major lower limb (hip, femur, tibia), as prolonged bed rest leads to complications like pneumonia and thromboembolic disease (stroke, heart attacks and pulmonary embolisms which can be fatal), bed sores, stiff joints, lead to permanent reduced function and loss of independence in elderly.
163
How do you reduce a bone with an angular deformity??
3 points of contact - 2 as a force needed to bend bone back in place and a counter force as a fulcrum at the site of the fracture.
Then plaster cast using these points of contact.
164
What are advantages and disadvantages of non-operative management of fractures?
What does this management include?
Cheap, easy to apply, can be taken off by patient for washing/physio, reduce risks of operation if properly used.
However immobilising joint near fracture means stiffness and muscle wasting (3x length in cast in physio), can't fully control fracture (instability risk), patient comfort (itching), pressure issues.
Includes; nothing, simple splints for comfort, devices to help control position (functional brace...)
Week 1: Radiographs for position check
Week 2: Final decision on non-op
Week 6-8: Cast removed, rehab commences, radiographs sometimes, normally discharge
Week 12: Radiographic evidence of union
165
What are advantages and disadvantages of operative management of fractures?
Less immobilisation, earlier rehabilitation and pain control, possibility of anatomical reduction and fixation (prevent future disability) - articular surfaces (joints) and forearm (pronation/supination) can loose function if not aligned.
However, expensive, complications (infection, neurovascular), can slow healing (strip bone of important peri/endosteum with stem cells needed for healing).
166
What are some absolute and relative indications for surgical management of a fracture?
Absolute indications:
Displaced intra-articular fractures,
Open fractures (wash-out prevent infection),
Pathological fractures (tumour),
Polytrauma to stabilise (especially long bones, reduce embolism and immobilisation)
Relative indications:
Failure of conservative management,
Fractures with a high risk of complications (AVN-hip/scaphoid, non-union, arthritis),
Morbidity of conservative management (lower limb fractures prolonged bed rest)
167
What are some features of high energy trauma?
Polytrauma - multiple body parts injured
Fracture patterns - complex/displaced
Soft tissue injuries - Wounds/open fractures, Tissue loss, Neurovascular, Other injuries (burns)
168
What are common features and treatments of wrist fractures?
Low energy old females/High energy younger
Treat with cast/splint if low energy, extra-articular, stable in cast with good reduction.
Operate (ORIF with plate and screws) if high energy, intra-articular, unstable in cast, poor reduction.
169
What are common features and treatments of ankle fractures?
Medium energy (young/middle ages) by inversion/eversion injury, ‘Going over’ on the ankle, sports, high-heels.
High energy - pilon fracture of tibia (smashed) by fall from height/RTA.
If in acceptable position/stable and uni-malleolar then treat with cast/moon boot (functional brace).
Surgical ORIF if failed conservative management, unstable, or bi-malleolar.
170
What are common features and treatments of tibial diaphysis fractures?
High energy - sport/fall from height/industrial accident.
Most need surgery - IM nail.
At risk of compartment syndrome.
171
What are common features and treatments of metacarpal fractures?
Direct impact from punching.
Inanimate sometimes but if animate (other person) then often get 'fight bite' from punchee's tooth - staph, strep, eikenella common with human bite so treat like open fracture - wash out and prophylactic antibiotics.
172
What are the most common limb-threatening injuries?
Open fractures, arterial injury, nerve injury, compartment syndrome.
173
What is an open fracture?
How should they be managed?
Bone penetrates skin - can go back in. Higher infection risk, causing osteomyelitis/chronic infection leading to amputation and more likely to non-union.
Get a good history - environment determines type of antibiotics.
Examine thoroughly - look (+photos), fell, move, neurovascular status.
Normally needs surgery to wash-out and reduce, then treat like other fractures (4Rs - resuscitate, reduce, restrict, rehabilitate).
