Bones Flashcards
what is the ft of bones
structure movement satbility protection fat store haematopoeisis mineral homeostasis
lamella bone =
mature. organised long fibril sheets.
osteons, haversian systems, canaliculi
woven bone =
immature. dissorganised short fibril sheets
what sectiion of the bone has the most compressive forces? and what part is designed to dissipate most
cortex metaphyseal trabecular (woven bits) arranged to dissipate force
what is micro-modelling
modelling of trabeculae to suit disspation of forces upon it
how many cycles of exercise is required to stimulate remodelling?
36 cycles, recovers after 8hrs
if there is v rapid stimulation of current bone what happens
fibrolamellar bone laid down around the vessels - weak. after time, this bone is replaced by lamellar bone which includes osteons around the b vessels instead
briefly describe the process of remodelling
damage bone removed by oc
1ry osteons form in cortex and trabeculae thicken and align in medulla
how long does it take for OC to remove none?
4wks
how long does it take OB to replace bone?
3 mths
describe the 6 types of fracture
- transverse - bending
- oblique - compressive
- spiral - torsion
- comminuted - high impact
- open - pierce skin
- closed - wi surrounding ST
descr stress remodelling
RSI (36x ++)
remodelling - fibrolamella laid down but then trabeculae resorbed to be remodelled into correct alignment
–> inc porosity and decr stiffness and strength
= failure likely
descr modified equine trainig
use gallop short bursts more
train to inc bone mass on dorsal and both lateral aspects (cf more medial increases)
why are greyhounds left at and right medial carpal/tarsal bones thickeded?
always run counter clockwise - matches the loading
what injury does poor equine training predispose them to?
thick dorsal and palmar MCB/MTB due to rapid appositional growth–> f#
3rd C/T bone f# along trabceulae
how can growth be stimulates
GH
genes
load
what is necessary in the development of bone to allow mineralisation
blood supply!
at what 2 area will endochondral ossification start from
GP in either physis of epihysis
why does the thickness of the trabecular increase liklihood of fracturing
because it cant absorb as much
what is fibrolamellar bone
weak, poorly mineralised
if deformation is elastic what changes happen? and if its plastic deformation - what changes happen then
elastic - rtns to normal when f removed. stimulates Modelling to increase stiffness and strength
plastic - permenantly changed after and REmodelling stimulated (pos due to microcracks etc)
why would a physiological load on bone cause a fracture
becuase it was diseased
- non-adaptive remodelling on eq/canine athlete
- metabolic bone dz (hyperPTH or vitD defic)
what are the causes of MBD
hyperPTH (removes Ca+ form bone)
vit d deficiency - not abs from GIT well, not reabs from kidney and not converted
diet or dz
name an eq disease of flat bone reabsorption (clue - california)
pulmonary silicosis = bone fragility syndrome flat bones (scapular mainly), also leads to respir. dz
what is feline osteodystrophy
destruction of nasal turbinates
what hormone might help osteoporosis
oestrogen
what are the 3 main aetiopatholigies are
abn endochondral ossification
abn maturation of cartilage
inappropriate relative growth
name some common ortho dz in the horse
osteo-chondrosis
physitis
angular limb deformities
flexural deform
name som ecommon canine ortho dz
osteochondrosis (re anconeal process, fragmented medial coronoid process)
hypertrophy psteodystrophy
legg-calves perthes
hip dysplasia
what do pigs get ortho dz-wise
osteochondrosis
what ortho dz do bovids get
osteochondrosis and flexural deformities
endochondral ossification happens at the metaphyseal GP and epiphyseal in initial development, however _______ should be fully ossified at birth
metaphyseal
when are cuboidal bones developed
by 3wo
at the GP (physis) what histological layers are there.
- restin cart
- prolif cart
- hypertrophic (swells)
- calcifcation zone (burst and mineralises)
- 2ry spongiosa - which gets reabs and modelled etc.
