Musculoskeletal System Flashcards
Definitions & terms for musculoskeletal:
Myocytes/myofibres:
a type of permanent cell. They have a limited ability to regenerate, but cannot undergo hyperplasia..
Describe the structural elements of bone and summarize the contribution of each to bone integrity and/or modelling and remodelling.
A. Mineral
1. Calcium
2. Phosphorus
B. Osteoid/Organic bone:
1. Type I collagen
2. Ground substance: water non-collegenous proteins (cytokines, adhesion molecules, enzymes), glycosaminoglycans, proteoglycans
Osteoclasts: from macrophages, processes rest on bone, remodel
Osteoblasts: have tools to build bone & react to chemical signals
Osteocytes: used to be osteoblasts, now live in haversian canals
Interpret the results of necropsy procedures conducted on specimens from the musculoskeletal system.
Grossly looking at the bone isn’t hard, but in order to do histopathology you would need to decalcify the bones.
Also combining rads with macroscopic changes are important.
Describe the process of normal endochondral ossification and list the primary causes of abnormalities of bone growth associated with endochondral ossification.
Endochondrial ossification:
Cartilage exists in three zones, resting, proliferating & hypertrophic zones. The hypertrophic zone will be going through maturing, degeneration & calcification, all orchestrated by chondrocytes
Outline the pathogenesis of chondrodysplasia and osteochondrosis.
.
Describe the contribution of parathyroid hormone, calcitonin and 1,25-(OH)2 Vitamin D to the regulation of bone metabolism.
.
Outline the pathogenesis of common metabolic alterations in bone such as rickets, osteomalacia, osteodystrophia fibrosa, growth arrest lines, hypertrophic osteopathy, vitamin A deficiency and toxicity, vitamin D toxicity, and vitamin C deficiency.
.
Outline the common causes and possible sequelae of osteitis.
.
Name the common neoplasms of bone and identify the species in which they commonly occur.
.
List the common inherited, congenital and degenerative diseases of joints and discuss the pathogenesis of each.
.
Identify the structural elements of muscle and describe how components of muscle fibers contribute to energy production and contraction
.
Outline the common causes of muscle atrophy.
.
Describe the normal sequence by which structural elements of muscle are altered in degeneration.
.
List the common causes of myositis and where appropriate identify the species in which they occur.
.
Describe the normal constituents of synovial fluid.
.
Describe the changes in synovial fluid constituents that occur in inflammatory and degenerative joint diseases.
.
Choose the appropriate diagnostic approach for tumours of the musculoskeletal system.
.
RIGOR MORTIS
A post-mortem normally pathologic change that involves the contraction of muscles as the energy stores are depleted, dependant on the energy in the muscle & the temperatures. (Relaxation due to muscle protein break down occurs 4 days later)
Disuse atrophy
Muscles waste away due to a lack of use
Atrophy
Decrease in the size of a muscle due to lack of stimuli
Denervation atrophy
A lack of stimuli from the motor nerves to a muscle due to an issue with the nerve providing the stimuli causing a rapid decrease in muscle size (loss of myofibrils leaving the sarcolemma & the nuclei, with eventual myofibre collapse & fibrosis)
Hypertrophy (work & compensatory)
Work hypertrophy is the result of increased workload. Compensatory hypertrophy occurs when individual myofibres enlarge to compensate for the loss of other myofibres. As myofibres enlarge, they can split so that several myofibres occupy a single endomyseal tube
Satellite cells and myoblasts regeneration
regenerate muscle best when the sarcolemmal tube is maintained. If there is disruption of the tube, they canbudandcrossadefector2to4mm,but fibrosis is the result of a more serious disruption.
Exertional myopathy
occurs with overly strenuous exercise, resulting in hypoxia of muscles and lactic acidosis. Animals that are borderline deficient in vitamin E or selenium are particularly prone. A multifocal monophasic myodegeneration is usually the outcome. Epaxial muscles and extensors of the hip are particularly affected.
Nutritional myopathy
is usually seen in herbivores in selenium deficient regions or where there is poor quality feed. Oxidative injury to actively contracting muscle is the intermediate step in the pathogenesis. The diaphragm, tongue, epaxial muscles and extensors of the hip (and the heart) are particularly affected.
Toxic myopathy
occurs with exposure of calves to doxycycline at 3 to 10 times normal dosage, and with ingestion of ionophores such as monensin and salinomycin that are added to cattle feed for their ‘growth promoting’ activities. While the heart is usually the most severely affected, skeletal muscle will become necrotic if the animal survives the initial acute toxic phase.