In ED, early antibiotics (Cefuroxime 1.5g TDS, or if pen allergy then Clindamycin, or Gentamicin if heavy contamination) and anti Tetanus (booster if none within 5 years). Stabilise quite quickly in splint/cast (like Thomas splint) to get correct length/alignment, bone back in and tamponade bleeding vessels. Also sterile saline soaked dressing, cover wound and photograph.
174
What is the Gustilo-Anderson classification?
For assessing open fractures, three grades according to size:
1. <1cm, simple low energy fractures, minimal soft tissue damage/contamination
2. 1-10cm, moderate energy injury, moderate soft tissue injury/contamination
3. Further broken into A/B/C: A/B >10cm, differentiated by plastic surgery needed (A - skin flap from local area, B - free flap, full thickness taken from somewhere else in body), 3C is high energy with arterial injury needing repair, generally includes partial amputations/mangled extremities)
175
What does surgical management of an open fracture include?
Primary:
Within 24hrs - wound debridement - remove all dead tissue and contaminants.
Skeletal stabilisation with intramedullary nail and external fixation.
Secondary:
Normally left open, allow for second look within 48hrs - tissue inspection, further debridement, plastic surgery need, wound closure.
176
What is the cause, signs and management of arterial injury in limbs?
Often seen as cold and pale/dusky foot, painful with no pulse below. Common in true knee disloactions.
Caused by kink in major vessel, disruption of a vessel structure (laceration/transection or intimal dissection).
Pulse loss can be due to arterial spasm/loss of blood elsewhere causing hypotension but assume arterial injury until proven otherwise.
It is a surgical emergency.
Resuscitate patient, realign and splint leg (then re-check vascular status), then surgical referral (ortho + vascular/plastics).
In surgery, extra-anatomical vascular shunt used to direct blood flow while ortho stabilises fracture, then vascular graft.
177
What are the types of nerve injuries in limbs after fractures?
Neurapraxia:
Nerve ischaemia from contusion/traction, structure intact, ion pump works again once cause is removed.
Axonotmesis:
Myelin sheath disruption, distal axon dies, but schwann cells and endoneurium still intact. Nerve recovers down pipe but scarred myelin sheath can prevent full recovery.
Neurotmesis:
Complete nerve division, no myelin sheath guide for regeneration to irreversible without surgical repair.
178
What are signs of compartment syndrome after a tibial shaft injury?
Initially comfortable but then severe increasing pain, not better with analgesia (strong opiates), feeling cast is too tight, numbness over dorsum of foot, pain on passive toe stretching, tight calf muscles, paraesthesia.
Pulse often normal.
179
What is compartment syndrome?
How do you manage it?
Normally with high energy trauma.
Increased pressure inside a fixed fascial compartment, resulting in reduced tissue perfusion, and severe muscle pain from pressure and ischaemia.
Tissues in compartment become ischaemic then necrotic, causing irreversible damage. Pressure increases further as soft tissue swells as it dies causing more hypoxic muscle and necrosis in viscous cycle.
Must be treated emergently as irreversible damage and amputation can occur. Fasciotomies ASAP - cuts in skin to allow bulging out of soft tissues.
Most common in leg, forearm and thigh.
180
What are the two categories of metabolic bone disease?
Disorders of Bone Remodelling
Disorders of Mineralisation
181
What are some metabolic disorders of bone remodelling?
Osteoporosis: resorption > formation (quantity not quality), deterioration in microarchitecture and compromised bone strength causes increased fracture risk
Paget’s disease: resorption and formation increased (abnormal localised bone remodelling, increased OC resorption, increased but disorganised bone formation)
Osteopetrosis: resorption decreased
182
What are some metabolic disorders of bone mineralisation?
Hyperparathyroidism (Primary – Adenoma, Secondary – Chronic hypocalcaemia),
Vitamin D-related disorders (Osteomalacia and rickets)
183
What are features of Paget's Disease of Bone?
Abnormal localised bone remodelling - increased OC resorption, increased but disorganised bone formation.
Bone produced is less elastic.
Abnormal osteoclasts and osteoclast precursors which are greater in size and number and become hypersensitive to stimulation.
