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DVM 2 - 1 > Locomotion 1 > Flashcards

Locomotion 1 Flashcards

1
Q

How do radio-graphic projections work in terms of terminology

A
  • Refers to the path taken by the X-ray beam through the structure where the primary beam enters the tissue and the second part where the beam exits
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2
Q

where does beam go with ventrodorsal projection

A

beam enters the abdomen ventrally and exits dorsally

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3
Q

Left lateral recumbency where does beam go

A

right side up, left side down -> gives left lateral projection
○ Names after the side through which the beam exits the body

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4
Q

What are the 3 main types of joints

A

1) fibrous
2) cartilaginous
3) synovial

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5
Q

Which thoracic vertebra is the anticlinal vertebra

A

11 - process change orientation

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6
Q

Where is the intervertebral fibrocartilaginous joint

A

the intervertebral disc comprises a pulpy nucleus within a fibrous ring and lies in the intervertebral space between the bodies of each adjacent vertebra

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7
Q

Where is the costovertebral joint found

A

there are two

1) between the head of the rib and the costal fovea
2) between the turbercle of the rib and the transverse process of the thoracic vertebra

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8
Q

where is the sternocostal joint found

A

the joint between the costal cartilage and the sternebra

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9
Q

where is the costochondral joint

A

the joint between the rib bone and the costal cartilage

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10
Q

on what aspect of the carpus is the carpal seasmoid located

A

medial palmar

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11
Q

sesamoid bone where form and function

A

Form within tendons and ligaments

1) increase the compressive strength of these structures
2) reduce the impact of friction as ligaments move across bones
3) increase the mechanical advantage of ligaments

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12
Q

what is the other name for the glenohymeral joint

A

shoulder joint

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13
Q

what bones make up the pelvic inlet and pelvic outlet

A

Pelvic inlet: Ilium crest, pubis (cranial), ilium

Pelvic outlet: ischium and caudal pubis

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14
Q

What are the 4 sesamoid bones associated with the stifle

A

1) patella
2) fabellae - medial and lateral
3) popliteal sesamoid

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15
Q

what does the stifle comprise of

A

femoropatellar and femorotibial joint

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16
Q

list 3 functions of bone

A

1) support where rigidity required
- levers for locomotion
- protection
2) houses haemopoietic tissues
3) calcium homeostasis

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17
Q

What are the 3 types of tissue within the bone

A 
1) all bones comprised of combination of:
o cortical (= compact) bone
o trabecular (= cancellous) bone – porous network
2) periosteum – connective tissue covering outer surface of bone (except at articular surfaces)
3) endosteum – all surfaces inside bone - including all the trabecular
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18
Q

3 regions of the bone

A

1) diaphysis (shaft - longer) – exclusively cortical bone surrounding marrow cavity
2) epiphysis at each end – mostly trabecular bone surrounded by thin shell of cortical bone
3) metaphysis between diaphysis and epiphyses – transition from mostly cortical to mostly trabecular

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19
Q

List the 3 sources of blood supply for the bone and what occurs in mature bone

A

1) nutrient artery enters diaphysis to supply marrow and cortical bone
2) metaphyseal arteries
3) epiphyseal arteries
Mature bone -> vessels from different regions anastomose -> no anastomosis between epiphyseal and metaphyseal vessels until skeletal maturity
§ due to cartilaginous growth plate

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20
Q

what is the venous drainage of bone marrow and cortical bone

A

drainage of bone marrow through veins accompanying nutrient, epiphyseal and metaphyseal arteries
o drainage of cortical bone to venules in periosteum

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21
Q

What is bone, and what is it composed of and what is the two types of bone as it matures

A
  • bone is a connective tissue
    • major component is type I collagen
    • several additional glycoproteins (many bind calcium)
    • hydroxyapatite (mainly calcium and phosphate) - mineralisation gives strength
    1) organised in layers (lamellae) in mature (lamellar) bone
    2) disorganised in immature (woven) bone (found in developing and healing bone - fast maturation
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22
Q

List the 6 bone cells

A

1) osteoblasts
2) osteocytes
3) bone lining cells
4) osteoclasts
5) bone marrow cells - haemopoietic and adipose tissue
6) blood vessel cells