Idiopathic myopathy
not associated with known causes is reported in horses. Some are associated with infection with Streptococcus and others are simply called ‘pasture associated myopathy’ and are thought to be a type of toxicosis.
MYOSITIS
Inflammatory myopathies occur periodically and cause either local or generalized disease. Most affect one area or muscle, but some are systemic. Bacterial myositis is either suppurative or necrohemorrhagic.
Immune mediated myositis
rare, but is recognized most commonly in the dog where the masticatory muscles (masseter and temporal) are usually affected. These muscles have a unique type of myosin (type II) that is the target of an immune response. The autoantibodies are directed to masticatory myosin binding protein-C (mMyBP-C). The serological test detects the autoantibody.
Clostridial myositis
very important in ruminants especially, but also in any animal that receives an intramuscular injection. Clostridium chauvoei, the cause of blackleg, is particularly interesting as the spores are disseminated to muscle following ingestion, and will sporulate when exposed to an anaerobic environment (bruising, trauma, injection) to form bacteria that release exotoxins that cause necrosis.
Atrophy of cachexia, malnutrition or senility
similar to other forms of atrophy, but usually spares the postural muscles.
How is muscle necrosis identified at necropsy?
The muscle is pale, soft and exudative (PSE of pigs), has white streaks (indicating mineralization) or is red and dry.
Order of injury with ischemia (decreasing order)
- Myofibre
- Satellite cell
- Fibrocyte
(Decreasing order)
Name some common agents of bacterial myositis
Streptococcus equi in horses, Arcanobacterium pyogenes in cattle, Corynebacterium pseudotuberculosis (CLA) in sheep, Streptococcus canis (necrotizing fasciitis) in dogs, Actinobacillosis (wooden tongue, lumpy jaw) in cattle are but a few of the more common.
Trichinella spiralis
a nematode with intramuscular larvae that can cause a verminous myositis.
Name the two primary neoplasms of muscle
Rhabdomyoma Rhabdomyosarcoma (agressive)
Lamellar bone
Type of bone where collagen is arranged in sheets; more compact
Trabecular bone
Spongy or cancellous bone, arranged in a matrix.
Haversian systems
Also known as osteons. Lamellar bone that is arranged in concentric layers.
Woven bone/reactive bone
Bone that is formed in a haphazard manner with the collagen fibrils interlaced
Where do osteocytes come from?
They were initially osteoblasts. Osteoblasts are cool worker cells with tools (stored in their matrix vesicles). They can make things with their mineral, ATP & Alkaline phosphotase. When they grow up they live in their lacunae, become osteocytes and are surrounded by bone matrix. They hang out with osteoblasts. Osteoblasts respond to the parathyroid hormone by increasing the calcium pump activity & stimulate osteoclasts.
Where do osteoclasts come from?
They are different than osteoblasts or osteocytes. They were once monocytes and have a brush border at the contact site with bone. They clean up things by sucking up hydrogen ions and eating collagen with proteases. They are like a dog eating leftovers on the floor.
Howship’s lacunae
This is a concavity formed in the bone by osteoclasts
What stimulates/inhibits osteoclasts?
Stimulates: Parathyroid hormone, cytokines (IL-1, IL-6, TNF, PG)
Inhibits: Calcitonin
Periosteum
Covers bone. It is a membrane of outer fibrous tissue with inner osteogenic layer. Over the physis it is called the perichondrial ring & produces cartilage. It is rich in nerves
What happens with a fracture
- Periosteum is disrupted, blood supply is interrupted, soft tissue damage & necrosis of bone
- Periosteum will react to form new bone along the surface (primary callus) if it has enough blood. Not enough blood supply? Will form cartilage. This first bone will be woven bone & be disorganized
- Secondary callus forms with laminar bone. This will improve with compression, adequate blood supply & stabilization
Exostosis
localized area of periosteal new bone formation as a response to periosteal trauma
What can cause a growth arrest line?
BVDV, malnutrition, canine distemper, lead poisoning -> this alter/stop endochondrial ossification
Chondrodysplastic breeds
Basset, Dachshund, Corgi, bull dogs: genetic generalized defective endochondral ossification
Osteopetrosis
Failure of osteoclasts to clean things up & the medulla fills with trabecular bone.
