Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVSOH 4 > Musculoskeletal Pathology > Flashcards

Musculoskeletal Pathology Flashcards

1
Q

Define bone malformations.

A

Primary structural defects due to localised errors in embryo development. Teratogens, genetic causes, in utero events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define bone deformities.

A

Alterations in shape or structure that was previously normally formed. Growth plates are most vulnerable sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the causes of bone deformities?

A

Infections (CDV, BVDV), toxins (Pb, vitamin A), undernutrition

Schmallenberg and blue tongue virus arrest foetal development at 50 days when spinal column and mandible are forming

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is chondroplasia?

A
  • Disorder of bone growth due to primary defect in formation of cartilage
  • Affects bones formed by endochondral ossification in cattle, dogs, sheep, cats and pigs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the aetiology of chondroplasia?

A
  • Often unknown ILO 1
  • Genetic defect (chondrogenesis) – breed selection
  • Secondary condition (lysosomal storage disease) – rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Distinguish generalised and localised chondroplasia.

A

Generalised – affect the whole skeleton, proportionate dwarfism, such as form hypopituitarism

Localised – restricted to certain bones, disproportionate dwarfism. Brachycephalic dogs and dachshunds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do angular limb deformities develop?

A
  • Forelimbs of fast-growing large breed dogs
  • Partial or complete premature closure of the growth plates – one part f the bone will grow while the other stops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a common site for angular limb deformities?

A
  • Distal ulnar physis is a common site
  • Ulna shorter than radius, casing radius bows dorsally decreasing carpus valgus and carpal laxity, as well as carpal and elbow subluxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define osteochondrosis.

A

Focal disturbance of endochondral ossification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens in physeal osteochondrosis?

A
  • Hypertrophic cartilage layer of growth plate
  • Hypertrophic chondrocytes remain viable
  • Well-demarcated wedge of retained cartilage in the physis (black arrows)
  • Sequalae if extensive growth plate involvement causing fracture and angular limb deformities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is septic ischaemic necrosis of bone?

A

Disrupts vascular supply to periosteum and/or trabecular bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of aseptic ischaemic necrosis of bone?

A
  • Trauma – vascular damage following fracture
  • Infiltrating neoplasm
  • Thromboembolism
  • Avascular necrosis of femoral head – Legg-Calvé-Perthes disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Legg-Calve-Perthes disease?

A

Femoral head bone replaced by fibrous tissue, femoral head collapse. Original insult is already gone by the time you see this in clinic so do not know why it happens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is osteopenia/osteoporosis?

A
  • Metabolic disease
  • Localised or generalised decreased of bone density and/or mineralisation
  • Cortical bone and trabeculae affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name the 3 mechanisms of osteopenia/osteoporosis.

A

Reduced bone matrix formation

Increase in bone resorption – fibrous osteodystrophy

Deficient mineralisation – rickets in growing animals and osteomalacia in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does osteoporosis occur by reduced bone matrix?

A
  • Generalised – protein and vitamin deficiencies and senile states
  • Immobilisation/reduced physical activity
  • Localised – poor irrigation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does osteoporosis occur from increased bone resorption?

A

Primary - parathyroid neoplasia

Secondary hyperparathyroidism:
- Nutritional – increased phosphorous, decreased calcium diet causing an increase in PTH
- Renal (chronic renal failure) – common especially in dogs
- Excess glucocorticoids – reduces Ca absorption in GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does osteoporosis occur from rickets/osteomalacia?

A
  • Vitamin D deficiency
  • Phosphorus deficiency
  • Imbalanced calcium: phosphorus ratio
  • Subsequent bone deformities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which species is osteoporosis due to deficient mineralisation common in?

A

Crested geckos with insufficient UV light have vitamin D deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is hyperplastic osteopathy?

A
  • Progressive, bilateral, periosteal new bone formation
  • Diaphysis and metaphysis of the abaxial aspects of 2nd and 5th metacarpals and/or metatarsals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is hyperplastic osteopathy secondary to?

A

A space-occupying lesion – intrathoracic tumours (paraneoplastic syndrome), inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the current theory of how hypertrophic osteopathy occurs?

A
  • Reflex vasomotor changes mediated by the vagus nerve
  • Increased blood flow to the extremities
  • Proliferation of connective tissue and periosteum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the routes causing bone inflammation?

