Musculoskeletal 4, 5 and Practical Flashcards
What is a joint?
What are the types of joints?
Joint- the area where two bones are attached for the purpose of motion
Syndesmosis- fibrous tissue connection- intervertebral
Symphyses- fibrocartilagenous disks, intervertebral disks
Diarthrosis- hyalin joint cavity and synovium, synovial fluid, articular epiphyseal complex
What makes up the synovium
Inner layer-
synoviocytes
Type A- macrophage-like- removal of material
Type B- fibroblast-like- production of synovial fluid
Type C- intermediate morphology
villous, vascularised, synovial fossa
Outer layer-
fibrous connective tissue
Describe how
Describe how joints respond to mechanical forces
- Compression from one bone to another through cartilage
- Inside the cartilage- aggrecans (hold water), collagen type 2, water and chrondrocytes
- Nourishment for cartilage is water-soluble for chondrocytes
- In compression, the water moves out into the joint cavity and allows recirculating and change
- The hydrostatic pressure increases with helps support the structure of the joint
- Distension- water back into cartilage allowing fresh nourishment
Describe cartilage homeostasis?
Metalloproteinases breakdown aggrecans and collagen
Chondrocytes prevent this with tissue inhibitors of metalloproteinases
Inflammation and degenerated matric product causes an increase in metalloproteinases
How do joints change with age?
Change of proteoglycan structures
- Decrease of aggrecans
- H2O binding capacity of cartilage reduced
- Reduction in elasticity/nutrition/O2 perfusion
- Increase in cartilaginous alterations
- Erosion mostly in friction sites
- Hyaline cartilage, vertebral discs and meniscus affected
How does cartilage respond to injury?
Cracks lead to fibrillation where chondrocytes join to form lacunae
Ebumation follows- cartilage gone- bone against bone (dads knees)
How does the joint synovium respond to injury?
Hyperaemia/oedema/exudate
This leads to capsular fibrosis
villous hyperplasia
pannus formation- capsule of structure grows over articular cartilage
What are the common names for degenerative joint disease?
What joints are more commonly affected?
How does it grossly appear?
How does it appear histologically?
DJD- osteoarthritis, arthrosis
Hip, shoulder, stifle, interphalangeal, metacarpophalangeal, older animals
Gross- roughening, yellowing and fibrillation of the cartilage, in more severe cases there may be ulceration and eburnation of the underlying bone with osteophytes and joint mice
Histology- loss of metachromatic staining in the superficial cartilage, formation of chondrones, reduced thickness of cartilage, synovial villous hypertrophy, mononuclear inflammation and fragments of degenerate/necrotic cartilage
What is the arrow pointing to?
Osteophytes
What types of haemorrhage can occur in joints?
What can cause a joint haemorrhage?
Intra-articular
Periarticular
- Traumatic
- Inflammatory
- Toxic
What are distortion, luxation, subluxation and ankylosis?
Distorsion- shot time dislocation of corresponding joint areas
associated conditions- ruptures of capsule/ligaments, haemorrhages
Luxation- persistent dislocation
Subluxation- partially/temporary dislocations
Ankylosis- loss of mobility
fusions of joints, fibrous/osteous connection, articular deformations
What are some examples of congenital DJD?
What are the different causes of joint inflammation?
What neoplasia can affect joints?
Congenital DJD-
Osteochondrosis
Hip dysplasia
Congenital patella luxation
Intervertebral disk disease
Spondylosis
Wobble syndrome
Inflammation-
Bacterial arthritis
Mycoplasma arthritis
Viral arthritis
Neoplasia-
Synovial sarcoma
Histiocytic sarcoma
What is the aetiology of osteochondrosis
What species does it affect?
Describe the pathology
How does it appear grossly and histologically?
What are the associated conditions?
Aetiology- rapid growth, overnutrition, mineral imbalances, trauma, genetic
Species-
Swine- femur, vertebrae, ulna
Dog- fast-growing males- elbow dysplasia
Horses- femur tarsus, metacarpopharyngeal
Pathology- ischaemic damage to growing cartilage, areas of necrosis, cysts, detachment
Gross- white foci progressing to cartilage ulceration
Histology- microcysts with necrotic material, retention of cartilage cores, hypertrophic chondrocytes
Associated conditions-
Osteochondritis dissecans, epiphyseolisis due to separation of articular cartilage
What dogs are affected by hip dysplasia?
What causes it?
Therefore how does it grossly appear?
Large dog breeds
Lack of conformity between the femoral head and acetabulum leading to subluxation and degenerative joint disease
Shallow acetabulum, subluxated femoral heads, roughened to eroded cartilage, sclerosis of subchondral bone
What species are prone to patellar luxation?