*** the resting cartilage is ‘above’ the new bone ( as its getting pushed upwards and bone grows underneath the cartilage)
what EC abn are there
- affect rate of growth
- directionof growth
- health are articular cart
what is osteochondrosis
chondrodysplasia (abn EC ossif)
results in thick retained hypertrophic cartilage
what is the pathogenesis of OCD (osteochondrosis)
- disruption of blood supply
- abn chondrocytes maturation
- defective matrix production
- persistence of hypertrophic chondrocytes (havent bURST AND CALICIFED)
if blood supply is disrupted, what is the result
impaired ability to withstand shearing forces
what is the patho-physiology of OCD
shearing forces cause separation of bone at osteochondral jct
cartilage flaps and fragmentation
exposed subchondral bone (eburnation)
clinical signs of OCD
arthritis
lameness
what is the aetiology of OCD
rapid growth - diet (incP:Ca balance; dec Cu:Zn balance), breed
+ trauma
hormones - test, GH, hyperinsulinaemia and hypothyroidism
what are subchondral cyst-like lesions
abn EC ossification from leaving the cartilage core - when it collapses = ‘cyst-like’ lesion
what is physitis and is it a concern
inflm or disruption of EC oss leading to lameness and stiffness
no -SELF LIMITING
What is hypertrophic osteodystrophy and what causes it? (dogs)
2-8mo, large breeds
cause - CDV infection, bacterial infection, XS vit+min,
pathogenesis - necrosis of metaphyseal vasculature
what are the signs of hypertrophic osteodystrophy
lame, fever, lethargy, pain
bilat and symmetrical lesions of long bones
abn diaphyseal bone, widened physis
SELF LIMITING
what is panosteitis and when does it occur and why
idiopathic cause
5-18mo
rapid growing large breeds
fibrosis of bone tissue (BM, endosteum and periosteum)
what are the signs of panosteitis (clinical and xray)
lame, shifting, lethargy, pain
inc medullary opacity, poor definition of trabeculae
SELF LIMITING
what is legg-calve perthes
4-11 mo toy breeds
idiopathic
avascular necrosis of the fem head, if the sub-chondral bone loses stability it collapses
what are the signs of legg-calve perthes
acute lameness, fracture of femoral head
osteolysis of fem head
what is the reason of hip dysplasia
genetic laxity of joint lig (lig of the head of the femur)
what causes the canine elbow dysplasia complex
- un-united anconeal
- OCD of humorous
- fragm coronoid process
what is shetland shoulder syndrome
abn humoural head + glenoid capsule
in angular limb deformities there is a word for both medial and lateral defomity - what are they
medial - varus
lateral - valgus
where might angular limb deformities happen
metaphyseal GP epiphyseal GP cuboidal bones metaphysis soft tissue laxity
what canine breeds get angular limb deformities
small - shitzhu
what is the reason behind canine angular limb deformities
asynchronous growth
what are the reasons behind flexoid limb deformities
disproportionate growth bw muscle/tendon and bone
what are the 2 forms of flexural limb deformity
congenital - neonate foals
acquired - rabidly growing foals, acute or chronic
what maj condition does osteochondrosis lead to
osteoarthritis
what is ‘arthritides’
conditons causing pain and dysfct of joints
what is seen with OA
dec pH, hypoxia, and dec IL-1 (and other inflm mediators prod by synovium)
–> causes MMP to be released and enzymes to break down cartilage
xray - osteophytes, enthesiophytes, SCB sclerosis
what are o-phytes
bone on joint margins
what are enthesiophytes
bone on ST insertion
what is sclerosis of the sub-endochondral bone
loses trabecular bone pattern
how do you tx OA
analgesia, reduce inflm (NSAIDs to reduce PGE2 and No released from synoviocytes or csteroids), limit articular damage (cartofen vet helps proteoglycan synth) and help healing if pos (HA+csteroids)
why shouldnt NSAIDs be used in wound healing
inhibit PMN migration
what surgical options are there for OA
arthrodesis - destroy cartilage and fuse
arthroscopy - assess, debride and replace joint
name some tx that are less well known, but used for joint diseases
bisphosphonates - antag against IL
poly-unsta FA - to reduce arachidonic acid (cod liver oil)
glucosamine/chondroitin - reduce PGE and NO
avocado, soya bean, vit+min - reduce IL and PGE2
desc the disease of IM-polyarthritis
chronic Ag stim and IC formed at the synovio-cytes
pyrexia, lethargy and joint swelling, shifting lameness
can be erosive (poor px)
and ead to 2ry OA
how is IM polyarthritis treated
csteroids (cyclosporin and azathioprine)
desc the process of disease of infective arthritis
bacteria in to joint
cause inflm, inc fluid, joint effusion, capillary dilation and release reactive O2spp which all damages the synovium more.
