Vet Muscle

Front 1

Muscular Hyperplasia "double muscling"

Back 1

Calves and lambs

Congenital Anomaly--increase in NUMBER of myofibers; size of each fiber is normal

Charolais, Belgian blue

--normally myostatin limits growth of skeletal muscle. mustation in myostatin leads to double muscling

Dystocia

Seen more in rump and shoulders, reduced body fat, thinner skin than normal

Front 2

Myofibrillar Hypoplasia "Splay leg" "Spraddle Leg"

Back 2

PIGS--congenital anomaly

Young piglets, splaying of limbs to the side. Affected muscles are atrophic, flabby, pale and wet

Hereditary small number of myofibrils in individual muscle fibers

Can be teratogenic--Zearalenone, mycotoxicosis

--choline or methionine deficiency

Front 3

Hyperkalemic Periodic Paralysis (HYPP)

Back 3

HORSES congenital anomaly

Autosomal Dominant in quarterhorses

Associated with post-anesthetic recumbency

1. Abnormal/delayed inactivation of sodium channel activity resulting in uncontrolled sodium influxes into the cell--membrane instability, continuous myofiber activity --> uncontrolled muscle twitching, weakness, collapse.

2. In response to all the sodium, potassium is released into the bloodstream

3. No gross lesions, just prominent muscling

4. Tx with low potassium diet, diuresis to increase potassium excretion

5. Sequelae: laryngeal muscle dysfunction: laryngospasms
Trembling, weakness
Metabolic Acidosis--pulm. edema, cardiotoxicity
Acute myoglobinuric nephrosis
if chronic--reduced muscle mass
severe acute myofiber necrosis

Front 4

Muscle Atrophy

Back 4

Reduction in muscle size caused by a decrease of myofiber diamters (loss of myofilaments in the sarcomeres)

Reversible if source of injury is removed

Histo: reduction in myofiber diameter with unchanged amt of connective tissue

Front 5

Denervation Atrophy

Back 5

Lack of tonic stimuli, muscle cells become atrophic

Due to loss of nerve function or generalized loss of the entire CNS motor unit

Damage to CNS or PNS

Examples:
Laryngeal Hemiplegia (roarers) due to damage of the left recurrent laryngeal nerve
Sweeney, after damage to the suprascapular nerve
Dogs with radial or brachial paralysis associated with trauma

Front 6

Disuse Atrophy

Back 6

Intact innervation (tonic stimuli) but reduced movement b/c of fractures, ruptured tendons, joint immobility, failure to use a painful leg, UMN damage, recumbency

--lesions localized to affeced groups of muscles--Type II fibers involved

Front 7

Muscular Dystrophy

Back 7

Group of diseases characterized by progressive weakness and muscular degeneration b/c of the absence or presence of abnormal musculr proteins (DYSTROPHIN)

1. Primary Defect: the myofiber itself. inadequacy of regenerative activity, innervation is sound

2. Degenerative changes --> loss of muscle fibers, progressive, reptitive, failed regeneration --> muscles are replaced by fat and fibrous connective tissue

3. Hereditary rare in animals:
Merino sheep: neuromuscular wkness, stiff gait, exercise intolerance
Canine x-linked muscular dystrophy: dystrophin def. in male golden retrievers
Myopathy of Labrador Retrievers--autosomal recessive, megaesophagus

Front 8

Responses of myofibers to injury?

Back 8

Degeneration
Necrosis
Regeneration

variable etiologies: trauma, ischemia, infarction, metabolic, toxins, infections

Front 9

Monofocal muscular lesions

Back 9

Confined to one site due to a single incident of trauma

Front 10

Multifocal lesions

Back 10

lesions/necrosis at multiple sites

Front 11

Monophasic lesions

Back 11

only one insult, a single episode. all lesions at same stage of necrosis/regeneration

Front 12

Multiphasic lesions

Back 12

ongoing insult (Vit E/Selenium deficiency) or continuous feeding of a toxin.