Clinical features are enlarged skull, bowing of long bones, large joint OA, fractures, nerve compression causing deafness.
Can be monostotic - affect one bone, or polyostotic - affect multiple bones (like hip and both femurs).
Can change causing malignancy (<1%), normally osteosarcoma (bone cancer from mesenchymal cells). Poor prognosis so pagen't disease patients monitored to try catch early.
184
What are the three phases that can exist within a bone with Paget's disease??
Lytic – Intense osteoclastic resorption
Mixed – resorption and compensatory formation
Sclerotic – predominant osteoblastic formation
185
What are the investigations and treatment of Paget's disease?
Radiographs/bone scans (active areas detected),
Bloods - elevated alkaline phosphatase (ALP) (bone turnover marker),
Histology - more and larger osteoclasts, disorganised woven bone, fibrous vascular tissue.
Treat by inhibiting osteoclasts (bisphosphonates - alendronate/pamidronate) , calcitonin is second line, arthroplasty if needed.
186
What is osteopetrosis?
Defective osteoclastic resorption (cannot acidify Howship’s lacuna, so can't resorb bone).
Bone is formed but not remodelled so is dense, no medullary canal.
Have a predisposition to fracture (as more brittle since less elasticity), especially transverse and have an increased risk of non/mal-union.
187
What is hyperparathyroidism?
What are the types?
Increase serum PTH as a result of excess production by parathyroid gland(s).
Primary hyperparathyroidism (most common): intrinsic abnormality of the parathyroid gland(s) causing pathological increase in PTH production. Caused by parathyroid adenoma in 85%.
Secondary hyperparathyroidism: increased PTH secretion from hypertrophic parathyroid glands, secondary to chronic hypocalcaemia/hyperphosphataemia due to Vit D deficiency/chronic renal disease.
Tertiary hyperparathyroidism: prolonged exposure to PTH causes parathyroid glands to become dysregulated and secrete PTH regardless of calcium level.
188
What are the main affects of PTH?
Increases bone resorption (OBs release more RANKL and less OPG, OCs differentiate and activate)
Increased renal hydroxylation of Vit D (active form of Vit D (calcitriol) produced which, increases RANKL release, increase intestinal uptake, increase renal uptake)
189
What are symptoms and signs of hyperparathyroidism?
‘Bones, stones, abdominal groans, thrones and psychic moans’
Bones - gout, pseudogout, arthritis, osteoporosis
Stones - kidney stones (from hypercalcaemia due to bone resorption) and increase Ca in urine
Abdominal groans, throans - constipation, GI ulcers, acute pancreatitis, polyuria
Psychic moans - fatigue, depression, forgetfulness and anxiety (from hypercalcemia)
190
How is hyperparathyroidism treated and diagnosed?
Diagnosed with serum calcium, phosphate and PTH concentrations.
Treatment depends on if primary/secondary cause.
Most primary is caused by a PTH adenoma and rest by other PTG intrinsic pathologies. Surgical removal of affected gland cures 97%.
Secondary treat underlying cause - like high dose vitamin D if deficient.
191
What is rickets?
Defects in mineralisation caused by inadequate calcium/phosphate prior to physeal closure.
Affects the zone of provisional calcification in the physes of long bones causing brittle bones with physeal cupping/widening, bowing of long bones, muscle hypotonia/weakness, flattening of skull, enlargement of costal cartilage, kyphosis, dental abnormalities, irritability, listlessness.
Can be:
Congenital – familial hypophosphataemic (inability of kidneys to absorb phosphate), or,
Acquired – Vitamin D deficient (lack of dietary Vit D intake/sunlight exposure; low Vit D levels lead to decreased calcium absorption; low Ca increases PTH, bone resorption).
192
What is osteomalacia?
Defects in mineralisation caused by inadequate calcium and phosphate after physeal closure.
Qualitative defect of bone, rather than quantitative defect like osteoporosis.