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23
Q

Osteoblasts where found, function and what mature to

A
  • round cells found on bone surfaces
  • secrete osteoid (mixture of bone matrix proteins) which then becomes mineralized to form rigid bone tissue
    ○ Mineralisation takes a few days to form
  • become osteocytes as they are embedded in the matrix they secrete
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24
Q

Osteocytes what look like, what structures do they possess and their function

A
  • small round cells within lacunae surrounded by bone matrix, less cytoplasm than osteoblasts
  • possess fine processes extending into canaliculi (fine channels)
  • processes form junctions with processes from other osteocytes and osteoblasts
  • thought to have a role in sensing of mechanical strain that bones are subjected to
    ○ Secrete molecules that travel through the canaliculi which send messages to the cells on the surface
    ○ May stimulate bone formation - too much mechanical strain for the bone at that time
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25
Q

Bone lining cells shape, where found and function

A
  • flattened cells covering resting bone surfaces

- capable of differentiating into osteoblasts

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26
Q

Osteoclasts shape, where found and function - how achieve this

A
  • large multinucleate cells
  • sparsely scattered on bone surfaces - small number
  • responsible for bone resorption:
    ○ adhere to bone through sealing zone, creating microenvironment between cell and bone surface
    ○ secrete hydrogen ions and lysosomal enzymes to degrade bone matrix
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27
Q

Organisation of bone tissue what are the 2 types hw organised and what contain

A

1) Trabecular bone
• network of bone plates and rods
• interspersed with spaces containing bone marrow and blood vessels
2) Cortical bone
• organised into Haversian systems (osteons):
○ longitudinal cylinders consisting of concentric bone lamellae surrounding a central blood vessel and nerve branches (vasomotor and sensory) within ‘Haversian canal’
• blood vessels within Haversian canals linked to each other through transverse ‘Volkmann’s canals’

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28
Q

Differentiation of bone cells what are the 6 different times this occurs

A

1) embryonic development
2) growth
3) maintenance
4) response to changing mechanical or metabolic needs
5) repair
6) other types of pathology

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29
Q

mesenchymal stem cells what bone cells do they produce, where located, what other cells produce

A
  • Osteoblasts, bone lining cells and osteocytes
  • located in most connective tissues, including bone marrow stroma
  • can differentiate into adipocytes and muscle cells
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30
Q

Active osteoblasts what occurs when secretion ceased

A

become osteocytes or bone lining cells, or undergo apoptosis when secretion has ceased.

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31
Q

Osteoclasts where derived and what become to stimulate bone resorption

A
  • derived from haemopoietic cells of monocyte/macrophage lineage (present in blood and bone marrow).
  • initially differentiate into mononuclear preosteoclasts, which fuse with each other to form multinucleate osteoclasts if there is continuing stimulus for bone resorption
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32
Q

Embryonic bone development what are the 2 ways and main difference

A

1) intramembranous ossification

2) endochondral ossification - requires cartilage

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33
Q

Intramembranous ossification what occurs and in which bones

A

• condensation of embryonic mesenchyme, followed by differentiation into osteoblasts and secretion of osteoid to form spicules of woven bone,
○ gradually forming a network of trabeculae to extend the bone
-> many of the skull bones

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34
Q

What are the 3 functions of cartilage

A

1) Support where flexibility required
2) Shock absorption - stifle joint also have menisci that adds in this
3) Smooth articular surface - unlike with bone

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35
Q

Cartilage what is it composed of and are there vessels present?

A

cells and extracellular matrix
• composition of matrix and ratio of cells/matrix varies with cartilage type
• usually avascular - some cartilage do have a vascular supply, if cartilage is very large chondrocytes cannot get diffusion from circulatory system outside cartilage

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36
Q

What is the only cell type found within cartilage, structure, function and how to know if just divided

A

Chondrocytes
• encased in lacunae within extracellular matrix
• proliferation results in occasional pairs of chondrocytes within lacunae (‘interstitial growth’)
○ Gradually push away as create extracellular matrix -> therefore in older animals will see chondrocytes fairly separated from each other

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37
Q

Extracellular matrix of cartilage what secreted by, what do the fibers resist and what are the fibers composed of