New lesions forming at same time that regeneration is taking place

Front 13

Classifications of lesions

Back 13

Monofocal Monophasic: local trauma

Monofocal Multiphasic: repeated local injury

Multifocal Monophasic: Myotoxicities (single exposure); metabolic disorders

Multifocal Multiphasic: nutritional deficiencies, muscular dystrophy

Front 14

Types of Degeneration

Back 14

1. Hyaline/waxy (ZENKER's)
2. Granular
3. Vacuolar (hydropic) degeneration--swelling of organelles, accumulation of glycogen w/in the myofiber, hypo/hyperkalemia

4. Fatty--accumulation of fat w/in the myofiber--lipid storage diseases...

5. Lipofuscinosis

Front 15

Degeneration

Back 15

Common sequel to myofiber injury, regardless of cause.

Can be reversible, unless to a certain point--then irreversible and necrosis follows.

Muscles appear pale (not confuse w/ veal calves, anemia, exsanguination, fat..)

If calcification extensive, muscles show white, chalky foci

Red discoloration if degenerated muscle w/ hemorrhage or release of myoglobin (rhabdomyelisis)

Micro: vacuoles, loss of striation --> swelling, hypereosinophilia, glassy/hyaline appearance --> rupture of fibers, retraction caps formed

Front 16

Dystrophic Calcification

Back 16

calcification of degenerated muscles is common in some diseases--

see white chalky foci

Micro: calcified fibers have granular bluish granules--use Von Kossa stain to verify Calcium

Front 17

Necrosis

Back 17

Due to: ischemia, hypoxia, free radical injury, chemical injury, infectious agents

1. Cell systems most vulnerable to necrosis: membranes, aerobic respiration, synthetic apparatus (proteins, enzymes), Genetic apparatus

2. 4 mechanisms associated w/:
Hypoxia/ischemia inhibit aerobic respiration--> ATP depletion
Generation of reduced oxygen species --> free radical inj
Defects in membrane permeability--> membrane dmg
Disruption of calcium homeostasis --> Ca influx

3. Can be Segmental or Total
Segmental: physical insults, toxemia, myopathies (toxic, metabolic, endocrine, nutritional), ischemia --> infarction, bacterial emboli
Total: extensive infarcts, massive trauma, burns

4. Lesions: pallor, dry, gritty
Micro: swollen, hypereosinophilic, fragmented sarcoplasm, persistent basal lamina, macrophage invasion, regen or fibrosis

Front 18

Role of Calcium overload in Necrosis

Back 18

Calcium-induced mitochondrial damage --> cellular degen and necrosis

Necrosis --> influx of calcium into the cell

Also the ingestion of toxic plants causes necrosis of tendons, ligaments

Front 19

White Muscle Disease

Back 19

Farm animals, young rapidly growing.

Associated with Vit E/Selenium deficiency, exacerbated by exercise, environment, nutition, toxicity.

In pigs--may occur w/ other VitE deficient syndromes--mulberry ht, hepatosis dietetica.

Diets high in unsaturated fat can contribute (increased Vit E requirement)

1. Cell membrane lipids are oxidized by free radicals due to lack of O2 radical-scavengers such as Vit E and selenium

2. Ca builds up in cells, CPK enzyme leaks out of cells, degenerated myofibers undergo necrosis.

3. Muscle activity elates to production of free radicals: muscles most severely affected: diaphragm, heart, tongue, intercostals (type I fibers)

4. Difficult to see path in mild cases. Lesions bilaterally symmetrical. fish flesh w/ calcification

5. HEART: LV in calves, RV in sheep.

6. Take samples of type I muscles

Histo: segmental degeneration (Zenker's, flocculant), hypercontraction w/ loss of striation, hypereosinophilia, fiber fragmentation, CALCIFICATION is severe; proliferation of myosatellite cells (attempt at repair) and macrophages

Front 20

Exertional Myopathies

Back 20

Group of dz,--> severe muscle degeneration following strenuous exercise.