A

Haematogenous - bacterial infections, vertebrae and metaphysis of long bones

Direct introduction – compound fracture/surgery

Direct extension – surrounding tissues e.g. tooth, joint infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the aetiology of acute septic periostitis?

A

Bacterial aetiology, formation of subperiosteal abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Distinguish fibrous and ossifying chronic periostitis.

A

Fibrous – thickening in the form of a tightly adhering fibrous plate

Ossifying – formation of new bone tissue
- Exostosis – regular contour and surface masses
- Osteophytes – irregular reliefs, spikes or ridges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the aetiology of osteomyelitis?

A
  • Bacterial aetiology
  • After open fractures or surgical interventions
  • Haematogenous spread
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Distinguish acute and chronic osteomyelitis.

A

Acute – origin in the bone marrow itself or in the bone tissue. Initial exudate > purulent > compression of the bone tissue > very painful

Chronic – progressive osteolysis, subperiosteal neoformation. Lumpy jaw, actinomyces bovis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Name the tumours that originate in bone cells.

A

Osteosarcoma/osteomas
Chondromas/chondrosarcomas
Fibromas/fibrosarcoma
Liposarcomas
Giant cell tumours
Haemangiomas/haemangiosarcomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Name the tumours that originate in bone marrow.

A

Lymphoma/leukaemia
Plasma cell myelomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the characteristics of osteosarcomas?

A
  • Association with infarction, fractures, and orthopaedic metallic implants
  • Tumour grows quickly, very invasive locally and painful
  • Early hematogenous metastasis is common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the common sites for osteosarcomas?

A

Proximal humerus
Distal radius
Femur
Distal ulna
Proximal tibia
Ribs
Vertebrae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is normal joint structure?

A

Even joint cartilaginous surface, bone/periosteum, synovial membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the response of joints to injury?

A
  1. Inflammatory cells, death of chondrocytes, synovial lining cells
  2. Activation of matrix metalloproteinases (MMPs) and lysosomal enzymes neutral proteases
  3. Degradation of matrix
34
Q

What is the consequence of joint cartilage having no perichondrium?

A

This limits nutrition/oxygenation supply and regenerative ability and can only receive from synovial fluid or vasculature so must work by diffusion which is a slow process that is easy to interrupt and means healing is slow too

35
Q

Why do you not feel pain in joint disease until quite far along?

A

There is no nerve tissue here so don’t feel damage for a long time, only when you get exposure of the subchondral bone does it hurt

36
Q

How is nutrition ensured in joint cartilages?

A

Ensured by the pumping promoted by the compression and decompression of the cartilage during movement

37
Q

How does joint pain develop?

A

Insult or reduced lubrication in the joint > fibres separate apart > become frilly in fibrillation > wear down even more > exposure of subchondral bone > pain

38
Q

What happens to the periosteum when you get a lot of inflammation in the joint?

A

Periosteum around the joint edges will form osteophytes

39
Q

How does chronic inflammation form as a response to injury in a joint?

A
  • Hypertrophy of synovial villus
  • Formation of fibrovascular tissue rich in macrophages originating from synovial membranes called a pannus
  • Degrades cartilage
40
Q

What 3 things are affected when there is degenerative joint disease?

A

Periosteum – new bone growth and osteophyte formation

Synovium – villous hypertrophy, hyperplasia, inflammation and pannus formation

Cartilage – erosion and fibrillation

41
Q

Describe the pathology of non-suppurative arthritis.

A
  • Non-suppurative arthritis means there is no pus in the joint, just inflammation and maybe fluid.
  • Viral or repetitive trauma will cause this. you get deposition of fibrin with the synovium and articular cartilage.
  • Hopefully this will resolve, the stimulus will clear away/viral infection cleared away and inflammation is resolved.
  • But if its carries on, we will get infiltrates of immune cells – lymphoplasmacytic synovitis and fibrous tissue causing pannus formation.
  • Pannus formation impeaches onto the joint surface which means you start to have more stimulus for inflammation.
  • This leads to further destruction of cartilage and possible infection of subchondral bone if infectious.
42
Q

Describe the pathology of suppurative arthritis.

A

Typically seen in farm animals and is bacterial in nature. Get infiltration of the joint by neutrophils responding to the bacteria. Ideally, this resolves from this. If not, neutrophils release lysosomal enzymes that break down indiscriminately, which may extend to periarticular structures. The result is the same, causing destruction of cartilage, regardless of infectious agent or non-infectious agent.

43
Q

What are the routes of infectious of joints?