A

synthesized and secreted by chondrocytes
• fibres (resist stretching) and amorphous extracellular material (resist compression)
• fibres composed of type II collagen
○ almost exclusive to cartilage - narrower and thinner than bone collagen (collagen type I)
○ not normally visible microscopically
- Determine the shape of the cartilage

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38
Q

amorphous extracellular material of cartilage what are the 2 main materials what do they form and what does this result in

A

composed of proteoglycans and hyaluronan (shapeless)
○ proteoglycans consist of core protein and sulphated glycosaminoglycan (GAG) side chains (polysaccharides)
○ proteoglycans form large aggregates with hyaluronan (a large non-sulphated GAG - no protein content)
§ GAGs (glycosaminoglycan) have multiple negative charge, therefore strongly hydrophilic - attract water
§ swelling pressure of hydrophilic proteoglycan aggregates counteracted by tension of collagen fibres, resulting in extremely high resistance to compression chondrocyte lacuna
§ Very important in shock absorption

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39
Q

What are the 3 types of cartilage

A

1) hyaline
2) elastic
3) fibrocartilage

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40
Q

Hyaline cartilage where found, what structure does it contain, appearance, how are cells arranges, and ratio of GAGs/collagen

A

found in:
○ respiratory tract (nose, larynx, trachea, bronchi)
○ ventral ends of ribs
○ articular cartilage (smooth, resilient, frictionless surface)
○ growth plates of growing long bones
- has a perichondrium (connective tissue structure that is continuous with the cartilage that connects it)
• white glassy appearance grossly
• cells arranged randomly except in growth plate, where arranged in columns
• high ratio of GAGs/collagen

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41
Q

Elastic cartilage where found, how different to hyaline cartilage, what structures within

A 
found in:
○ external ear
○ epiglottis (part of larynx)
○ Arytenoid cartilage 
• more flexible than hyaline cartilage
• elastic fibres in matrix
• has perichondrium
42
Q

Fibrocartilage where found, what structures make it unique and ratio of GAGs/collagen

A

found in:
○ intervertebral discs
○ Menisci - more flexible - located between two bones to provide additional shock absorption
○ points of attachment of tendons and ligaments to bone
○ cardiac skeleton - structure around the valves
• low ratio of GAGs/collagen
• no perichondrium
• chondrocytes arranged in lines between bundles of fibres perichondrium

43
Q

Endochondral ossification what does it begin with and the 6 steps

A

begins with formation of cartilage model, followed by formation of primary centre of ossification

1) Hypertrophy of chondrocytes mid-diaphysis
2) formation of periosteal bone collar from mesenchymal stem cells -> osteoblasts
3) death of hypertrophic chondrocytes
4) invasion of cartilage by osteoclasts and blood vessels
5) resorption of cartilage matrix by osteoclasts
6) deposition of bone on cartilage remnants by osteoblasts

44
Q

Endochondral ossification what other 6 steps occur after the primary centre of ossification has developed

A

1) chondrocytes in cartilage are still proliferating at the end of the bone -> formation of epiphysis
2) primary centre of ossification continues to enlarge
3) primary trabeculae in mid-shaft is resorbed to form marrow cavity which grows
4) formation of at least one secondary centre of ossification in epiphyseal cartilage at each end, through process similar to that for primary centre
5) growth continues at the growth plate (b/n primary and secondary center) through proliferation of chondrocytes
6) closure of growth plate following puberty

45
Q

What are the 3 behaviours of chondrocytes during endochondral ossification and what regulated by

A

1) proliferation -> stimulated by growth hormone which acts through insulin-like growth factor-1 -> stimulated by locally secreted bone morphogenetic proteins (BMPs)
§ inhibited by signalling through fibroblast growth factor (FGF) receptor 3
2) Cartilage matrix secretion - stimulated by IGF1 and BMPS
3) hypertrophy - bone morphogenetic proteins (BMPs)
§ inhibited by signalling through fibroblast growth factor (FGF) receptor 3

46
Q

List 3 behaviours of invading cells during endochondral ossification and what regulated by