What is the pathogenesis?
How does it grossly appear?
Toy breeds of dogs and horses
Path- anatomical defects of the joint, hypoplasia of the ridge of the femoral trochlea
Gross- luxation or subluxation of the patella
Medial- toy breeds
Lateral- giant breeds, horse
[Can lead to haemorrhage]
What can cause intervertebral disk disease?
What species are affected?
What is the pathogenesis?
How does it grossly appear?
How does the histology become affected?
What are the associated conditions?
Congential or aging
Dogs- daschound, basset, pekinese
Pathology- degeneration of nucleus polposus leading to rupture of annulus fibrosis causing herniation of nucleus polposus
Gross- ventral or dorsal herniation
2 dorsal herniation types
Type 1- Massive herniation resulting of degenerate nucleus material
Type 2- partial herniation- bulging of outer lamellae and intact dorsal ligament
Mainly T12-L2
Histology- Chondroid metaplasia of nuclear polosus or mineralisation
Ac- paresis, spondylosis, haemorrhage, inflammation with type 1, fibrocartilagenous embolism with type II
What disease is this image showing?
What are the arrows highlighting?
What is the aetiology, and what species are affected?
Describe the pathology and gross appearance
What is the associated condition
Spondylosis
Blue arrows- disk degeneration without herniation, loss of disk material
Red arrows- spondylosis/ankylosis
Aetiology- degenerative, age-associated
Species- bulls, pigs, dogs
Pathology- secondary to degeneration of ventral annulus fibrosis
Gross- formation of osteophytes at the ventral bodies to intervertebral spaces
Associated conditions- ankylosis
What is the technical name for wobblers syndrome?
What is the aetiology?
What is the pathology?
What does it do and cause?
Cervical vertebral stenotic myelopathy- wobbler
Aetiology- malformation
Species- horses (TB, QH), dogs (Doberman, great dane)
Pathology-
cervical vertebral instability- the spinal cord is damaged when the neck is extended or flexed
cervical static stenosis- compression/extension occurs regardless of the position of the neck due to thickening of ligaments
Causes compression of the spinal cord and therefore neurological disorders
What is arthritis?
What are the different types?
What is periarthritis?
Arthritis is inflammation of joints
Synovitis
Chondritis
Osteitis
Osteochondritis
Periarthritis- outer capsule adjacent tissue inflammation
Can be mono/polyarthritis
What agent can cause bacterial arthritis?
Describe the pathogenesis?
How does it grossly appear?
What is histology?
Agents- streptococcus, staphylococcus, E.coli, Actinobacillus equi, Haemophilus parasuis
Path- young animals due to septicaemia (polyarthritis) in adults due to penetrating wounds (monoarthritis)
Gross- purulent, fibro-purulent arthritis with or without periarthritis and haemorrhage
Histology- degenerated neutrophils associated with bacteria, haemorrhages, necrosis- chronic lymphocytes and plasma cells with villous hyperplasia
What agents cause mycoplasma arthritis in swine, goats, sheep, and cattle?
How does it grossly appear?
How does it appear histologically?
Swine- Mycoplasma hyorhinis
Goats- M. mycoides
Sheep- M. capricolum
Cattle- M. mycoides
In young animals
Gross- sero-fibrinous arthritis, villous hyperplasia
Histology- sero-fibrinous reaction with mononuclear inflammation, villous hyperplasia, perivascular inflammation and synovial lymphoid follicle formatoin
Where are synovial sarcomas most commonly found (species, breed, location)
How do they grossly appear?
What are the three types?
How do they appear histologically?
Large breed dogs, most commonly middle-aged, are usually found near a weight baring joint- stifle, elbow, shoulder, tarsus
Indistinct borders and may infiltrate along fascial planes- may be cystic
Synovioblastic- epithelial
Fiboblastic
Biphasic
Cells are polygonal to spindleoid, oval, prominent nuceli. May be clefts or cavities containing proteinaceous to mucoid material and lined by a poorly defined layer or malignant cells
How large can myocytes be?
Label this diagram
In what order do these muscle connective tissue layers go?
Epimysium
Endomysium
Perimysium
Endomysium- outer most
Periphysium- middle the diddle
Epimysium- inner most
Describe how a muscle contracts
What is the difference between Type I and Type II muscle fibres?
- Excitation-contraction coupling- leads to calcium release from SR
- Causes actin to bind to myosin
- ATP causes the release of actin to myosin- process restarts
Type 1- slow twitch, oxidative, fatigue resistant
Type IIA/B- fast-twitch, glycolytic, rapidly fatigue
What agent causes malignant oedema in what species?
Describe its pathogenesis?