Causes:
Diet, Malabsorption (eg coeliac disease), Renal osteodystrophy, Alcoholism, Tumour, Drugs that cause Vit D deficiency/Phosphate homeostasis disruption/Altered bone mineralisation
Presentation:
Bone and muscle pain, Atypical fractures (Femur/femoral neck fractures), Proximal muscle weakness, Fatigue, Hip arthritis with protrusion (acetabulum protrudes past ilioischial line)
193
What are insufficiency fractures?
Type of stress fracture, cumulative result of repeated normal loading on abnormal bone.
Different from fatigue fracture (normal bone, abnormal stress).
194
What are vertebral wedge fractures?
Compression fractures, very common in osteoporosis, from insufficiency/low energy trauma, often affecting multiple levels.
Vertebral body crushes making wedge shape rather than normal rectangle.
Can accumulate throughout the thoracolumbar spine, significantly changing posture (thoracic kyphosis), causing progressive deformity of height loss, reduced pulmonary volume, protruding abdomen, constipation, early satiety (full from less food, causing weight loss and malnutrition). This is because reduced space in thoracic and abdominal cavities.
Also more accident prone as can't look up and centre of gravity is forwards.
Treatment is reducing bone loss, analgesia and physio. Sometimes kyphoplasty (balloon inserted into crushed vertebrae, inflated and filled with bone cement).
195
What are fragility fractures?
Almost always osteoporotic, normal forces fracturing abnormal bone.
196
Describe proximal humerus fractures cause and treatment.
Caused by simple fall (often osteoporotic).
Treated in a sling - collar and cuff (strip of foam filled fabric going around neck and wrist) as this doesn't holds elbow so weight of arm is traction holding in good position. Early physio.
Surgery if more complex (often in older as more likely to be more fragments).
For all treatment, outcomes are variable - most loose some RoM in shoulder and instability lifting arm up.
197
Describe wrist fracture types and management.
Very common, especially females, distal radius fractured. Rare in young so DEXA.
Can be volar/Smith's (hand anterior to radius) or dorsal/Colles' (hand posterior/dorsal to wrist).
Often shortening occurs - hand pushes into crushed radius.
Management options for best functional outcome:
1. Acceptable position (minimally displaced extra-articular) - cast
2. Unacceptable position, likely stable if reduced (dorsal displacement/simple intra-articular component) - trial of manipulation under anaesthetic/cast
3. Unacceptable position, unstable even if reduced (volar displacement, complexity, intra-articular step) - ORIF
198
Describe pubic rami fractures mechanism and treatment.
Normally fall backwards from standing, land on buttocks, causing both superior and inferior pubic rami to fracture (as this is part we sit on and ring so normally break in 2 places).
Conservative management - short bed rest, early mobilisation with physio.
199
What is management of a hip fracture?
Almost all surgery as bed rest leads to muscle wasting, loss of mobility, bed sores, pneumonia, pulmonary embolism, death.
Try get early mobilisation.
Type of surgery depends on if above femoral neck base (intracapsular) or below it as if above, arteries likely torn.
If below, further divide into inter-trochanter or sub-trochanter.
Intracapsular:
Fix with cannulated hip screws if undisplaced
Arthroplasty (hemi if low demand/dementia, total if active/cognitively intact/high function) if displaced
Extracapsular:
Intertrochanteric - sliding hip screw
Subtrochanteric - intramedullary nail
200
What fracture is related to bisphosphonate use?
What is management for this?
Atypical femoral fractures.
Insufficiency fracture - no trauma. Due to osteoclasts unable to heal microtrauma.
Pattern: subtrochanteric, lateral cortex, transverse, increased cortical thickness with old cortical 'breaking' around it. Lucent line on radiograph.
Aim to prevent complete fracture with intramedullary nail. Also review bisphosphonate treatment.
201
What is the outcome of pediatric fractures?
Thick periosteum means can have more conservative management as keep in place, so non-union is rare, and greater remodelling potential, healing quicker than adults. Much less morbidity that in adults with bed rest/immobilisation, don’t get as much joint stiffness, muscle atrophy, pulmonary embolism, pneumonia, bed sores.