bacteria hide in synovium + fibrin clots = chronic inflm
–> OA
how do you dx septic arthritis
synovio-centesis = get EDTA (TP and WBCC) and plain (C+S)
when might an septic arthritis not cause lameness
if its draining
what does lymes dz cause (borellia)
shifting lameness (D) = non-erosive arthrpathy. 90% PMN in the synoviocentesis tx - doxycycline
what are tendons made of
type1 collagen
what are ligaments made of
90% type1; 10% type2 collagen
which is more serious - flexor or extensor tendon injuries? why?
flexor
high loads and E stored, if lacerated - cant heal well wi the sheath. (50% heal rate)
what is the most common soft tissue injury of the horse
SDFT (90%)
what does the SDFT do
support fetlock and store E
how hot does a tendon get at gallop
45 degrees, and 17% strain (yet it can fail at only 10%)
what is the manica flexoria
part of the SDFT that wrap around the DDFT as it goes through the fetlock canal (when the SDFT is outside, not inside)
what would you see in u/sound
reduce echogenicity
learn the SDFT and DDFT look like on ultra-sound and all the -itis-es
sorry….
what is seen on u/sound in SDFT tendonitits
focal an-echoic lesions
loss of borders
swelling
(fetlock sinking and lameness)
how do you tx tendonitis
cold hose box rest NSAIDs support dressings neurectomy
what is the accessory lig to the DDFT
check ligament
how do you tx a desmitis
cold hosing, box rest - also pos desmotomy
stem-cells and PLT-rich plasma
shockwava therapy
neurectomy
why is the px annular sheath (at level of sesamoids) sometimes cut ‘desmotomy’
because if the flexor tendons in the sheath are inflm - cant expand = more pain than nec
where is it that the patella gets ‘hooked’ when locked
med trochlear ridge - quads unlock it
what causes gastrocnemius rupture
rotation force (foot stuck) por px
what are the signs of peroneus tertias rupture
stifle flex AND hock ext (not okay..) poor px
how does the SDFT luxate
inserts on the tuber calci on calcanean process so luxate = falling off - lateral trauma
name some equine myopathies
- neurogenic atrophy (motor neurone dz)
- white muscle dz (vitE;Se)
- acute or chronic exertional rhabdomyolysis (unfit, calm down)
- non-exertional rhabdomyolysis (clostridia or inj-site abscess)
- atypical myoglobinuria (sycamore)
what are the fracture classifications for open fractures
grade 1 = bone was out, but now back in
grade 2 = bone outside, neither bone nor ST missing
grade 3 = missing bone and ST
2 common avulsion fractures are…
lat malleolus (ulna) tibial tuberosity (tibia)
desc the basic fracture healing process
- form clot (200% strain)
- dev inflm and oedema
- cell proliferation
- cartilage and bone for = callus dev
- —for callus to form the strain must be
where does the blood suppy for fx healing come from - as it will have lost most of the medullary arterial supply
surrounding ST AND the periosteal arteries (dont lose any periosteum)
fracture can heal either directly or indirectly - desc brief differences
direct -
how can you achieve external co-aptation
IM pins cerclage wires screws - lage and positional plate - compression, neutral, buttress external fixators - good if highly communited
what is the ideal lavage
19G, 100ml/g in a 20ml syringe
what banages are good for intial assessment
wet-dry and silver and hydrogel