A

1) vascular endothelial growth factor (VEGF) stimulates angiogenesis
2) BMPs stimulate osteoblast differentiation from bone marrow stromal cells
3) receptor activator of NFkB ligand (RANKL) stimulates osteoclast differentiation - REQUIRED

47
Q

What can lead to chondrodysplasia and give an example

A

Mutations in genes regulating endochondral ossification
Genes encoding for
• cartilage matrix proteins
• hormones or growth factors that regulate endochondral ossification, or:
○ their receptors
○ intracellular mediators of their effects
a mutation in the aggrecan (cartilage proteoglycan) gene responsible for ‘bulldog dwarfism’ (severe chondrodysplasia) in Dexter cattle

48
Q

What does the timing of ossification and growth plate fusion based on and when for primary and secondary ossification centers in different species

A

Dependent on the species and the breed
Primary -> of major limb bones form before birth in all domestic mammals
Secondary of major limb bones present at birth in ungulates (hooved - need to have well developed limb bones - need to run from predators) but not in dog and cat

49
Q

What are the 2 processes involved with shaping of bone during growth and why does this occur

A

1) formation through osteoblastic activity on selective bone surfaces
2) resorption through osteoclastic activity on other bone surfaces
NEED TO MAKE BONE LARGER BUT NOT THCK
in response to changing mechanical loads or bone injury

50
Q

What are the 4 general steps in growth of long bones

A

1) Increase diameter of diaphysis via formation
2) Expand marrow cavity - more room for bone marrow to provide more stem cells and blood cells -> therefore resorb bone within the cavity
3) Retain shape, wide at epiphysis for muscle attachments before narrow at diaphysis so not too heavy -> resorption of periosteal surface
4) growth in length through chondrocyte proliferation in the growth plate

51
Q

What are the responses to mechanical loading and how do they come about

A

This is done via production of molecules from osteocytes (detect strain and produce molecules through canaliculi)

1) loading stimulates formation (osteoblasts) and suppresses resorption (osteoclasts), leading to thickening of trabeculae and/or cortex; this may result in a change in shape or volume of bone.
2) unloading stimulates resorption and suppresses formation, leading to thinning of trabeculae and/or cortex.

52
Q

Remodelling of bone mechanism and what surfaces does this occur on

A

Mechanism -> within cortical bone, osteoclasts tunnel through bone longitudinally, followed by osteoblasts which deposit concentric lamellae of bone to fill in the tunnel, leaving space for blood vessel, thus forming new osteon.
occurs on periosteal and endosteal surfaces, as well as within cortical bone

53
Q

List 3 main factors that activate osteoblast activity during bone modelling, remodelling, repair and pathology

A

1) sex steroid hormones (oestrogen, testosterone), BMPs (bone morphemic proteins), other growth factors
2) mechanical load
3) inflammatory cytokines and prostaglandins

54
Q

List 3 main factors that activate osteoclast activity during bone modelling, remodelling, repair and pathology and what are these factors mediated by

A

1) PTH (calcium homeostasis, especially during pregnancy and lactation)
2) mechanical unloading (e.g. rest periods following training – horses)-
3) inflammatory cytokines and prostaglandins
○ most of these effects mediated by osteoblasts – hormones and cytokines stimulate RANKL expression in osteoblasts

55
Q

What are the 4 main stages during cellular fracture repair and are the stages highly defined

A

1) inflammation
2) soft callus formation
3) hard callus formation
4) remodelling
- stages are sequential but may be considerable overlap -> no clear differentiation

56
Q

What are the 4 main stages in inflammation during fracture repair

A
  1. Disruption of vascular integrity leads to formation of a haematoma.
  2. Haematoma contains coagulation factors which attract granulocytes, lymphocytes and macrophages into haematoma.
  3. Inflammatory cells secrete cytokines including interleukins-1 and -6, and growth factors, BMPs -> recruitment of mesenchymal stem cells
  4. Granulation tissue formed through:
    ○ growth of capillaries into haematoma
57
Q

