Muscle Pathology Flashcards
Since muscle is such a metabolically active tissue, when there is a problem, what are two things you need to consider?
Nutrition and toxins
What are some signs of muscle disease?
Atrophy, hypertrophy (response of a muscle tissue to outside stimulus), swelling/ oedema, weakness (nutrition, innervation, etc.), muscle spasm (calcium, neural muscular junction problem), abnormal gait (weakness or problem with innervation, may be changes in bone or tendon too), oesophageal dysfunction (a lot of species have skeletal muscle in oesophagus)
What is the best indicator of muscle damage from a blood test?
Serum Creatinine Kinase
Cachexia
Loss of muscle conditional from malnutrition or following cancer for example
With a traumatic wound to muscle, what are clinical considerations long term?
Keep joints moving, it will repair itself and regain function.
Major consideration with muscle direct injury?
Vascular injury and causing necrosis. Increasing pressure locally can close off blood vessels. If pressure exceed vascular or arterial pressure we can get necrosis. e.g. horse in lateral recumbency during surgery- weight on any muscles (or organs really)
Indirect injury to muscles?
Blood borne (pathogens, toxins, immune complexes), immune mediated damage
Physiological muscle dysfunction?
Excess tension or excess force it can rupture (i.e. wild animal in captivity), exercise induced damage, loss of innervation (i.e. trauma), anything that causes a loss of blood supply (= necrosis, you will lose muscle function), endocrine/ electrolyte imbalance (disrupting calcium you can get necrosis, e.g. malignant hyperthermia in pigs)
Genetic muscle dysfunction?
Usually structural- improper innervation, lack of function of neural muscular junction. Muscle doesn’t define how it functions until it get innervated
Nutritional/ Toxic effects on muscle?
Deficiency of selenium/ vitamin E (whiteness in muscle = necrosis), toxic plants, feed additives, toxins
a. Blood vessel
b. Perimysium
c. Epimysium
d. Fasicle
e. Endomysium
f. Muscle fiber (cell)
Swelling of muscle tissue inside the fascia, what happens?
Fascia puts pressure on the blood vessels, lose blood supply and ischaemia.
Where does the pain come from in a muscle injury?
Nervous problem. Even if it is muscular dystrophy, the pain is from the inflammation, not the muscle itself.
What are satellite cells and what is their function?
Stem cells that generate new tissue when muscle is injured. Very few satellite cells. Signals from macrophages cause them to come out of acquiesence.
Where is the nucleus for a skeletal fiber?
Nucleus is always on the periphery. If the nucleus is in the middle, it can be a marker of damaged muscle (possibly chronic, but either way the damage is happening now)
What are the different types of muscle fibres? Resistance to fatigue?
What stains dark in muscle fibers?
Which type of muscle fibers use what kind of fuel?
What are the relative size comparisons?
Lots of Mitochondria (so the most in slow twitch type I)
*low glycolytic capacity compared to fast twitch (especially type IIb)
* the white fibers do not have much mitochondria in them ( quite large compared to the ones with mitochondria)
Motor Unit
What is true regarding a fiber type and its innervation?
A motor nerve and all of the muscle fibers it innervates. Within one muscle there can be multiple motor units.
**Each muscle fiber in a muscle is only innervated by one nerve.
**All slow oxidative fiber types are only innervated by nerves which innervate slow oxidative fibers.
What are the two manifestations of atrophy?
Symmetric and Unilateral
Why does a muscle atrophy?
Lack of trophic support coming from the nerve (growth factors, for example). Not about loss of neural musclar junction and electrical activity. Depending on the typer of innervation the pattern of atrophy is unique.
What are the differential effects of atrophy; fibre types?
As you get older, what type fibres do you lose first?
Type 2 fibres- think of elderly, can’t catch themselves when they trip up because they have lose their fast fibers.
What is this?
Atrophic fibre surrounded by normal fibres.
What are you looking at here?
Large group of atrophy, generalized. Increased concentration of nuclei (haven’t increased the number, just the density)
What happens when we lose innervation?
- Atrophy of fibres because we’ve lost trophic support
- Another motor neuron sprouts and attaches– if they are different type fibers– then the fibers can convert to the motor neuron
Hypertrophy- compensatory in response to loss of functional fibres (increased load on the remainder)
Alterations in normal metabolic processes
What is a neuromuscular junction?
Motor neuron meets the individual muscle fibre. Not physical, just very close. Should only see one NMJ per muscle fiber (multiple end buds of the nerve, but it is all one NMJ).
Necrosis (probably blood vessels cut off in this case)
Pale streaks
Mineralization, myofibre necrosis, or mineralization, infiltration by fat or collagen
Necrosis- internalized nuclei, pale staining areas.
Inflammation
Hyaline Degeneration happens first
Contraction of the muscle fiber (hypercontracts), do not have nice striations, it looks glassy (smooth and shiney)
Second: you get floccular degeneration
Lose muscle nuclei. Lost all of the structure of the skeletal muscle fibre.
In skeletal muscle damage, you can also see mineralization. Calcification. In this section, a lot of inflammation and mineralization. Once you get mineralization, you are losing function because you’ve disrupted the sarcomere.
Giant Cells (satellite cells in the context of skeletal muscle)- no scaffold to know where to regenerate. “Bags of cells”- disorganized. You still get muscle fibres but very disorganized and function is compromised.
Compartment syndrome
Increased intramuscular pressure leading to ischaemia myodegeneration
Muscles surrounded by tight fascia.
White Muscle Disease
Selenium/ vitamine E deficiency
They are antioxidants. Skeletal muscle is highly metabolic, uses oxygen, creates oxygen free radicals, if you don’t have the system to clear those- you can get damage to muscle. Selenium and vit E are very important.
Myofibril degeneration. Esp. livestock with rations like silage, proprionic acid (creates glucose) but it breaks down and affects viatmin E.
Exertional Myopathy (Capture Myopathy)
What are some types?
What is an effective regenerative gap width?
e.g. Wild animal in captivity- if the animal moves around too much- you rupture your muscles, myofibrils, blood vessels.
If exercise induced, usually the animal has an underlying metabolic nutritional defect.
*Can also be exertional rhabdomyolysis in horses
Effective regeneration- 2-4 mm gap
If gap is above 2-4 mm, the repair becomes ineffective. There is a limit on how well you can regenerate an injury.
Kink in muscle fibre (compared to the others). Kink suggests hypercontraction. They don’t run in a nice parallel way.
Gas bubble formation in necrotic muscle- blackleg. In infection, you get a lot of gas. If it gets big enough it will start occluding blood vessels. You can see it is a gas bubble because it is lined nicely.
Muscular Dystrophy
Dogs with muscle weakness and atrophy due to muscular dystrophy. Also fat builds up in muscle.