How does it appear grossly and histologically?
Clostridium speticum- ruminants, horses, swine
Path- bacteria penetrate muscle through a slim wound then produce toxins and cause tissue damage
Gross- severe oedema, gas bubbles, cellulitis that dissects the muscle fibres
Histology- muscle fibres are eosinophilic, necrotic, not many neutrophils
What causes blackleg?
Describe its pathogenesis
How does it appear grossly and histologically?
Ac?
Clostridium chauvoei- cattle and sheep
Path- activation of latent spores in the muscle that colonised previously, spored are ingested and subsequently, dissemination through blood occurs and colonise the muscle- reactivated by stressors
Gross- muscles are dark red, oedematous with a dry centre and porous patter (gas bubbles)
Histology- necrosis, gas bubbles
Ac- liver and kidney degeneration, pleuritis, myocarditis
What is the name for muscle tumours?
Which species are more commonly affected?
How do they appear histologically?
Rhabdomyoma or rhabdomyosarcoma
Dogs and horses
Histo- morphological variants- subdivided into round cell, spindle cell and mixed. Cross striations are indicative of sarcometric differentiation- strap cells and racket cells
An 8-year-old female Cocker spaniel dog is presented at your clinic with a large welling localised on the distal femur. The animal is PTS and submitted for necropsy.
Provide a gross description
Provide a morphological diagnosis
Gross- femur, focally extensive mass localised within the distal diaphysis of the femur involving the medullary cavity and expanding caudally to the periosteum through focal discontinuity of the bone cortex. There are black multifocal areas of haemorrhage with central areas of tissue rarefaction (necrosis). The cranial portion of the cortex exhibit mild thickening.
MD- Oestosarcoma
Look at the picture provided and identify:
Mitotic figures
Neoplastic cells
Areas of haemorrhage
Osteoid formation
A 10-year-old male cat is presented with severely abnormal kidney function parameters with an enlarged and soft maxilla. The animal is found dead a few days later.
Provide a gross description
Provide a morphological diagnosis
Kiddy cortex is affected by a multifocal to coalescing wite to tan firm bulging areas
MD- kidney severe, multifocal to coalescing, chronic, intersititial nephritis
10 yo male cat with severely abnormal kidney function parameters and enlarged and soft maxilla
On this digital slide of the bone turbinates- identify active osteoclasts, mineralised bone
Considering gross and histological changes-
what is the name of the condition in the bone
what is the pathogenic link between kidney and bone lesions
Condition- fibrous osteodystrophy
Pathogenic link-
- chronic kidney lesion, damage to glomerular filtration
- Phosphorous retention- increase in PTH
- Increase in osteoblasts activity with mineralised bone reabsorption and mesenchymal cells
- Failure of differentiation into osteoblasts with the production of collagen
- Lack of collagen reabsorption by osteoclasts
A 10-year-old German shepherd that has been put to sleep for an end-stage lymphoma exhibits pathological changes at the hip joint
Provide a gross description of the lesion
Provide a name for the condition
Provide the cause
Gross- acetabulum is shallow and the femur head is flattened. In both areas, articular cartilage is lost (bone eburnation). Ligament teres are absent. There is thickening and roughening of the synovia all around with diffuse projections (villous hyperplasia)
Condition- Hip Dysplasia
Provide the cause- genetic conditions
The 10-year-old lab found with discomfort including pain on leg palpation and breathing difficulty. An X-ray of the chest is provided, the animal is put to sleep
Provide a gross description of the lesion
Provide the name of the condition
Explain the link between the pulmonary lesion and the bone lesion
Gross description- there is a diffuse complex, multilobular, coral-like new bone proliferation extending on the periosteum of all the bones.
Condition name- Marie’s disease, hypertrophic osteopathy
Link
Space occupying lesion, changes in haemodynamics of blood to limbs- increase vascularization of periosteum- excessive periosteal new bone formation
A foal is found dead, with a history of poor nutrition. During necropsy, you find pathological lesions in the adipose tissue and muscle
Provide a gross description
Provide a morphological diagnosis
GD- approximately 70% of the muscle there are linear, parallel multifocal to coalescing/focally extensive white streaks
MD- muscle, diffuse/multifocal to coalescing, acute/subacute, muscle necrosis/myositis
Briefly describe this slide
Identify intact myofibres and rhabdomyolysis
Considering history, gross and histological features- what can cause the change?
Description- 60% of the left slide is affected by diffuse fragmentation of myofibres with associated infiltrating macrophages and other inflammatory cells (rhabdomyolysis)
Cause-
Poor nutrition causes vitamin E and selenium deficiency- therefore not having normal anti-oxidant activity causing membrane damage