Soft callus formation what is the result and the 4 stages

A

This stage, where present, involves formation of a fibrocartilaginous tissue around fracture ends.
1) Mesenchymal stem cells differentiate into:
○ chondrocytes, which proliferate and secrete cartilage matrix
○ fibroblasts, which generate fibrous tissue
2) Cell proliferation and matrix production stimulated by growth factors, including PDGF, FGFs, IGFs and BMPs.
3) Fibrocartilaginous plug forms between fracture fragments, providing some stability - not rigid as isn’t bone
4) Chondrocytes undergo hypertrophy, in preparation for vascular invasion and replacement by bone (endochondral ossification)

58
Q

Hard callus formation what are the 2 main steps and what is needed

A

Formation of mineralised bone matrix, either:
1) replacing fibrocartilaginous soft callus, or
2) where no soft callus present, directly within the fracture gap and/or on existing bone surfaces.
• Mesenchymal stem cells differentiate into osteoblasts and secrete bone matrix (usually woven bone), under influence of BMPs.
• High oxygen tension critical for osteoblast differentiation, thus hard callus formation requires adequate vascular supply.

59
Q

Callus remodelling what occurs and the steps

A

Remodelling of the woven bone hard callus into original lamellar bone configuration (trabecular and/or cortical)
• Resorption by osteoclasts and replacement by osteoblasts:
○ on periosteal and endosteal surfaces
○ within cortex (osteonal remodelling)

60
Q

Walk what is the sequence and how many beats

A
  • slow and each limb lands separately in sequence
    ○ Hind followed by lateral fore followed by contralateral hind etc = walk
    ○ LH, LF, RH, RF
    § Can hear 4 beats
61
Q

Trot what is the sequence and how many beats

A
  • can be fast – and diagonal pairs of limbs land together
  • Left hindlimb landing and taking off with the right forelimb and vice versa
    ○ LH & RF, …….. RH & LF, (diagonal pairs)
  • 2 beats
62
Q

Pace what is the sequence and how many beats, what occurs with dogs

A
  • can be fast – lateral pairs of limbs land together
  • Left hindlimb landing and taking off with the left forelimb and vice versa
    ○ LH & LF, …….. RH & RF, (lateral pairs)
  • 2 beats
  • Dogs can cross over from pace and trot
63
Q

Canter how many beats, what are the 2 main types and how differentiate

A
  • has 3 beats and can be either rotational or transverse
    1) rotational – one lateral pair of limbs land together - much more stable at the back
    2) transverse – one transverse pair of limbs land together
  • not done unless got strong back, will wobble slightly
64
Q

Describe the sequence in Left and right lead of transverse cancers

A

1) Left lead diagonal (transverse)->
□ Right hindlimb, left hindlimb + right forelimb land together, Left forelimb
2) Right lead diagonal (transverse)->
□ Left hindlimb, right hindlimb + left forelimb land together, Right forelimb

65
Q

Describe the sequence in Left and right lead of rotational cancers

A

1) Left lead rotatory ->
□ Left hindlimb, right hindlimb + right forelimb, left forelimb
2) Right lead rotatory ->
□ Right hindlimb, left hindlimb + left forelimb, right forelimb

66
Q

Gallop what is the sequence, the types and number of beats

A
  • is faster than canter and the diagonal or lateral pair land separately in fast succession (hind limb then forelimb) so there are 4 beats instead of 3
    ○ Therefore there are also the transverse and rotatory gallop - instead of landing together land in quick succession
    § LH, RH, …., LF, RF, ………. (transverse, right lead)
    § LH, RH, …., RF, LF, ………. (rotatory, left lead)
67
Q

What does each stride consist of

A

consists of a support phase and a swing phase

68
Q

What are the 3 main ways to identify the gait

A

1) Symmetry
1. Symmetrical eg walk, trot, pace, hop movement of limbs are bilaterally symmetrical
2. Asymmetrical eg canter, gallop. movement of limbs are different on left and right sides.
- Speed – asymmetrical generally faster.
2) Rhythm – 1 beat = hop
○ 2 beats = trot or pace
○ 3 beats = canter
○ 4 beats = walk or gallop
3) Fix attention on one limb, then a pair of limbs
- Both diagonals together = trot
- Both laterals together = pace
- Both hind together = hop

69
Q

What are the 2 main objective analysis for the gait

A

1) Such as lameness locator -> gives relative movement of the four limbs
§ Can give objective comparisons with the effect of nerve blocks or other treatments on the gait are possible
2) Hoof-mounted device -> gives movements of limbs in real time
§ This allows direct measurement of the effects of methods of hoof preparation and horseshoe design as well as the working surface on the hoof movement.

