Musculoskeletal 4, 5 and Practical Flashcards

(55 cards)

1
Q

What is a joint?

What are the types of joints?

A

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

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2
Q

What makes up the synovium

A

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

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3
Q

Describe how

A
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4
Q

Describe how joints respond to mechanical forces

A
  • 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
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5
Q

Describe cartilage homeostasis?

A

Metalloproteinases breakdown aggrecans and collagen

Chondrocytes prevent this with tissue inhibitors of metalloproteinases

Inflammation and degenerated matric product causes an increase in metalloproteinases

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6
Q

How do joints change with age?

A

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
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7
Q

How does cartilage respond to injury?

A

Cracks lead to fibrillation where chondrocytes join to form lacunae

Ebumation follows- cartilage gone- bone against bone (dads knees)

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8
Q

How does the joint synovium respond to injury?

A

Hyperaemia/oedema/exudate

This leads to capsular fibrosis

villous hyperplasia

pannus formation- capsule of structure grows over articular cartilage

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9
Q

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?

A

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

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10
Q

What is the arrow pointing to?

A

Osteophytes

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11
Q

What types of haemorrhage can occur in joints?

What can cause a joint haemorrhage?

A

Intra-articular

Periarticular

  • Traumatic
  • Inflammatory
  • Toxic
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12
Q

What are distortion, luxation, subluxation and ankylosis?

A

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

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13
Q

What are some examples of congenital DJD?

What are the different causes of joint inflammation?

What neoplasia can affect joints?

A

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

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14
Q

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?

A

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

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15
Q

What dogs are affected by hip dysplasia?

What causes it?

Therefore how does it grossly appear?

A

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

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16
Q

What species are prone to patellar luxation?

What is the pathogenesis?

How does it grossly appear?

A

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]

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17
Q

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?

A

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

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18
Q

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

A

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

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19
Q

What is the technical name for wobblers syndrome?

What is the aetiology?
What is the pathology?

What does it do and cause?

A

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

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20
Q

What is arthritis?

What are the different types?

What is periarthritis?

A

Arthritis is inflammation of joints

Synovitis

Chondritis

Osteitis

Osteochondritis

Periarthritis- outer capsule adjacent tissue inflammation

Can be mono/polyarthritis

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21
Q

What agent can cause bacterial arthritis?

Describe the pathogenesis?

How does it grossly appear?

What is histology?

A

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

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22
Q

What agents cause mycoplasma arthritis in swine, goats, sheep, and cattle?

How does it grossly appear?

How does it appear histologically?

A

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

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23
Q

What agents can cause viral arthritis, in what species?

How does it appear grossly and histologically?

What are the associated conditions?

A

Aetiology- caprine arthritis encephalitis virus CAEV (goats), Marfia visna (sheep)

Gross- villous hypertrophic chronic non-suppurative arthritis

Histology- villous hypertrophy, mononuclear inflammation

Ac- pneumonia, mastitis, encephalomyelitis

24
Q

What causes rheumatoid arthritis?

What is pathogenesis?

Gross?

Histology?

Ac?

A

Aetiology- autoimmune- dogs/cats

Path- local activation of the complement cascade in response to immune complexes

Gross- polyarthritis, generalised. particularly involves tarsal, carpal and phalangeal joints. Oedema, instability, pannus formation and thickened brown capsule

Histology- hypertrophy and hyperplasia of synovial villi, lymphoplasmacytic inflammation, haemosiderophages and pannus