Lesions similar to WMD bu affect major muscle masses with mainly TYPE II fibers.

Examples: Azoturia, Tying up, Azoturia-like syndrome, Capture myopathy

Front 21

AZOTURIA
Paralytic Myoglobinuria, "monday morning disease", Exertional Rhabdomyolysis, Paralytic Myoglobinuria

Back 21

Dz of HORSES--strenuous exercise after a long resting period. Weakness, reluctant to move, diaphoresis, sweating, myoglobinuria, recumbency, renal failure, acidosis, death...

1. Etiology: Electrolyte abnormalities, Se deficiency, exercise forced after eating...

2. Gross: muscles of the extremities are swollen edematous, DARK (from myoglobin) and kidneys are DARK BLACK. If horse survives, muscles become pale, atrophic

3. Histo: segmental degen and necrosis with little to no calcification. Chronic dz = fibrosis, atrophy
Toxic myoglobinuric injury to kidneys--death

5. Sequelae: death from cardiac/renal injury
Recovery and repeated episodes --> atrophy
Recovery w/ regeneration

Front 22

Tying Up
Set fast, acute rhabdomyolysis, transient exertional rhabdomyolysis

Back 22

Mild, rapidly regressive form of azoturia
No gross lesions
Micro: mild rhabdomyolysis. rare myoglobinuria

Front 23

Azoturia-like Syndrome in Cattle

Back 23

ZEBU/wild cattle
Assoc w/ handling/transport over long distances.
Similar dz in racing greyhounds after intense muscular exertion

Front 24

Capture Myopathy

Back 24

Acute, often fatal myopathy of wild mammals/birds.
Preceded by chase, struggle/transport.

Acidosis pronounced

Bilaterally symmetrical muscle degen, pale edematous muscles, hemorrhage, tendon rupture

Can cause death from CHF

Front 25

Toxic Myopathy

Back 25

MONENSIN tox, Poisonous plants, Gossypol

Susceptibility based on:
metabolic uniqueness of tissue
selective binding of myotoxin

Lesions: ill-defined, pale streaks in myocardium and skeletal muscle
occasionally muscle necrosis causing myoglobinuria

Ex:
Ionophores, Toxic Plants, Gossypol, Drugs/chemicals, Mycotoxins

Front 26

Ionophores

Back 26

Monensin, Salinomycin, Narasin--causes myofiber necrosis in HORSES and cattle, sheep dogs, horse most susc.

Ionophores facilitate movement of cations across cell membranes--> disruption of normal ionic equilibrium --> Ca overload --> necrosis

Death from cardiovascular collapse/shock

Lesions: monophasic multifocal segmental necrosis, pallor, regen, fibrosis

Front 27

Toxic Plants for myopathy

Back 27

Cassia: horses, cow, sheep/goats

Karwinskia: sheep/goats

Eupatorium: cattle

Front 28

Gossypol

Back 28

muscle necrosis. in cotton seeds

Front 29

Drugs/chemicals/mycotoxins

Back 29

IM injections--locals, Abs, supplements can cause hemorrhage/necrosis

Mycotoxins: Penicillium and Aspergillus.
--> staggers, muscle necrosis secondary to sustained muscular contractions

Front 30

Hypokalemic Myopathy in COWS
(electrolyte abnormality)

Back 30

CATTLE: profound weakness/recumbency.
Hypokalemia d/t anorexia and ketosis, glucocorticoids, IV admin of glucose or insulin

1. Decreased potassium in muscle interferes w/ normal muscle cell fxn. Myofiber necrosis d/t altered mitochondrial activity/focal ischemia from vasoconstriction, also interferes w/ cardiac conduction

Lesions: iscemic necrosis from recumbency; myofiber necrosis, vacuolated myofibers

