Path 2 - Muscles - Disturbances of Growth, Physical Injury, Circulatory, Degeneration & Necrosis

sihirlifil's version from 2017-04-29 14:57

Disturbances of Growth

Question Answer
What are the disturbances of growth? (5)Atrophy
Infiltration (fat, glycogen)
Muscular dystrophy
**What is atrophy?Decrease in size of cells that have gained full development
**Types of atrophyDenervation atrophy
Disuse atrophy
Malnutrition & cachexia
Denervation atrophy pathogenesis?Brain/spinal cord damage --> loss of central control
Peripheral nerve injury
Always accompanied by paralysis
Disuse atrophy pathogenesis?Diminished level of work, removal of source of nutrition or stimulation --> cell shrinkage --> decrease in size of tissue/organ
Etiology of denervation atrophy in the CNS (5)Disk protrusion
Chronic meningitis
Metastatic lesions
Localized spinal malacia
Etiology of denervation atrophy in the PNS (4)Trauma
Pressure by disks
What happens with equine laryngeal hemiplegia?Damage to left recurrent laryngeal nerve --> denervation atrophy
What is Sweeney?Damage to the suprascapular nerve in horses (atrophy of supraspinatus and infraspinatus muscles)
Damage to which nerves usually cause denervation atrophy in dogs?Radial or brachial plexus paralysis (and atrophy of associated muscles)
**Which muscle fibers are affected by denervation atrophy?Both Type I and Type II (diffuse atrophy)
Sequelae of denervation atrophy?Denervated muscle may be re-innervated if the neural sheaths are not physically disrupted
Muscle fiber atrophy reversed if fxnl connections between nerve and muscle fibers re-established
How does disuse atrophy usually occur?Secondary to inactivity/limitation of movement:
Fractures, tendon rupture
Joint immobility
Painful leg
UMN damage
**Where are the lesions of disuse atrophy?Type II preferentially; flabby, shrunken muscles
Atrophy due to malnutrition & cachexia: etiology?Most common form of muscle atrophy
Severe helminthosis (ostertagiasis, fasciolasis)
Chronic debilitating diseases (TB, Johne;s disease)
**Atrophy due to malnutrition & cachexia: lesions?Type II preferentially; small, thin, dark, sticky, flabby
How does senile atrophy look?Similar to atrophy of cachexia
Yellowish-brown to dark brown color (lipofuscin) (particularly diaphragm)
Pressure atrophy is caused by?Prolonged pressure on muscle (abscesses, tumors, parasitic cysts)
Lesions of atrophy: summary (7)Decreased size and weight of muscles
Decreased size of fibers
Degeneration and necrosis of fibers
Prominence of skeleton
Progressive loss of function
Recovery if cause is removed
Muscle atrophy: gross appearance?Reduced in volume, pale, flabby
Muscle atrophy: microscopic appearance?Myofibers become smaller in diameter, angular, separated by increased fatty connective tissue (fatty infiltration)
What is hypertrophy?Increase in size of muscle by an increase of fiber size (become enlarged, not just increase in number
No new cells Formation of new myofilaments
**Etiology of hypertrophyIncreased workload (physiologic or pathologic)
Physiologic, pathologic (compensatory), idiopathic, iatrogenic
**What is muscular dystrophy? Seen in who?Progressive, hereditary, degenerative (+/- abnormal proteins) in cattle, sheep, dogs, cats, chickens
**Characteristics of muscular dystrophy?Intact innervation
Inadequate regeneration
Primary defect in myofibers (variations in fiber diameter, vacuolar degeneration, fiber splitting, central cores)
Muscle weakness, stiff gait, exercise intolerance
**Muscular dystrophy is inherited in who?Merino sheep
Duchenne type dogs (X-linked dystrophin deficiency)
What is labrador retriever myopathy (HMLR)?Inherited, autosomal recessive; muscle weakness, bunny hopping, exercise intolerance, collapse during exercise
Lesions of HMLR?Deficiency of Type II muscle fibers, poor muscling, +/- megaesophagus (aspiration pneumonia!), segmental necrosis and regeneration
**Which nerve fibers are affected in congenital myopathies?Type I
**Which nerve fibers are affected by endocrine disease?Predominantly Type II
Hypothyroidism, Hypercortisolism