However physeal injuries before maturity can cause growth abnormalities/arrests, can be difficult to diagnose (because of physis and ossification centres on radiographs) and treat.
202
What is cartilage?
Connective tissue with chondrocytes (cell) and lacuna (bubble around them).
This exists in the matrix made of ground substance – hyaluronic acid, chondroitin sulphate, keratin sulfate, a lot of water (70%).
Fibres present depends on type of cartilage but often collagen type 2 and elastin.
203
What are some properties of cartilage?
No blood vessels or nerves.
Nutrition by diffusion so needs to be permeable.
Elastin fibres makes fibres flexible, weight-bearing and resistant to shear forces.
Resiliant because of high water content.
Slippery means low friction for joints.
Lack of blood vessels means heals slowly - poor regenerative capacity.
204
What is hyaline cartilage?
Articular cartilage.
An amorphous but firm matrix, flexible and resilient.
Collagen fibres form an imperceptible network
Chondroblasts (spherical) produce the matrix,
once mature, chondrocytes sit in their lacuna (bubble around them).
Function: They support and reinforce, resiliant cushioning preperties and resist compressive stress.
Found in most of embryonic skelton, end of long bones, joints of epiphesis, costal cartilage of ribs, nose.
205
What is elastic cartilage?
Similar to hyaline but a lot more elastic fibres so highly bendable.
Function: maintain shape of structure while allowing flexibility
In outer ear, larynx, epiglottis.
206
What is in the ECM of articular cartilage?
70% water - more at joint surface, less deep
15% collagen - mainly type 2 (gives tensile strength)
15% proteoglycans - hydrophilic (attracts water) more deep to try pull water in, gives compressive strength
207
Describe the zonal structure of articular cartilage.
Why is this important clinically?
Superficial zone:
Collagen fibres arranged parallel to joint surface/movement of joint, so good at resisting shear rubbing force
High in type 2 collagen (C2), low in proteoglycans (PG) - even though highest water content
Middle (intermediate) zone:
Collagen oblique
Thickest layer
Deep zone:
Collagen perpendicular, crosses tidemark - would be weak point if some collagen didn't cross it to anchor
More PG - draws water in
Tidemark:
Separates articular cartilage from calcified.
Lacerations crossing tide mark healing will involve subchondral bone so have a blood supply and stem cells, so deeper laceration fares better as long as it crosses.
208
How do lacerations above and below the tide mark in hyaline cartilage heal differently?
Superficial laceration (below tidemark):
No healing due to avascularity, chondrocyte proliferation
Deep laceration:
Fibrocartilage healing; Haematoma, stem cells, vascular ingrowth
209
How does cartilage respond to stress?
(Physiological/moderate running/excess/immobilisation)
Physiological stress:
Stimulates matrix synthesis, inhibits chondrolysis
Moderate running:
Increases cartilage thickness and proteoglycan content
Excess stress:
Suppresses matrix synthesis, promotes chondrolysis
Immobilisation:
Cartilage thinning and softening, proteoglycan loss
210
How does cartilage change with age (A) and osteoarthritis (OA)?
Water:
A - Decreased
OA - Increased
Modulus/stiffness:
A - Increased (less elastic)
OA - Decreased (more elastic)
Chondrocytes:
A - Fewer but increased size
OA - Cells cluster (late stage)
Proteoglycans:
A - Decreased size
OA - Proteoglycans unbound from hyaluronate
Collagen:
A - Increased collagen crosslinking/brittleness
OA - Collagen disorganized (increased collagenase)
211
What is cellulitis?
Bacterial infection of the skin and subcutaneous fat, most commonly caused by staphylococcal/streptococcal
212
What is an abscess?
How are the treated?
Closed collection of pus, made of dead WBC and bacteria, can't get out but some may have small point of discharge (punctum).
Pus under pressure can make patient unwell and infections caused by abscess normally don't respond to antibiotics (lack of penetration to cavity).