Osteogenesis imperfecta
Genetic disease where osteoblasts can’t produce type 1 collagen, so in the cortex there is a lack of bone due to the deficient secondary spongiosa (I assume there is enough collagen to form the primary spontiosa)
Congenital hyperostosis of pigs/Craniomandibular osteopathy of dogs
For some reason in the radius of pigs and the mandible/maxilla/occipital/temporal bones of dogs, they can get a huge periosteal reaction and subsequent new bone formation.
Name the 4 main metabolic bone diseases
Osteoporosis: old/soft -> hormones
Rickets: young/soft -> vitamin D
Osteomalacia: old/soft -> vitamin D or calcium
Osteodystrophy: defective bone -> metabolic - phosphorus/clacium
Rickets
Same as osteomalacia in mature What: Bone fails to mineralize/soft Why: Low vitamin D or phosphorus How: Growth plate enlarges sue to no formation of primary trabeculae, but osteoid is still forming. Who: Young (osteomalacia - old)
Osteoporosis
What: Bone is lost, but rest of bone is normal
Why: Disuse, old, starvation/malnutrition, possibly low Ca
How: Bone is lost
Who: Older animals
Osteodystrophy
What: Too much parathyroid hormone, osteoclasts go nuts
Why: Calcium deficiency/phosphorus excess
How: Meat only diets fed, osteoclasts start to resorb bone & leave fibrous tissue; can also happen due to renal fibrous osteodystrophy
Who: any age
Dystrophic growth of the bone. It is defective bone development that is usually attributable to renal disease or to disturbances in calcium and phosphorus metabolism.
Necrosis of bone - how does this appear grossly
Dead bone is dry, white or demarcated from other bone by a red border
Osteomyelitis
inflammation of bone or bone marrow, usually due to infection.
Legg- Perthes disease
Toy breed dogs (often) will lose blood supply to their femoral heads. These will necroses, become a sequestrum. and eventually be taken away/collapse and remodelled.
What is osteomyelitis?
Inflammation of the bone. (Diskospondylitis in the spine). It’s caused be bacteria being blood borne and creating a inflammatory reaction next to bone and an acidic environment once it becomes supprative. Thromobosis & necrosis of the bone makes this all worse. New bone tries to stabilize things, but it’s not a good environment for it, so it might get worse.
What are bacteria that commonly cause osteomyelitis?
Truperella pyogenes (Arcanobacterium) - pigs/cows
Streptococcus zooepidemicus/Salmonella - horses
Unusual in dogs & cats. (blastomyces or coccidioides)
More likely in the young.
Lumpy jaw is caused by
Arctinomyces bovis
Inflammatory conditions in dogs
Hypertrophic osteodystrophy (HOD) - inflammatory lesion of the metaphysics in young usually large breed dogs adjacent to the physis Panosteitis: young growing dogs, periosteal/endosteal new bone formation associated with bone pain -> self limiting
Name some things that stimulate exostoses (periosteal new bone formation)
- Trauma
- Primary/secondary bone neoplasia
- Osteomyelitis
- Degenerative Joint disease
- Bioposies
(others as well)
Hypertrophic osteopathy (HO)
Periosteal new bony formation around the distal bones due to central issues (e.g. pulmonary neopalsia, heart worm etc)
Osteochondroma
Usually an indicental finding where a exostoses forms with a cartilaginous cap near the physis. May change to be neoplastic. Can be virally associated in cats.
Fibrous dysplasia
Incidental finding (usuallly in the bones of young animals where there are radiolucent areas that are filled with fibrous tissue and woven new bone.
Bone cysts - 3 types
Subchondral
Simple
Aneurysmal
Subchondral bone cysts
Adjacent to joints affected with DJD or osteochondrosis
DJD vs. Osteochondrosis
DJD - herniation of joint fluid into articular cartilage excavating the bone
Osteochondrosis - no bone, but excess cartilage dies
Simple bone systs
INcidental findings, clear or serosanguinous fluid & fibrous tissue lining. Can continue to expand & cause local defomity
Aneurysmal bone cysts
Develop in areas of infarction, ateriovenous shunt, haemorrhage or other vascular anomaly. Bone cysts must be differentiated from cystic cavities with neoplasms
Bone neoplasms
Most common in dogs: osteosarcoma (poor prognosis, locally aggressive)
Others: ossifying fibroma, fibrosarcoma, chondroma, chondrosarcoma, osteoma and osteosarcoma.
Most common secondary neoplasm of bone
transitional cell carcinoma
Important components of a joint
articular cartilage, subchondral bone and joint capsule.
Articular cartilage is composed of what?
Water, a gell that contains chondrocytes, type II collagen fibres & proteoglycans