Front 31

Hypokalemic Myopathy in CATS

Back 31

Generalized weakness w/ ventroflexion of the neck

1. Hypokalemia --> hyperpolarization of the cell membrane, secondary excessive permeability to Na.
Decreased K interferes w/ muscle cell fxn, myofiber necrosis, abnormal cardiac conduction

Etiology: abnormal muscle energy metabolism
Ischemia from vasoconstriction
Decreased K in diet
Increased K in urine--renal disease
2ndary to GIT dz, inappropriate fluid therapy
Hyperthyroidism. increased activity of Na-K-ATPase

LESIONS: myofiber necrosis +/- chronic interstitial nephritis

Front 32

Other Electrolyte abnormalities causing myopathies?

Back 32

Hypernatremia in cats
Hypophosphatemia in Cows

hypokalemia in both

Front 33

Porcine Stress Syndrome (PSS)
Malignant Hyperthermia, Pale Soft Exudative Pork, "Herztod", Black muscle disease

Back 33

Hereditary hypermetabolic syndrome

1. Respiratory and metabolic acidosis,
Myoglobinemia,
Hyperkalemia,
High blood lactate, Hyperthermia,
Cardiovascular collapse, Death

Any type of stress can trigger

Also in dogs and horses

PATH: inherited defect in intracellular uptake, storage and release of Ca ions. excess Ca in the cell --> consumption of ATP progresses to degen and necrosis. Denaturation of sarcoplasmic protein leads to movement of intracellular water into interstitium

Lesions:
Gross--muscles w/ TYPE II fibers are pale and wet (interstitial edema). Cut--water oozes
Pulmonary edema, accumulation of clear fluid in abdominal/thoracic cavities
Micro: early myofiber degen, necrosis, edema; may be acute necrosis of cardiac muscles

Front 34

Compartment Syndrome

Back 34

Ischemic Injury Myopathy

1. Degeneration and necrosis of muscles surrounded with heavy aponeurosis (conn. tissue)
occurs in poultry--deep pectorals.
--muscular expansion in a non-expandable compartment, resulting in vascular compression, ischemia, infarction of muscle fibers

Can be preceded by flapping of wings. lesions occur a few hours later--necrosis of supracoracoid muscles

Front 35

Hypothyroidism as a myopathy

Back 35

1. Clinically = generalized weakness, muscle atrophy, megaesophagus; CK and AST are normal

2. Path: decreased thyroid hormone affects muscle mtabolism --> skeletal myofiber weakness, atrophy.
Peripheral neuropathy (axonal degen)--damage to motor nerves --> denervation atrophy, NM weakness

3. LESIONS: marked type II atrophy in DOGS

4. Dx: selective Type II atrophy and evaluation of thyroid function

Front 36

Hypercortisolism as an endocrine myopathy

Back 36

1. Clinically: stiff pelvic limb gait, increased bulk and tone of proximal thigh muscles, muscle weakness

2. Etiology: increased cortisol production or steroid excess

3. path: prolonged steroid admin causes peripheral neuropathy resulting in denervation atrophy of many myofibers with regen.

4. Lesions: overall muscle atrophy
variation in myofiber diameter, splitting, necrosis
bilateral adrenocortical hyperplasia +/- a tumor

5. Dx: selective TYPE II fiber atrophy, denervation atrophy, avaluate adrenocortical fxn and serum cortisol

Front 37

BLACKLEG
Black quarter, Symptomatic Anthrax, Emphysematous Gangrene.

Back 37

Hemorrhagic Myositis caused by Clostridium chauvoei

1. Ingestion of soil containing spores--spores to GIT --> spores to muscle

2. Muscle injury/hemorrhage--change in local invironment causes germination of spores in muscle. Exotoxins, edema, myonecrosis, emphysemia, toxemia

3. Affects large muscle masses,. muscles are black with gas and crepitate on palpation.

Rancid odor in affected tissue. milde interstitial/sq edema peripherally to the lesion. Fibrin tags

Diffuse serosal hemorrhages, early bloat, pulmonary edema.