70
Q

Muscle damage what could be the cause and how long till occur

A
  • Possible nerve damage if not painful
  • This occurs within a short period -> weeks if complete
  • If incomplete nerve damage then less obvious muscle damage
71
Q

AEC what is it, what is it composed of and how two tell the difference between layers

A

AEC = Articular Epiphyseal Complex is the zone of endochondral ossification beneath the articular cartilage (on the tip of the bone) in growing animals.
- The AEC is composed of a layer of articular cartilage (AC) and a subjacent layer of growth (epiphyseal) cartilage (EC).
The deeper growth cartilage is vascularised unlike the articular cartilage

72
Q

Chondrodysplasia what is it, where occur, what results in and example

A
  • Defect in the formation of cartilage
  • Physis and/or AEC
  • Causes often undetermined
  • Affected animals generally show disproportionate dwarfism (short legs with normal sized or dome shaped heads)
    NOT ALWAYS A DEFECT -> certain breeds
    EXAMPLE - bulldog calves - The animals are grotesquely malformed with protruding tongue; thick, rotated and abducted limbs; absent hard palate; and umbilical hernia and protruding viscera.
73
Q

Osteochondrosis where generally occur what species most likely affected and clinical manifestations

A
  • Focal failure of endochondral ossification
  • Articular-epiphyseal complex (AEC) > metaphyseal growth plate
  • Most species can be affected -> most likely in pigs, horses and large breed dogs
  • Clinically manifestations generally about the effect on joints -> degenerative joint disease
74
Q

What is the pathogensis of osteochondrosis and what look like grossly

A

Path
1) necrosis of blood vessels in immature growth cartilage
2) necrosis of cartilage
3) endochondral ossification does not occur focally - leading to a retained core of cartilage within the bone
4) cleft -> cartilage flap -> joint mouse OSTEOCHONDRITIS DISSECANS
Grossly - lesions weel demarcated, thickens, white foci on articular cartilage, large clefts and flaps

75
Q

Osteogenesis imperfecta what is it, where occur, result in

A
  • Defect in type 1 cartilage -> growth plates no affected as primarily type 2 collagen
  • Collection of diseases, result in poor quality collagen or decrease in high quality collagen
  • Acute fractures mandibles and major limb bones, fracture callceous can be present at birth
76
Q

Aetiology of osteochondrosis

A

Multifactorial
• Genetic predisposition - certain breeds of dogs, often the larger breeds
• Trauma or excessive weight bearing
• Rapid growth - young fast growing animals most susceptible
• Hormonal factors

77
Q

Osteopetrosis what is it, what are the 2 ways it can occur and typical gross appearance

A
  • defect of osteoclastic function → poor remodelling of the primary spongiosa (mineralised cartilage matrix) → increased bone fragility.
    1) Can be inherited:
    2) Acquired condition often associated with in utero viral infections that damage osteoclastic precursors, eg canine distemper, BVD, FeLV in cats
    Grossly
  • butterfly shape bone
78
Q

What are the 3 main metabolic bone diseases and there general causes

A
  • Causes nutritional or hormonal imbalances -> can get multiple diseases in the same animals
    1) Fibrousosteodystrophy
    2) Osteoporosis
    3) Rickets/osteomalacia
79
Q

Osteoporosis how does it occur, consequences and list the 3 main causes and causes within

A
  • The bone is reduced in amount, but normally mineralised (normal quality)
  • Bone resorption > bone formation
  • Consequences are secondary fractures and hypocalcaemic crisis
    1) Nutritional deficiencies - livestock
  • copper (lambs and calves) calcium (increases parathyroid or high phosphorus diets)
    2) Endocrine disorders
  • Hyperadrenocorticism - Glucocorticoids inhibit collagen synthesis, osteoblastic differentiation, and stimulate osteoclastic bone resorption
    3) Disuse - paralysis, fractures, confinement -> stablised at a lower bone density
80
Q