Incision and drainage, then wash out.
213
What could an acute monoarthritis be?
GRASP:
Gout
Reactive arthritis
Autoimmune/arthritic
!Septic arthritis!
Pseudogout
214
What are the investigations for suspected septic arthritis?
What are the pathogens involved normally?
Bloods: inflammatory markers - FBC, CRP, ESR; Peripheral Cultures; Uric acid
Radiographs
Joint Aspiration - Clear (normal), Purulent (infection), Blood stained (infection)
90% non-gonococcal: staph aureus 50-80%, streptococcus 15-20%, haemophilus influenzae 20% (infants 6mo-2yrs)
Gonococcal: Young, sexually active; Knee
IVDU: Pseudomonas Aeruginosa (immunocompromised), Fungal/ Candid
215
What is the management for septic arthritis?
1. Aspirate - to dryness, send for urgent gram stain
2. Antibiotics - empirical (best guess), 1st line Fluclox/BenPen
3. Washout - in theatre
4. Microbiology - discuss with microbiologist for sensitivities
5. Monitor - continued surveillance
6. Long-term antibiotics - 8 week course guided by micro advice
216
How do you diagnose gout and pseudogout?
Bloods - Possibly raised serum urate (but can be normal during active flare)
Aspiration - Monosodium urate crystals in gout, Calcium pyrophosphate dihydrate crystals in pseudogout
One of the tests involves shining polarised light through it
217
What is reactive arthritis?
Aseptic arthritis.
Occurs 2-6wks after bacterial infection elsewhere: Gastroenteritis (salmonella, campylobacter), Gastrourinary infection (chlamydia, gonorrhoea)
Treatment – NSAIDs, physiotherapy, steroid joint injections
Also called Reiter’s syndrome;
Predisposition in HLAB27 positive (85%)
Polyarthropathy, conjunctivitis, urethritis often in combo (‘Can’t see, can’t pee, can’t climb up a tree’)
Joint & eye changes often severe
218
What are autoimmune/arthritic causes of monoarthritis?
Acute flare of a chronic condition:
Osteoarthritis,
Rheumatoid arthritis,
Polymyalgia rheumatica,
Seronegative spondyloarthritidies -Ankylosing spondylitis/Psoriatic arthritis/Enteropathic arthritis/(Reactive arthritis)
219
What are the Seronegative spondyloarthritidies and properties of them?
What gene is responsible for them?
Ankylosing spondylitis - fusion (ankylosis) of the spine, Enthesitis (insertion oftendons/ligaments/fascia), Sacroiliitis (lumbosacral pain), Uveitis, <45 y/o,
Psoriatic arthritis - severe in DIPJs of fingers with soft tissue changes - stereotypical silvery skin plaques, uveitis, and dysmorphic nails; (can progress into arthritis mutilans - destruction and gross deformity of hands/feet),
Enteropathic arthritis - IBD/Crohn's/ulcerative colitis too,
Reactive arthritis,
Undifferentiated spondyloarthritis
HLAB27 gene
220
What is rheumatoid arthritis symptoms?
Chronic systemic autoimmune disease caused by cell-mediated immune response against soft tissue and bone, affects almost every body system - mainly small hand joints, shoulders, elbows knees (sometimes spine, hips, feet).
Affects distal joints first, symmetrical, significant stiffness >30mins, erosion of joint surfaces cause deformity.
Nodules around fingers/elbows.
Positive bloods for RF and anti-CCP but incomplete forms are common.
221
What are rheumatoid arthritis risk factors?
Female 3x likely
Genetics - Human leukocyte antigen (HLA) subtypes (strongest risk factor) and Major histocompatibility complex (MHC)
Epigenetic modifications to genomes
Smoking
Infections
Periodontitis (gum disease)
Microbiome (western diet)
222
What is involved in the aetiology and pathophysiology of rheumatoid arthritis?