Histo: segmental degen, necrosis, edema, neutrophils; bacteria rarely seen in tissues

Front 38

Gas Gangrene (Malignant Edema)

Back 38

Hemorrhagic Myositis
Caused by Clostridium septicum, C. perfringens, C. novyi, C. sordelli, C. chauvoei.

All but carnivores affected

Entry through a wound, spores in soil and feces.

Need optimal conditions--wounds with low oxygen tension. areas cold on palpation, crepitation, toxemia

Lesions gross: locally extensive, mostly connective tissue; severe edema, minimal emphysema, hemorrhage, skin discoloration
histo: edema, cellulitis, minimal myositis. FA test.

Front 39

Gas gangrene vs. Blackleg

Back 39

Blackleg: high myositis, low cellulitis. some edema, high emphysemia

Malig Edema: low myositis, high cellulitis, high edema, high emphysema

BOTH: organisms give off exotoxins:
injury to capillary endothelium
altered permeability--edema and hemorrhage
lysis of myocytes --> necrosis
gas bubbles--> produced during replication of clostridial organisms

Front 40

Purpura Hemorrhagica in Horses

Back 40

SUPPURATIVE MYOSITIS
--Immune mediated myositis.
Post-STREPTOCOCCAL Infection

Edema of head/limbs, leukocytoclastic vasculitis, petechial hemorrhages in mucosae, associated with strangles (Strep equi)

Front 41

Eosinophilic Myositis of ruminants

Back 41

Etiology: sarcocystosis, immunologic injury --Autoimmune rxn against type IIc fibers of masticatory muscles.

Cattle: focal necrosis w/ large # of neutrophils
--degenerate SARCOCYSTS present, can cause hypersensitivity
--Lesions have well-demarcated green foci (will fade to white with air exposure)

Large # of eosinophils give green color. Focal necrosis, fibroplasia in prolonged lesions.
Eosinophilic granulomas can develop.
Calcium salts often deposited in necrotic core
Sarcosporidia may be present

Front 42

Masticatory Muscle Myositis of dogs (esp GS)

Back 42

Rare, acute/relapsing eosinophilic myositis.
Swollen, painful jaws, blood eosinophilia.

Atrophic myositis in long-nosed breeds can be same condition, just acute/chronic

Path: antibodies against protein in type IIc fibers in masticatory muscles??

Gross: swollen, pale, greenish; unilateral/bilateral, atrophy if chornic. may involve ANY muscle in ruminants

Histo: acute: fiber necrosis w/ edema and marked infiltration of eosinophils in masseter, temporal and pterygoig muscles.
Chronic: fibrosis, atrophy and infiltrates of lymphocytes and plasma cells

Sequelae: atrophy

Front 43

Granulomatous Myositis

Back 43

Systemic Mycoses, TB, Metazoal parasites (Trichinella, cysticercosis)

Lesions: white firm masses in muscle

Examples: TB, Actinobacillus (wooden tongue), Actinomycosis (lumpy jaw), Botryomycosis (staph aureus), Fungal granulomatous myositis (blastomycoses)

Front 44

Myastehenia Gravis

Back 44

DISORDER OF NEUROMUSCULAR JXN

sporadically seen in dogs and cats, dz of the post-synaptic membrane - motor end plate, causing weakness, severe fatigue from mild exercise

1. 2 types:
Congenital: inherited where animals are born with reduced # of ACh receptors
autosomal recessive in Jack Russels, Springer spaniels, smooth fox terriers--same

Acquired: breed dispositions: dogs: akitas, GSpointers, chihaurha, rotts, dobies, dalmations, newfoundlands. cats = abyssinians
--> animals develop IgG antibodies against ACh receptors in postnatal life.
Dramatic improvement after admin of anti-cholinesterase drugs (neostigmine)

Histo: muscle atrophy (disuse);

Sequelae: Megaesophagus, Dysphagia, Aspiration Pneumonia, Thymoma