Osteoporosis what bones mainly affect and the gross lesions

A
  • portions of bones with large component of cancellous tissue, such as vertebral bodies, flat bones (scapula and ilium), and the metaphysis of long bones.
  • bones are light, brittle with thin cortec and large medullary cavity, formation of transverse reinforcement
81
Q

Rickets/osteomalacia when is which, cause and result in

A
  • Vit. D and/or phosphorus deficiency (mainly pregnant or lactating cattle grazing)
  • Young animals -> rickets
  • Adults -> osteomalacia
  • Defective mineralisation of physeal cartilage at sites of endochondral ossification (rickets) and of osteoid matrix (rickets and osteomalacia)
82
Q

Vitamin D where get from and the 3 functions

A

can get from sunlight and diet
Function -
1. Enhances absorption of P and Ca from small intestine
2. Stimulates release of P andCafrombone (resorption)
3. Enhances resorptioncincthe kidney

83
Q

Rickets/osteomalcia where do the lesions generally occur list 3

A

Lesions most prominent at sites of rapid growth where cartilage contributes most significantly to skeletal growth (e.g. physis of proximal humerus, distal radius, ribs, femur

1) retained cartilage in trabecular bone -> extends into metaphysis
2) growth plate much thicker -> failure of cartilage to mineralise
3) shape -> shorter, broader, thickened and uneven growth plate

84
Q

Fibrous osteodystrophy (FOD) what does it occur with and why, what are the 2 types and types within

A

FOD occurs with hyperparathyroidism due to increased production of parathyroid hormone (PTH).

1) primary hyperparathyroidism - functional parathyroid adenomas and carcinomas
2) secondary hyperparathyrodism
1. nutritional secondary hyperparathyroidism
2. renal secondary hyperparathyroidism

85
Q

why is hyperparathroidism a problem with bone

A

Increased PTH secretion → Increase bone resorption and release of calcium and phosphate from the bone.
Effect of PTH on bone: stimulation of bone resorption.

86
Q

Secondary hyperparathyroidism when common, example and pathogenesis of both types

A

1) nutritional -> common with young growing animals on low-calcium-high-phosphorus diet
Eg - dog and cat all meat diet
Path - increased PTH -> bone resorption (rubber jaw)
2) Renal
- Skeletal lesions develop secondary to chronic, severe, renal disease; most common in dogs (“rubber jaw”)
Path - decreased GFR -> decrease Ca and P absorption in GIT -> increase PTH etc.

87
Q

What are the gross result from hyperparathyroidism

A

BIG HEAD - bilaterally enlarged mandibles

  • Increased axillary bones
  • Obstruct nasal passages
  • Teeth can become loose and partially burried
  • trabecular and cortical bone -> rubbery
  • dog and cat mainly get rubber jaw
88
Q

Toxic osteodystrophies what are the main 2 ones

A

1) flurosis

2) hypervitaminosis A

89
Q

Flurosis what result in, how occur and how do lesions occur

A

when fluroide present in chronic excess is capable of inducing characteristic bone and teeth lesions.
cause - ingestion of small amounts of fluoride compounds over long periods
teeth -> Fluoride disrupts ameloblasts→ irregular enamel matrix, rate of formation, and rate of mineralisatio -> oxidation of exposed dentin -> dark discoloration
Bone -> mechanism unknown

90
Q

Hypervitaminosis A what common cause in cats and lesion can cause, what are the 2 main lesions overall and are they reversible

A
  • generally diets of liver
    cats -> fed livers over long period form exostoses, spine may also become fused
    1) osteoporosis - reversible if stop feeding high vitamin A foods
    2) physeal lesions -> narrowed - irreversible
91
Q

Osteomyelitis where generally occur and 4 main routes of infection, what result from and main

A 
- There is a strong predilection for sites of active endochondral ossification
○ metaphysis and epiphyses of long bones and vertebrae
Routes of infection:
1) Haematogenous MOST IMPORTANT
•Bacteremia/septicaemia
2) Direct implantation
•Wounds,fractures
•Penetrating trauma
3) Local infections
•From adjacent tissueseg.arthritis
4) Non-infectious 
•Local periosteal injury
92
Q

what is the Pathogenesis of haematogenous osteomyelitis and what are the 3 anatomic factors favouring metaphyseal localisation

