Musculoskeletal 5 Flashcards
What are the four ways muscle injury can result?
Due to:
- Denervation - loss of connection with peripheral nerve - loss ofboth Type I/II
- Disuse - lack of muscle activity - typically loose type II
- Malnutrition/Cachexia/Starvation - protein catabolism + loss of fibres
- Endocrine disturbance - loss/excessive influence from hormonal activity
What is required for regeneration to be able to occur?
- Regeneration requires presence of basal lamina + satellite cells - myocytes themselves cannot regeneration
What does fibrosis in the muscle occur?
Occurs when basal lamina has been destroyed. It can follow an non-fatal injury + may be associated with atrophy
When does mineralisation occur?
Associated with:
- Necrosis
- Primary myopathies
- Vitamin D toxicity
Name the two different myopathies below and describe the difference between them:
Polyphasic - a combination of multiple different myopathies - indicative of ongogin injury
Monophasic myopathy - only one stage so more likely to be indicative of a single insult
What are the four main clinical signs that are observed due to muscle disease?
- Lameness
- Recumbancy
- Excercise intolerance
- Renal signs - myoglobinuria (acute Rhabdomyolysis - can present just with renal signs)
What is the name of the condition that is shown below?
Exertional Rhabdomyolysis - myofiber damage caused by primary excercise stress
What are the symptoms of capture rhabdomyolysis and what is the cause?
Clinical signs: Animals exhibit dyspnea, weakness, muscle tremors, muscle rigidity, hyperthermia
Cause: Increased circulating catecholamines due to stress
What is the suspected cause of canine exertional rhabdomyolysis?
Possibly associated with underlying dietary deficiencies - Vit E/Sel, Ca:P imbalance
What would be the effect of a defect in the production of myostatin?
Excessive uncontrolled muscle proliferation
What would be the effect of a defect in the production of dystrophin?
Lack of dystrophin would cause decreased building of muscle mass
What is the pathogenesis of malignant hyperthermia and what other clinical signs may be seen (other than that shown below)?
- Defect in Ca++ channel (ryanodine receptor - RYR 1) - caused by stress, halothane, depoalarising muscle relaxant
- Ca++ channels remain open - prolonged myofiber contraction + muscle rigidity
- Hyperthermia + acute myonecrosis result in acute myonecrosis
Maliganant hyperthermia:
- Tachycardia
- Dyspnea
- Metabolic acidosis
What is the effect of hypothyroidism?
- Myofiber atrophy - associated with alterations in carbohydrate metabolism + energy loss from glycolysis + glycogenolysis - peripheral neuropathy w/axonal degeneration leading to denervation atrophy of type 1 and 2 fibres
How does hyperthyroidisim lead to muscle atrophy?
Increased catabolic state leads to negative energy balance
How does hyperadrenocorticism result in myofiber atrophy?
Increased catabolism + inherited synthesis of muscle proteins