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Path 2 - Muscles - General, PM, Congenital

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sihirlifil's version from 2017-04-29 14:56

General

Question Answer
Fxnl unit of muscleMyocyte (actin (I band) & myosin (A band) filaments)
Muscle fiber type ISlow twitch, oxidative, fatigue resistant, aerobic
High mitochondrial & fat content, low glycogen
Muscle fiber type IIaFast twitch, oxidative AND glycolytic, fatigue resistant
Intermediate mitochondria, fat, glycogen
Muscle fiber type IIbFast twitch, glycolytic, fatigue-sensitive, anaerobic
Low mitochondrial & fat content, high glycogen
What makes up a motor unit?Motor neurons (within CNS)
Axon branches
Myofiber
**Each motor unit goes exclusively to either type I or II fibers**
Mutlinucleation is important forRegeneration
Sarcolemma is?Basement membrane (resistant to insults, penetrable by macrophages, responsible for regeneration)
Classification of muscle disease (DICE2N3): D = Degenerative (ischemia, nutritional, toxic, exertional, traumatic)
Classification of muscle disease (DICE2N3): I = Inflammatory (bacterial, viral, parasitic, immune-mediated)
Classification of muscle disease (DICE2N3): C = Congenital and/or inherited (anatomic defects, muscular dystrophy, congenital myopathy, myotonia, metabolic, malignant hyperthermia)
Classification of muscle disease (DICE2N3): E2 = Endocrine (hypothyroidism, hypercortisolism)
Electrolyte (hypokalemia, hypernatremia, other imbalances)
Classification of muscle disease (DICE2N3): N3= Neuropathic (peripheral neuropathy, motor neuropathy)
Neuromuscular junction disorders (myasthenia gravis, botulism, tick paralysis)
Neoplasia (primary, secondary)
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Postmortem

Question Answer
**What is rigor mortis?Contraction and stiffening of muscles that fix the position of the joints after death of an animal as energy stores are used up
Order of rigor mortis?Jaws --> trunk --> extremities
Onset of rigor mortis? peak? disappears?2-6 hours
Peak 24-48 hours
Gone by 72 hours
**Why does rigor mortis happen?Lack of oxygen --> energy production ceases --> no energy to pump Ca2+ out of cell
Glycogen depletion (lack of ATP production to maintain relaxation)
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Congenital / Inherited

Question Answer
**Muscular hyperplasia of calves and lambs: hereditary in who? Which gene is affected and whats going on?European breeds of cattle (Charolais, Belgian blue)
Myostatin gene mutation- proliferation promoted, increase # myofibrers (same size) --> double muscling
Muscular hyperplasia of calves and lambs: lesions? Advantage/disadvantage?Increased muscle mass, reduced body fat, thinner skin
Meatier carcass BUT dystocia!
**Myofibrillar hypoplasia: happens in who? Aka?PIGS
Splayleg, spraddle/straddle legged
Myofibrillar hypoplasia: what does it look like?Impaired ability to stand and walk, muscular weakness of hind limbs, limb abduction; atrophic, flabby, pale, wet muscles
Failure of normal development in dogs/rabbits?Diaphragmatic hernia
Myofibrillar hypoplasia: Etiology?Fewer myofibrils in myofibers (inherited)
Teratogenic: Fusarium mycotoxicosis (F2) depresses piglet growth in utero, weak splay-legged piglets
Choline or methionine deficiency (essential for ACh synth)
Glycogen storage diseases: etiology?Missing of defective enzyme
Lesions of glycogen storage diseaseVacuolar myopathy of neurons, hepatocytes, cardiac & skeletal muscles (--> cardiomyopathy)
Polysaccharide storage myopathy (PSSM): happens in who? What is it?HORSES (quarter, warmblood, draft-related) inherited autosomal recessive
Abnormal polysaccharide accumulation (normal muscle fiber size)
What does EPSSM look like clinically?Recurrent exertional rhabdomyolysis
Stiff gait
Symmetric muscle atrophy
Weakness (bilateral pelvic limb or generalized)
Pathogenesis of EPSSMCarbohydrate metabolic disorder --> insufficient energy production
Lesions of EPSSMMuscles pale pink or diffusely red
Acute myoglobinuric nephrosis (pigment nephrosis)
Reduced muscle mass if chronic
Which type of fiber is affected by EPSSM?Type II
Which stain do you use for EPSSM?PAS positive sarcoplasmic deposits
Hyperkalemic periodic paralysis (HYPP): what is it? who gets it?Inherited autosomal dominant mutation in the sodium channel gene of QUARTER HORSES
What's happening biochemically in HYPP?Delayed inactivation of sodium channel activity --> uncontrolled sodium influxes into the cell, altered voltage --> continuous myofiber electrical activity
How does potassium relate to HYPP?Potassium is released into the extracellular space in response to increased intracellular sodium (=hyperkalemia)
Cardiotoxicity! Can collapse and suddenly die from heart failure
Gross lesions of HYPPLimited to prominent muscling
Treatment for HYPPLow-potassium diet; diuresis
Sequelae to HYPPLaryngeal muscle dysfunction (spasms)
Trembling, weakness, collapse
Metabolic acidosis (cardiotoxicity, pulmonary edema)
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