A

Bacterial entry via umbilicus, skin or mucous membrane → septicaemia → bacteria lodge in metaphyseal capillaries → thrombosis → infarction → osteomyelitis

1) Capillaries invading mineralising growth cartilage (primary spongiosa) make sharp loops
2) Capillaries are fenestrated and open into sinusoidal vessels causing sluggish blood flow, thrombosis and necrosis
3) Phagocytosis in sinusoids is inefficient

93
Q

Mandibular osteomyelitis (lumpy jaw) what is the primary cause in cattle, what type of inflammation and what occurs

A
  • Lumpy jaw is a primary disease of cattle caused by Actinomyces bovis
    ○ A. bovis is an obligate pathogen of the oral cavity; the surface tissues must be injured (e.g. penetrating trauma) for deeper invasion to occur
  • Osteomyelitis follow direct extension of the infection from the gums and results in a chronic pyogranulomatous reaction.
  • In the bone there are multiple foci of bone resorption -> The periosteal proliferation is excessive therefore the mandibles are enlarged.
94
Q

List the 4 main primary neoplasms of bone and the cell in which they derive

A

1) oesteosarcoma - osteoblast
2) Chondrosarcoma - chondrocytes
3) lymphoma
4) multiple myeloma - plasma cells

95
Q

What are the 4 common sites for oesteosarcoma and the general rule

A 
Most common sites
- Distal radius 
- Proximal tibia 
- Distal femur 
- Proximal humerus 
Generally away from the elbow towards the knee
96
Q

Oesteosarcoma when common, what lead to, does it metastasise and prognosis

A
  • Rare in other species apart from cats and dogs where most common - accounts for 80% of all primary bone tumours in dogs
    ○ Most common in large breed dogs
  • Generally middle aged to older dogs -> can occur in smaller dogs
  • Most combination of production and lysis of bone
  • Early metastases to the lungs generally and to other organs -> Poor prognosis even with treatment
97
Q

Oesteosarcoma what look like grossly, histologically and what predispose to

A

Grossly
- Haemorrhages
- Can totally destroy the bone
Histological
- Proliferation of neoplastic osteoblasts
- Normal bone formation can occur
- Production of osteoid (eosinophilic material) needs to be present
- Osteoclasts, spindle cell population that produce osteoid
Predispose to pathological bone fractures
Painful

98
Q

Chondrosarcoma what type of tumour, where occur, difference from oestosarcoma, treatment and gross appearance

A
  • Malignant tumour in which cells produce neoplastic chondroid and fibrillar matrix but never directly produce osteoid or bone
  • Flat bones, ribs and sternum
  • Can cross joint spaces UNLIKE OESTOSARCOMA
  • Treatment -> more likely to be successful as metastasise later and generally if occur to the lungs
    Grossly
  • Waxy/gelatinous appearance
  • White/grey
  • Large size and lobulated
99
Q

Lymphoma cause, what lead to, what other organs commonly involved

A
  • Multicentric causes generally
  • Eccentric bone infarction from the lymphoma due to ischemia secondary to infiltration of the marrow cavity
  • Calves generally get sporadic lymphoma, can also get involved of liver, spleen
  • Lysis of bone
100
Q

Multiple myeloma what occurs, where main place and what can lead to

A
  • Plasma cells replacing existing bone marrow cells
  • Lysis of bone
  • Most commonly occurs spinal column, ribs, skull and long bones
  • Can lead to patholgoical fractures
101
Q

Secondary tumours how occur and what are the common ones

A
  • Direct extension or metastasis
  • Carcinomas generally metastasise to bones more commonly
  • Osteosarcomas can metastasise to other bones
102
Q

Hypertrophic (pulmonary) osteopathy - Marie’s disease what does it result in, cause, common bones affected and gross lesions

A
  • Results in new bone formation
    Cause - is a space occupying lesion in the thorax (tumours, large abscesses or granulomas)
  • Dogs - neoplasm, horses - granulomatous disease
  • Common bones affected are: radius and ulnar, metacarpals, tibia and metatarsals
    Gross lesions - will continue to progress if mass lesion isn’t removed, if it is removed than will regress

DVM 2 - 1 (31 decks)

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