A
  • Haematogenous spread
  • Spread from osteomyelitis
  • Spread from soft tissue
  • Diagnostic or therapeutic procedures
  • Penetrating damage
44
Q

What is canine immune mediated polyarthritis?

A
  • Inflammatory but sterile
  • Deposition of immune complexes in joints
45
Q

What is the pathogenesis of canine immune mediated polyarthritis?

A

Cell mediated response > rheumatoid factor (IgG) > immune complexes form in joints > activation of innate immune defences > inflammation > pammus formation, synovitis, erosion of cartilage and fibrillation

46
Q

What is osteochondrosis?

A
  • Abnormalities in growth cartilage of joint
  • Vascular disruption, genetic, nutritional, trauma, biomechanical, anatomical factors
  • Initial lesional usually unknown but involves (focal) failure of endochondrial ossification
47
Q

What is osteochondrosis dissecans?

A

Progression of osteochondrosis resulting in fracture of fragments into the joint

48
Q

What is the pathogenesis of osteochondrosis dissecans?

A
  • Ischaemic necrosis in AE cartilage (vascular disturbance means bone stops growing properly and you get a wedge underneath the cartilaginous surface)
  • Failure/delay in ossification and focal weakness in subchondral bone
  • Fissure forms through articular cartilage which causes a fault line in the cartilage
  • Fissure grows and cartilage flap detaches
49
Q

Distinguish modelling and remodelling.

A

Modelling – change of shape and contour of a bone in response to normal growth, mechanical use, disease

Remodelling – constant resorption of old bone and replacement by now (normal turnover). Allows repair of micro-fractures and relatively constant result but gradual loss of bone mass with age

50
Q

What is the bone response to trauma regardless of cause?

A
  1. Haemorrhage
  2. Necrosis initially
  3. Resorption of damaged/dead tissue by osteoclasts
  4. Regeneration of new matrix produced by new osteoblasts
51
Q

What is the pathogenesis of fracture repair?

A
  1. Fracture
  2. Blood clot formation
  3. Clot infiltrated by fibroblasts which try to stabilise the fracture so that healing can occur (if not stabilised, healing will be delayed and we will have issues)
  4. Primary callus formation that is predominantly made up of cartilage and have lots of osteoplastic activity
  5. Secondary callus over a few months
  6. Will always have a lump over where bone has fractured
52
Q

What is the aetiology of fractures?

A

Trauma by excessive force
Abnormal bone, minimal trauma, normal use
Abnormal composition (nutritional/metabolic disease)
Inflammation
Neoplasia

53
Q

What are the complications of fracture repair caused by?

A
  • Insufficient oxygen supply
  • Instability – callus formation will not be proper and will get lots of fibrous tissue or a misaligned diaphysis or poor congruence in joints
  • Infection
  • Poor nutrition
  • Necrotic bone
  • Unsuccessful fixation
  • Underlying pathological condition
54
Q

What is sequestrum?

A

Fracture at growth plates and large amounts of bone that fail to be resorbed which must be surgically removed

55
Q

What is the muscle response to injury?

A
  1. Fibre swelling, eosinophilia, loss of striations
  2. Fragmentation – coagulative necrosis, calcification
  3. Macrophages infiltrate and clear debris
  4. Satellite cell hypertrophy and migration – they are there to repair muscle
  5. Satellite cells (muscle stem cells) become myoblasts
  6. Myoblasts fuse to form myotube
  7. Plasmalemma reforms
  8. Nuclei return to periphery (myofibre)
  9. Cross-striations reappear
56
Q

What is the myofibre response to injury?

A

Severe damage > necrosis > fibrosis as healing process was not possible

With plasmalemma damage, enzymes leak out – creatine kinase (CK), aspartate aminotransferase (AST)

57
Q

What are the adaptations to injury of muscle?

A
  • Atrophy – denervation, disuse, malnutrition, cachexia, senility
  • Hypertrophy – response to demand
  • Irreversible damage – necrosis and fibrosis
58
Q

What is disuse atrophy?

A
  • Lameness, immobilisation or recumbency
  • Muscles not subjected to repeated tension
  • Rapid decrease in size of muscle
59
Q

What is metabolic disorder atrophy?

A
  • Malnutrition, cachexia, senility
  • Wasting diseases (parasitism, neoplasia)
  • Muscle catabolism – reserves nutrients for vital organs
  • Neoplasia – circulating cytokines
60
Q

How might endocrinopathies cause atrophy?