Genetic predisposition triggered causing:
1. Citrullination - Conversion of amino acid Arginine into Citruline. Modified protein is immunogenic (becomes an antigen and triggers autoimmune response)
2. T-cell mediated immune response - Soft tissues then cartilage then bone - Citrullinated protein (antigen) processed by B-cells, B-cell presents to T-cell (HLA), T-cell activates B-cells (cytokines), B-cells produce autoantibodies (RF and anti-CCP)
3. System-wide effects:
Release of acute phase proteins (like CRP) from the liver - pro‐inflammatory cytokines stimulate synovial fibroblasts to release their own cytokines;
Synovium transitions to pannus - TNF‐a;
Breakdown cartilage - matrix metalloprotease;
Bone erosions - T-cells/M-CSF activate RANKL
Inflamed synovium - Prostaglandins/nitric oxide cause vasodilatation, swelling, pain
223
What is Pannus?
Grossly thickened synovium as a result of inflammation - Autoimmune attack on synovium, Hypervascularity, Hypertrophy/granulation.
Spreads between and over joint surfaces, Erodes and infiltrates bone, Swelling of joint.
224
What are the stages of rheumatoid arthritis?
1. Susceptibility to the disease - no autoimmunity evidence/arthritis but may have raised CRP/anti-CCP. Fab to start treatment here.
2. Undifferentiated arthritis - inflammatory arthritis symptoms, some synovial changes.
3. Established RA - synovial grossly transformed into pannus which then erodes cartilage and bone.
225
What joints deformities are most likely with rheumatoid arthritis?
Small joints first:
Swan neck deformities of fingers (hyperextension at the PIPJ and flexion at the DIPJ),
Z-deformities of thumb (flexion at the MCPJ and hyperextension at the IPJ),
Finger MCPJ deformities with ulnar deviation (subluxation of these joints like from extensor tendon slipping over/rupture),
Varus knee deformties (foot angled towards midline) or valgus (foot away from midline) causing windswept knees (exclude from ankylosed - fused - hip).
226
What are extra-articular symptoms of Rheumatoid Arthritis?
Bursitis (fluid filled bursa around elbow tip);
Subcutaneous/rheumatoid nodules (painless lumps at elbow/fingers/internally-gallbladder/lungs/heart valves);
Tendons - rupture, inflammation;
More likely to have: Myocardial infarction/Stroke/Infection/Non-Hodgkin’s lymphoma;
Life expectancy reduced by >10 years.
227
What are red flags of rheumatoid arthritis?
Atlantoaxial instability - subluxation where C1 slides forwards on C2, causing spinal cord compression, present with back of head/neck pain, numbness/weakness down arms, sudden death when head moves suddenly.
Pericarditis - heart lining inflammation. Urgent echocardiogram and treatment with steroids.
Scleritis - sudden onset eye pain and lactimation. If untreated, the whole sclera involved leading to thinning, possible perforation and blindness.
228
What investigations should be done for rheumatoid arthritis?
CRP and ESR - baseline to monitor disease activity with treatment
Auto-antibodies produced by B-cells, activated by T-cells:
IgM Rheumatoid Factors (RF) - Reasonable sensitivity (70-80% patients with RA) but not very specific (some infections/autoimmune diseases, 5-10% of healthy people)
Anti-cyclic citrullinated peptide (anti-CCP) antibodies - Good sensitivity(96-98% patients with RA, 50% in early RA, can predate symptoms by years), Much better specificity
Imaging - erosive arthritis (loss of joint space, subchondral erosions from pannus, joint ankylosis, 'gull-wing' appearance), subluxations/disloactions
229
What is the management for rheumatoid arthritis?
Maximise the long‐term health related quality of life (HRQL) - max funtion, min pain. Treat early.
Abrogation of inflammation - stop/prevent inflammation as this is what causes destruction and progression.
Base on disease activity - alter based on clinical and biochemical response; minimal effective dose as pharma side effects.
Disease-modifying anti-rheumatoid drugs (DMARDs) early to control symptoms and delay progression.