Physical Injury & Circulatory disturbances

Question Answer
Physical injury: One example of a specific conditionFibrotic and ossifying myopathy of Quarter horses (torn hamstring)
Heals with fibrosis and ossification
Causes of muscle rupture?Diaphragmatic (eventration)
Rent in fascial sheath (eventration)
Racing greyhounds: muscle rupture during strenuous exercise
Cattle: Tearing (myorrhexis) in adductor muscles of cattle on slippery gound
Circulatory disturbances of muscle: (4)Hemorrhage
Thrombosis, embolism and infarction
Ischemia (degenerative myopathy)
Lesions of hemorrhage? Etiology?Swelling, red to black
Myositis, septicemia, trauma
How common is muscle infarction? Lesions? Example?RARE- well-developed collateral circulation
Hemorrhage and necrosis in infarcted muscle, thrombus
Thrombosis of iliac artery in CAT and horse (saddle thrombus) --> Pain, paresis, pulselessness, poikilothermy, pallor
Congestion: etiology? lesions? example?Localized or generalized stasis (backup of blood on venous side)
Dark red muscles
Ruminal tympany (bloat) results in congestion of muscles cranial to the thoracic inlet
What is a bloat line? What does it look like?Rumen occludes blood vessels as it enlarges during bloat
Cervical esophagus is congested, thoracic esophagus mucosal surface is pale
Extensive congestion of cervical region (muscles and tissues) extending into the head

Degeneration & Necrosis

Question Answer
What's the problem with diagnosing muscle necrosis?Stereotyped response- lack of etiologic specificity of reactions
Histopathologic interpretation: Monofocal?Confined to one site, could be due to single incident of trauma (e.g. IM injection)
Histopathologic interpretation: Multifocal?Mostly systemic disease, necrosis at multiple sites
Histopathologic interpretation: Monophasic?Only one insult (e.g. overly strenuous exercise (exertional myopathy) or toxin fed on one occasion)
At necropsy, all lesions at the same stage of necrosis/regeneration
Histopathologic interpretation: Multiphasic?Ongoing insult (e.g. Vit E/Se deficiency, continuous toxin feeding)
New lesions (segmental necrosis) forming simultaneously with regeneration
Monofocal monophasic:Local trauma
Monofocal multiphasic:Repeated local injury
Multifocal monophasic:Myotoxicity, metabolic disorders
Multifocal multiphasic:Nutritional deficiency, muscular dystrophy
Gross appearance of muscle degenerationWhite, chalky foci (streaks): severe extensive calcification
Red: hemorrhage, rhabdomyolysis (release of myoglobin, myoglobinuria, tubular dmg to kidney)
Microscopic appearance of muscle degenerationVacuoles, loss of striation
Hypereosinophilia (of cytoplasm! not infiltration)
Glassy, hyaline (Zenker's)
Dystrophic calcification (granules in myofibers, Von Kossa stain)
Most common lesion of degenerationHyaline degeneration (swollen, lose striation, homogenous, acidophilic)
How can degeneration cause ischemia?Fibers swell, compress local vasculature
Necrosis: mechanisms of cell injury (4)Ischemic and hypoxic injury (inhibit aerobic respiration = ATP depletion
Free radical injury (generation of ROS)
Chemical injury
Infectious agents
Necrosis: most vulnerable to necrosis (4)Cell membranes
Aerobic respiration (mitochondria)
Synthetic apparatus (proteins, enzymes)
Genetic apparatus
Necrosis: mechanisms (4)ATP depletion (hypoxia, ischemia inhibit aerobic respiration)
Free radicals (generation of reduced oxygen species)
Membrane damage (defects in permeability)
Calcium influx (homeostasis disrupted)
Segmental necrosis: (5)Physical insults
Myopathies (toxic, metabolic, endocrine, nutritional)
Ischemia infarction
Bacterial emboli
Total necrosis: (3)Extensive infarcts
Massive trauma
Large burns
Necrosis: clin path indices of muscle damage?CK, AST, myoglobin
Calcium overloading: etiology, causes, lesions?Ca-induced mitochondrial damage (dystrophic) --> damage to plasmalemma --> influx of Ca into cell
Old age, idiopathic, toxic plants
Glistening, chalky, opaque foci
What has to be intact for regeneration?Success depends on integrity of the Sarcolemma
Sequence of events during regenerationNecrosis --> macrophage infiltration --> phagocytosis --> prolif of satellite cells, myoblasts, myotubes --> growth and differentiation of myofibers

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