MSK Pathology 2

Question 1

Bone responses to trauma…
1. modelling.
2. remodelling.

Answer 1

1. change of shape and contour of a bone in response to normal growth, mechanical use, disease.
2. constant resorption of old bone and replacement by new (i.e. normal turnover).
   - allows repair of micro-fractures.
   - relatively constant result
   – gradual loss of bone mass with age.

Question 2

Series of events in bine following trauma.

Answer 2

Haemorrhage.
Necrosis - initially.
Resorption - of damages/dead tissue by osteoclasts.
Regeneration - new matrix produced by new osteoblasts.

Question 3

Fracture - repair.

Answer 3

Blood clot in fracture site.
Infiltration of fracture site by collagen and fibroblasts to stabilise the fracture site and allow healing.
Primary callus forms in weeks.
- predominantly made up of cartilage with lots of osteoclastic activity.
Secondary callus forms in months.

Question 4

Fracture aetiology.

Answer 4

Traumatic:
- normal bine, excessive force.
Pathological:
- abnormal bone, minimal trauma, normal use.
- abnormal composition (nutritional/metabolic disease).
- inflammation.
- neoplasia.
- osteomyelitis.

Question 5

What are complications of fracture repair caused by?

Answer 5

Insufficient O2 supply.
Instability.
Infection.
Poor nutrition.
Necrotic bone.
Unsuccessful fixation.
Underlying pathological condition.
Sequestrum.

Question 6

Types of fracture?

Answer 6

Simple.
Comminuted.
Open or compound.

Question 7

Muscle response to injury and healing.

Answer 7

Fibre swelling, eosinophilia, loss of striations.
> Fragmentation (coagulative necrosis, calcification).
> Macrophages infiltrate and clear debris.
Satellite cell hypertrophy and migration from periphery.
> satellite cells align down segment of damaged muscle, fuse together and form myotube after transforming to myoblasts.
> Myotube allows plasmalemma to reform.
> Nuclei return to periphery (myofibre).
> Cross-striations reappear and new muscle is formed.

Question 8

Myofibre responses to healing.

Answer 8

Depends on extent of damage.
Severe - necrosis and then fibrosis.
Plasmalemma damage causes enzymes to leak out:
- creatine kinase (CK), aspartate aminotransferase (AST).
Extent and phase can indicate type of cause.

Question 9

Muscle response to injury - adaptation.

Answer 9

Hypertrophy - response to demand.
Atrophy - denervation, disuse, malnutrition, cachexia, senility.

Question 10

Disuse atrophy.

Answer 10

Lameness, immobilisation or recumbency.
Muscles not subjected to repeated tension.
Rapid decrease in size of muscle.

Question 11

Metabolic disorders.

Answer 11

Malnutrition, cachexia, senility.
Wasting diseases (parasitism, neoplasm).
Muscle catabolism - reserves nutrients for vital organs.
Neoplasia - circulating cytokines e.g. TNF.

Question 12

Muscle atrophy - endocrinopathy.

Answer 12

Direct or secondary (via neuropathy).
Hypercortisolism (endogenous / exogenous).
Hypothyroidism.
If muscle atrophy generalised, get weakness, distended abdomen, megaoesophagus.

Question 13

Denervation atrophy.

Answer 13

Muscle not innervated in the first place, so cannot be used so atrophy.
Not as common.

Question 14

“Double Muscling”.

Answer 14

Congenital.
Muscular hyperplasia.
Increased amounts of normal sized muscle fibres (hyperplasia).
Myostatin gene defect - normally limits skeletal muscle growth.
Beef cattle - esp. Belgian blue.
– Dystocia!

Question 15

X-linked Muscle Dystrophy (Duchenne type).

Answer 15

Congenital.
Lack of dystrophin (protein that strengthens the muscle fibres).
- repeated bouts of myonecrosis, leading to fibrosis.
Golden and Labrador retriever, Irish terrier, Rottweiler.
Female carriers - second X chromosome compensates.
Males - stiffness, exercise intolerance, difficulty swallowing.
Also affects heart muscles.
Px fairly poor.

Question 16

Myotonia.

Answer 16

Congenital.
“Fainting goats”.
Inherited Cl- ion channel defect.
Continues contracture of muscle after neutral stimulus has ended.
Stiff gait and muscle spasms.
“Sawhorse stance”.
“Fainting” (10-20 sec).

Question 17

1. Ischaemia affecting the muscle.
2. Cell sensitivity to ischaemia from most to least.

Answer 17

1. Vascular disorder.
   Muscles highly vascularised.
   Results from occlusion of major arteries or widespread vascular damage.
   Caused by:
   - occlusion of large vessels (infarction).
   – e.g. FATE, vasculitis, heartworm.
   - compression.
   – e.g. ‘Downer cow’, post-anaesthetic myopathy in horses.
   - swelling of muscle w/in a non-expandable compartment (“Compartment Syndrome”).
2. Type 1 Myofibres (oxidative).
   Type 2 myofibres (glycolytic/mixed).
   Satellite cells.
   Fibroblasts.