Ac- aseptic necrosis, arthosis

25
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
26
What breed of dogs are more commonly affected by histiocytic sarcoma? How does it appear grossly and histologically? Pathology?
Flat coat, golden and lab retrievers Gross- rapidly growing, locally aggressive, often in close proximity to a joint- originates from dendritic cells in the synovial membrane. Soft-tissue swellings close to major joints, nodular to diffuse synovial thickening with grey-pink tissue Hist- synovium and capsule infiltrated by malignant histiocytes which have large abundant eosinophilic cytoplasm, anisokaryosis with large irregular nucleoli, frequency mitotic figures and multinucleate cells Pathology- locally aggressive and frequently metastasise
27
How large can myocytes be? Label this diagram
28
In what order do these muscle connective tissue layers go? Epimysium Endomysium Perimysium
Endomysium- outer most Periphysium- middle the diddle Epimysium- inner most
29
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
30
Describe muscle response to injury
Segmental necrosis- regeneration * Damage occurs- if only affecting muscle cells and not basal lamina * Macrophages enter and remove necrotic debris * Satellite cells enter and differentiate into myotube- elongate * They proliferate and replace and restore muscle fibre * Basal lamina keeps myotube in the correct structure If basal lamina is damaged- the structure of satellite cell cannot be maintained leading to more fibrosis and even adipose tissue or mineralisation
31
What can cause muscle atrophy? Describe the pathology of muscle atrophy How does it appear histologically? What are the associated conditions?
Lack of use, cachexia, aging, endocrine disorders, denervation Pathology- lack of proper nervous/endocrine stimulation of myofiber, reduced nourishment Histology- reduction in the size of the myofibrils, chronically- substitution by fibrous tissue or fat Associated conditions- Cachexia- serous atrophy of fat Endocrine- skin conditions
32
What is congenital muscle hypertrophy? What species does it affect? Describe its gross appearance and histology? Why is it negative?
A congenital disorder that causes defects in the myostatin gene and causes a gross increase in muscle size Affects- Belgian blues and sheep Gross- increased muscle size- thighs, rumps, loin and shoulder Histology- increased number/size of normal fibres within affected muscle Was supposed to be better for consumption but it ain't tasty
33
What species does splay leg affect? What causes it? How does it appear histologically?
Pig Fail to sustain quadrupedal position- splay leg attitude Histology- reduced myofibre diameter with decreased myofibrils within muscle fibres and increased cytoplasmic glycogen
34
What species are affected by muscular dystrophy? Pathogenesis? Gross and histological appearance?
Dogs and cats- inherited X linked Pathology- defects in the gene coding for dystrophin- a sarcolemmal associated protein Gross- Dog- muscular atrophy, pale white streak in muscles Cat- muscular hypertrophy, particularly over the neck and shoulder, oesophagus and diaphragm Histology- Dogs- large dark fibres, necrotic fibres, regenerated fibres and mineralisation Cat- marked variation in fibre size with numerous hypertrophied fibres often with internalised nuclei polyphasic necrosis with mineralisation and minimal endomysial fibrosis
35
Describe the pathology of malignant hyperthermia? How do the muscles appear histologically and grossly?
Genetic- pigs Path- mutation in ryanodine receptor- dysregulation of excitation-contraction coupling. Characteristed by unregulated release of calcium from SR, leads to excessive myofiber contraction and causes a severe increase in body temp Gross- animals have pale, soft, wet and exudative muscles and develop rapid rigor mortis Histology- oedema and there may be multifocal monophasic injury with hypercontraction
36
How can myasthenia gravis be acquired or congenital? What are the associated conditions?
Acquired- circulating autoantibodies against skeletal muscle acetylcholine receptors which leads to a severe decrease in the number of functional receptors Congenital- born with defective NMJs- larger surface area and reduced acetylcholine receptor density Ac- thymoma, episodic collapse
37
What causes nutritional myopathy? Describe the pathogenesis How does it appear grossly and histologically? What are the associated conditions?
Selenium and vitamin E deficiency- calves, lambs, swine and foals Path- lack of antioxidant activity causes membrane damage and rhabdomyolysis Grossly- lesions are bilaterally symmetrical, there are multifocal white streaks parallel to the fibre direction with mineralisation of cardiac and skeletal muscle Histology- multifocal and polyphasic degeneration of the contractile components of muscle cell Ac- adipose tissue necrosis- yellow fat disease in horses
38
What are the other names for exertional myopathy in horses? Describe the pathology of the disease Histo Ac
Exertional myopathy- equine exertional rhabdomyolysis, Monday morning disease Path- aerobic production of ATP is not sufficient- production of ATP by anaerobic glycolysis, lactic acid as catabolite- toxic- membrane damage- rhabdomyolysis- myoglobin in blood- myoglobinuria Gross- occurs mainly in the gluteal, femoral and lumbar muscles Histology- selective necrosis of type II fibres with hyper-contraction Ac- haemoglobulinuria
39
What causes bacterial myositis? How does it occur? How does it appear?
Streptococcus zooepidemicus- horses Arcanopbacterium pyogenes- cattle, sheep Corynebacterium pseudotuberculosis- horses, sheep, goats Pasturella multocida- cats Traumatic or bacteriaemia Gross- suppurative lesions, abscesses
40
What is wooden tongue? What species does it affect? How does it appear grossly and histologically? What is the name for the disease in pigs and horses?
Wooden tongue is chronic pyogranulomatous fibrosing nodular myositis due to agent actinobacillus ligneresii in cattle Gross- fibrosing, granulomatous Histologically- central focus of radiating clubs of amorphous, eosinophilic material associated with bacteria and neutrophils Botryomycosis
41
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
42
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
43
What parasites can cause parasitic myostitis?
Neospora caninum- dog Toxoplasma gondii- dogs/cats Trichinella spiralis- pigs Sarcocystis spp- horses, cattle, sheep, goats, camelids, pigs Cysticercus spp- cattle, sheep, dogs, pigs
44
What causes eosinophilic myositis? How does it appear grossly and histologically?
Sarcocystis spp- bovine, ovine Gross- well-demarcated, green focal stripes or patches Histology- eosinophilic, myofiber hyper-contraction, necrosis and separation of endomyseal sheaths and perimyseal trabeculae, there may be fibrosis with lymphocytes, plasma cells and histiocytes
45
What is masticatory muscle myostitis? What species does it affect? What is the pathogenesis? Gross and histo?
Immune mediated myositis Dog Path- autoantibodies against myosin type M2- only present in masseter, temporal and pterygoid Gross- atrophy of mastication muscles Hist- Acute- eosinophilic myositis Chronic- fibrosis, multifocal lymphocytes
46
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
47
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
48
Look at the picture provided and identify: Mitotic figures Neoplastic cells Areas of haemorrhage Osteoid formation
49
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
50
51
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- 1. chronic kidney lesion, damage to glomerular filtration 2. Phosphorous retention- increase in PTH 3. Increase in osteoblasts activity with mineralised bone reabsorption and mesenchymal cells 4. Failure of differentiation into osteoblasts with the production of collagen 5. Lack of collagen reabsorption by osteoclasts
52
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
53
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
54
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
55
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