1st line - Monotherapy with conventional DMARDs (cDMARDS) - methotrexate,
Alternatives: sulfasalazine, leflunomide, hydroxychloroquine.
Combined with short term glucocorticoids during flare.
Monitor disease activity - gradual reduction/stopping drugs.
Step-up strategy - add further cDMARDs in combination then consider bDMARD (biological) , eg TNF-a inhibitors, rituximab
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What is osteoarthritis?
How can it be classified?
A heterogeneous group of disorders with similar pathological/radiological features, characterised by degeneration of articular cartilage, remodeling of subchondral bone and formation of osteophytes.
Primary -
localised,
generalised (often nodal in post menopausal women).
Secondary -
developmental (eg hip dysplasia, slipped epiphysis),
traumatic (eg intra-articular fracture, menisectomy, occupational, hypermobility),
metabolic (eg alkaptonuria, haemachromatosis, Pagets),
endocrine (eg acromegaly),
inflammatory (eg RA, gout, haemophilia, joint sepsis),
aseptic necrosis (eg corticosteroids, sickle-cell disease),
neuropathic (eg diabetes, syringomyelia, tabes dorsalis)
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What are symptoms of osteoarthritis?
What are radiological features?
Pain – worse on use of joint
Stiffness – mild in the morning, severe after immobility
Loss of movement
Pain on movement/restricted range
Tenderness (articular/periarticular)
Bony swelling
Soft tissue swelling
Joint crepitus
Can cause deformities. Often Spine, DIPJ, knees, hips.
Radiograph:
Narrowing of joint space
Osteophytosis
Altered bone contour
Bone sclerosis and cysts
Periarticular calcification
Soft tissue swelling
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What are ways of differentiating OA from RA?
OA:
Distribution (DIP and PIP), Bony swelling, Limited stiffness
RA:
Distribution (MCPJs, PIPJs, carpal bones, spares DIPJs), Soft tissue swelling, Stiffness prominent, Symptoms and signs of systemic inflammation, Serology, Erosions (without osteophytes or sclerosis)
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What are risk factors for osteoarthritis?
Modifiable local risk factor (leads to susceptible joint):
muscle strength, physical activity, occupation, joint injury, joint alignment, leg length inequality
Modifiable systemic risk factors (leads to predisposed individual):
obesity, diet, bone metabolism
Non-modifiable systemic risk factors (leads to predisposed individual):
age, sex, genetics, ethnicity
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What are the cellular/molecular hallmarks of ageing?
What happens to chondrocytes and matrix metabolism as they age?
Genomic instability
Telomere attrition
Epigenetic changes
Loss of proteostasis
Dysregulated nutrient sensing
Mitochondrial dysfunction
Cellular senescence
Stem cell exhaustion
Altered intercellular communication
Chondrocytes:
Mitotic activity decreases
β galactosidase increases
Epigenetic hypermethylation increases
Telomere length decreases
Matrix:
Type II collagen turnover decreases
Aggrecan turnover decreases
Accumulation of glycation end products
Cleavage products of matrix molecules (e.g. fibronectin)
Antioxidant defences decrease
All this leads to:
Decline in proprioception
Decrease in muscle strength (sarcopenia)
Changing shape of bones (hip and CMC joint of thumb);
which can cause OA
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What does non-pharmacological management of osteoarthritis consist of?
Education
Self-management
Weight loss
Regular telephone contact
Aerobic, muscle strengthening and water based exercises
Referral to a physical therapist
Use of a stick
Shoe insoles and knee braces
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What does pharmacological management of osteoarthritis consist of?
Paracetamol
Topical and oral NSAIDs (both non-selective with misoprostol/PPi and selective COX-2)
Duloxetine
Topical capsaicin
IA steroids
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What does surgical management of osteoarthritis consist of?
Considered when everything else fails.
Total joint replacement (arthroplasty)
Osteotomy
Knee fusion
Knee aspiration and debridement in case of locking
+ combination of non-pharmacological and pharmacological modalities