Question 18

Why should you turn a large recumbent animal regularly?

Answer 18

If been recumbent too long then moved, can get a sudden release of metabolic toxic product and breakdown products, causing Systemic Inflammatory Response Syndrome.
If toxins make way to the heart at high enough conc., the heart can stop.

Question 19

Compartment syndrome.

Answer 19

Swelling of vigorously exercised muscle in a non-expandable compartment.
- muscles surrounded by fascia and bone.
Increased IM pressure so vascular occlusion.
Supracoracoideus muscles of turkeys, chickens = Green Muscle Disease.

Question 20

White Muscle Disease.

Answer 20

Deficiency in antioxidants - selenium +/or vit E.
- oxidative injury to myofibres.
– necrosis and mineralisation.
Common.
Cattle, horses, sheep, goats.
Neonatal animals from selenium-deficient mothers.
Muscles w/ yellowish-white to chalk-white streaks.
With myocardial involvement
- cardiac failure leading to death.

Question 21

Exertional myopathy.

Answer 21

Rhabdomyolysis.
Build up of lactic acid.
Acute myonecrosis initiated by considerable exertion.
Myoglobinuria causes acute renal failure.
Horses - “tying up”/exertional myopathy.
Dogs - racing greyhounds and sled dogs.
Wild/exotic animals following capture and/or immobilisation.

Question 22

Bacterial myositis.

Answer 22

Direct penetration - dirty needles.
Haematogenous spread.
Extension of nearby infection (cellulitis, osteomyelitis, arthritis).
Suppurative - pyogenic bacteria e.g. T. pyogenes.

Question 23

Bacterial myositis clostridia spp.

Answer 23

Anaerobic bacteria.
Toxins released by bacteria causes vascular damage and ischaemia in order to make an anaerobic environment in which they can thrive.
Clostridium chauvoei - ‘Blackleg’.
- mostly outdoor / beef cattle.
- drying necrosis.
- strange sweet smell.
Clostridium septicum - ‘Malignant oedema’.
- horses, ruminants.
- dirty needles!
- wet and exudative.
– build up under skin.

Question 24

Immune-mediated myositis.

Answer 24

Masticatory muscle myositis (Eosinophilic Myositis).
- dogs (golden retrievers, dobermans).
- production of antibodies to type 2M myosin – unique to masticatory muscles.
- acute (swelling and pain); chronic (muscle atrophy).
- irreversible damage.

Question 25

Tetanus.

Answer 25

Toxic myopathy.
Spastic paralysis.
Bacterial - clostridium tetani.
- Tetanospasmin – exotoxin.
–> exotoxin = toxin that is being produced by a bacteria and secreted into its environment for a reason
Horses most sensitive.
- also cattle, pigs, dogs, cats.
Growth of spores in anaerobic wounds leads to Tetanospasmin entering bloodstream and targeting NS, which stops the release of inhibitory NTs GABA.
Sawhorse stance.

Question 26

Botulism.

Answer 26

Toxic myopathy.
Flaccid paralysis.
Bacterial - Clostridium botulinum.
Botulinum - exotoxin.
Horses, cattle and birds.
Ingestion of exotoxin (e.g. in feed) leads to growth of spores within GIT (shaker foals), the toxin then enters the bloodstream and targetd NS, preventing ACh release from the presynaptic vesicles.

Question 27

Myasthenia Gravis.

Answer 27

Immune-mediated paralysis.
Flaccid paralysis.
Auto-immune disease - anti-acetylcholine receptor IgG antibodies.
Associated with thymoma or thymic hyperplasia - poor T-cell regulation.
– over-production of T-cells.
–> some escape.
—> escaped T-cells recognise Ach receptors.
—» activate B cells to produce immunoglobulins which bind onto ACh receptors.
—»> ACh can no longer bind to ACh receptors so unable to get transmission from the nerve to the muscle and don’t get activation of muscles.
Acquired - GSDs, Golden Retrievers.
Congenital (rare) - Lack of ACh receptors, JRT, Smooth Fox Terriers.
Clinical signs = muscle weakness and megaoesophagus.

Question 28

Muscle neoplasia.

Answer 28

Relatively uncommon.
Rhabdomyomas - benign.
– larynx, dog.
Rhabdomyosarcoma - sometime younger animals.
Associated tissues - fibrosarcoma, hemangiosarcoma, infiltrative lipomas.
Metastatic - less common than metastases to bone.