A
  • Hypercortisolism (endogenous/exogenous) – exogenous glucocorticoids break down glucose and when they run out of glucose will break down muscle
  • Hypothyroidism
61
Q

What are the clinical signs of generalised muscle atrophy?

A

Weakness
Distended abdomen (muscle can no longer hold it up)
Megaoesophagus

62
Q

What is denervation atrophy?

A
  • Rapid atrophy – all myofibers innervated by damaged nerve
  • Myofibers shrink leaving nuclei
63
Q

What is x-linked muscle dystrophy?

A
  • Lack of dystrophin (protein that strengthen muscle fibres)
  • Causes repeated bouts of myonecrosis and fibrosis
64
Q

What is the effect of x-linked muscle dystrophy?

A
  • Female carriers cause second X compensates
  • Males – stiffness, exercise intolerance, difficulty swallowing
  • Also affects heart muscles
65
Q

What is myotonia?

A
  • Fainting goats
  • Inherited Cl-ion channel defect
  • Continued contracture of muscle after neural stimulus has ended
  • Stiff gait and muscle spasms
66
Q

What are the causes of vascular disorders causing ischaemia of muscles?

A
  • Occlusion of large vessels (infarction)
  • Compression
  • Swelling of muscle within a nonexpendable compartment - compartment syndrome
67
Q

What are the causes of ischaemic occlusion of blood vessels for muscles?

A
  • Various capillary anastomoses and collateral circulation
  • Feline aortic thromboembolism of iliac trifurcation in the cat
  • Vasculitis
  • Angiostrongylus, dirofilarial
68
Q

When can compression cause ischaemia for muscles?

A
  • ‘Downer cow’, post-anaesthetic myopathy in horses
  • External pressure on capillaries > increased perfusion pressure
69
Q

What is systemic inflammatory response syndrome?

A

If left on one side for prolonged period of time, you can get a release of toxic metabolic breakdown production causing systemic inflammatory response syndrome – which if in high enough concentration and reaches the heart, can cause the heart to stop

70
Q

What is ischaemic compartment syndrome?

A
  • Swelling of vigorously exercised muscle in non-expandable compartment – muscles surrounded by fascia and/or bone
  • Increased intramuscular pressure causes vascular occlusion
  • Supracoracoideus muscles of turkeys, chickens
71
Q

What is white muscle disease?

A

Selenium and vitamin E deficiency cause oxidative injury to myofibres
With myocardial involvement causes cardiac failure and death

72
Q

What is exertional myopathy?

A
  • Acute myonecrosis initiated by considerable exertion
  • Myoglobinuria hit the kidneys causes acute renal failure = brown urine
73
Q

What is the aetiology of bacterial myositis?

A
  • Direct penetration – dirty needles
  • Haematogenous spread
  • Extension of nearby infection
74
Q

What is masticatory muscle/eosinophilic myositis?

A
  • Production of antibodies to type 2M myosin-unique to masticatory muscles
  • Acute – swelling and pain
  • Chronic – muscle atrophy
75
Q

Describe the histology of immune mediated myositis?

A

Pink = protein, purple = nuclei. Inflammatory cells are starting to infiltrate and separate these muscle fibres apart. Cause fibrous tissue formation and necrosis of the muscle.

76
Q

What is the aetiology of tetanus causing spastic paralysis?

A
  • Bacterial – clostridium tetani
  • Tetanospasmin
77
Q

What is the pathogenesis of tetanus causing spastic paralysis?

A

Growth of pores in anaerobic wounds > tetanospasmin enters the bloodstream, and targets nervous system > stops release of inhibitory neurotransmitters GABA

78
Q

What is the aetiology of botulism causing flaccid paralysis?

A
  • Bacterial – clostridium botulinum
  • Botulism exotoxin
79
Q

What is the pathogenesis of botulism causing flaccid paralysis?

A

Ingestion of exotoxin (e.g. in feed) and growth of spores within GIT (shaker foals) or wound infection (rare) > toxin enters the bloodstream and targets the nervous system > prevents Ach release from presynaptic vesicles

80
Q

What is myasthenia gravis?

A

Anti acetylcholine receptor IgG antibodies

Associated with thymoma or thymic hyperplasia – poor T cell regulation

81
Q

What are the clinical signs of myasthenia gravis?

A

Muscle weakness
Megaoesophagus

CVSOH 4 (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions