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Pathology II Master > Muscle (AH) > Flashcards

Muscle (AH) Flashcards

Crossed with class notes, TQs and Muzzy review.

1
Q

Type I mm fibers

A

redslow twitchsmallmore mitochondriano glycogen

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2
Q

Type II mm fibers

A

White fast twitchlarge less mitochondria more involved in atrophy II A = oxitative + glycolytic. II B = glycolytic.

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3
Q

***What is the process that leads to Rigor Mortis?

A

decreased O2 –> decreased ATP –> decreased Ca2+ ATPase pump activity –> decreased Ca removal –> sustained contraction.

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4
Q

How does Rigor Mortis progress?

A

Start - 2hrs
Max - 24-48 hrs
Dissipates - 72 hrs.
Starts at jaw and trunk and then goes to extremities.

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5
Q

In what breeds of cattle is muscular hyperplasia hereditary? *Why does it happen?

A

Charolais and Belgian Blue. Mutation of myostatin gene –> double muscling

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6
Q

What spp. gets myofibrillar hypoplasia?

A

Pigs

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7
Q

Etiology of myofibrillar hypoplasia?( 3)

A
  1. Hereditary - decreased number of myofibrils in muscle fibers.
  2. Teratogenic - Toxins (F. graminearum = F-2 toxin = mycotoxicosis) –> depressed growth in utero.
  3. Choline or methionine deficiency –> decreased Ach synthesis and energy production.
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8
Q

Pathogenesis of Polysaccharide storage myopathy in horses?

A

Carbohydrate metabolic disorder –> insufficient energy production –> decrease in mm. –> Acute myoglobinuric nephrosis (pigment nephrosis)

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9
Q

Etiology of Glycogenoses (glycogen storage Dz)?

A

Missing or defective enzyme (inherited) –> accumulation of glycogen

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10
Q

What is Myotonia?

A

Channelopathy. Inability of myofibers to relax resulting in spasmodic contractions.

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11
Q

Etiology of HYPP?

A

Genetic mutation of skeletal mm sodium channel gene –> delayed inactivation of sodium channel activity –> uncontrolled twitching and hyperkalemia in bloodstream.

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12
Q

HYPP sequelae?

A

Laryngeal mm dysfunction. Trembling, weakness, collapse. Metabolic acidosis –> cardiotoxicity and pumonary edema. Can be fatal.

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13
Q

What is Arthrogyposis?

A

Muscle hypoplasia due to lack of muscle innervation during gestation.

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14
Q

Lesions of Arthrogyposis?

A

Atrophy and dysplasia of muscles Fibrosis → Curvature and rigidity of joints = Crooked limbsPossibly born dead

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15
Q

Etiology of Arthrogyposis?

A

Infectious:

  1. viral (BVD, Akabane)
  2. vaccinations druing 1st trimester (ruminants) for Rift Vally fever, wesselbron virus, bluetongue. Non-infectious:
  3. inherited in suffolk lambs
  4. Plant poisoning (lupinus spp.) causes decreased movement in utero
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16
Q

What is the primary defect associated with Arthrogyposis?

A

Always associated with spinal and brain abnormalities.

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17
Q

What is mm atrophy?

A

Decrease in size of cells that have gained full development

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18
Q

Mm atrophy etiology?

A
  1. Diminished level of work

2. Removal of source of nutrition or stimulation (more common)

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19
Q

What are the types of mm atrophy?

A

Denervation - lack of tonic stimuli.
Disuse - decrease of tonic stimuli.
Malnutrition and cacexia - small, thin, dark mm.
Senile- similar to malnutrition + lipofuscin.
Pressure

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20
Q

Which type of atrophy effects both type I and II fibers. What about the others?

A

Denervation = I and II fibers.

The rest = only type II.

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21
Q

Give three examples of denervation atrophy syndromes

A
  1. Equine lyaryngeal hemiplegia (roaring).
  2. Damage to suprascapular nerve in horses (sweeny).
  3. Radial or brachial paralysis in dogs associated with trauma.
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22
Q

Lesions of denervaiton atrophy?

A

Diffuse atrophy involving BOTH type I and II fibers

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23
Q

Lesions of Disuse atrophy?

A

Mainly involves Type II fibers.

Flabby shrunken muscles.

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24
Q

What is the most common form of Atrophy?

A

Atrophy of malnutrition and cachexia.

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25
Q

Etiology of atrophy of malnutrition and cachexia? (5)

A

Malnutrition, Starvation, Severe helminthosis, Chronic debilitating diseases (TB, Johne’s Dx), Neoplasia

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26
Q

Lesions of atrophy of malnutrition an cachexia?

A

type II fibers involved.

Small, thin, dark, sticky, flabby mm.

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27
Q

Lesions of senile atrophy?

A

Lipofuscin –> yellow brown color, especially in diaphram.

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28
Q

What causes pressure atrophy?

A

Prolonged pressure of muscles from abscesses, tumors, parasitic cysts

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29
Q

What is Hypertrophy?

A

Incease in size of mm by an increase in fiber size. No new cells, just bigger size.

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30
Q

Etiology of hypertrophy?

A
  1. physiologic - athletic training, pregnant uterus.
  2. Pathologic (left cardiac ventricular hypertrophy.)
  3. Idiopathic (esophagus, ileum - horses).
  4. Iatrogenic - steroids.
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31
Q

Lesions of hypertrophy?

A

Dark red. Increase in myofiber diameter. Increased myoglobin. Larger cellular organelles.

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32
Q

What is steatosis?

A

Defective myofiber development –> replacement of muscle tissue by adipose tissue.

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33
Q

How do mm affected by severe steatosis appear?

A

Soapy, marbling appearance. Not clinically significant.

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34
Q

What is muscular dystrophy?

A

Progressive degeneration due to abnormal muscle proteins (ex: dystrophin).

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35
Q

Etiology of muscular dystrophy? (2)

A
  1. Idiopathic: Primary defect in myofiber itself w/ inadequacy of regen activity (innervation is sound)
  2. Hereditary- Marino sheep, Canine X-linked mm dystrophy, HMLR
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36
Q

General lesions of muscular dystrophy?

A

Failed attempts to regenerate –> Fibrosis.

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37
Q

Clinical presentation of HMLR?

A

In young dogs. Bunny hopping. +/-megaesophagus –> aspiration pneumonia.

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38
Q

What is the defect in dogs with Canine X-linked mm dystrophy?

A

Dystrophin deficiency. Duchenne type

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39
Q

What specific condition is associated with mm rupture?

A

Fibotic and ossifying myopathy (torn hamstring in quarter horses).

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40
Q

Sequelae of ruptured mm.?

A

Diaphragmatic rupture or rent–> eventration. In racing greyhounds –> muscle ruptrue during strenuous activity.Tearing from slipping cows

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41
Q

Lesions of congestion?

A

swollen, red to black.

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42
Q

What is an example of mm congestion?

A

Bovine ruminal tympany (bloat)

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43
Q

Lesions associated with bloat?

A

Cervical esophagus is red.
Thoracic esophagus is pale (white).
Extensive congestion of cervical region extending to the head. ==> bloat line.

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44
Q

Thrombosis, Embolism, and infarction lesions?

A

hemorrhage and necrosis in infarcted muscle, thrombus

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45
Q

What are the three responses of mm to injury?

A

degeneration, necrosis, regeneration

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46
Q

What is true about etiology of degeneration/necrosis?

A

There is a stereotyped response making it hard to determine etiology.

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47
Q

Histopathological interpretation of degeneration/necrosis

A

Monofocal monophasic - local trauma.
Monofocal multiphasic - repeated local trauma.
Multifocal monophasic - single exposure to mycotoxins or metabolic disorders.
Multifocal, multiphasic - nutritional deficiency or muscular dystrophy.

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48
Q

Gross lesions of mm degeneration?

A

Degenerated mm. appear pale.

      1. Chalky/white = severe calcification.
        1. Red = hemorrhage/ rhabdomyolysis (myoglobin release)**
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49
Q

Micro lesions of mm degeneration? (6)

A

Vacuoles and loss of striations followed by swelling, hypereosinophilia, glassy or hyaline appearance (Zenker’s necrosis)
Finally, segmental rupture of fibers and formation of retraction caps

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50
Q

When is mm degeneration irreversible?

A

once necrosis ensues

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51
Q

Ddx for degeneration?

A

gross lesion = pallor.

Muscle pallor can also indicate pale muscles of veal calves, enemia, exsanguination, fat.

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52
Q

What are the mechanisms of cell injury that lead to necrosis?

A
  1. Ischemic and hypoxic injury –> ATP depletion.
  2. Generation of reduced oxygen species –> Free radical injury .
  3. Defects in membrane permeability –> membrane damage.
  4. Disruption of calcium homeostasis –> calcium influx –> mitochondrial damag
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53
Q

Gross/Micro lesions of necrosis?

A

Gross: pallor, dry gritty.
Micro: swollen, hypereosinophilic, fragmented sarcoplasm, persistent basal lamina, magrophage invasion, regeneration or fibrosis.

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54
Q

What are the main categories of degenerative myopathies?

A

Nutritional, Exertional, Toxic, Electrolyte, Stress, Ischemic, Endocrine, (Muscular Dystrophy)

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55
Q

TQ What is the pathogenesis of nutritional myopathies?

A

Decrease in Se / Vit E–> –> Lipid peroxidation –> damage to CM –> Ca2+ influx –> Mitochondrial damage –> segmental necrosis

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56
Q

Lesions of WMD?

A

Myofiber necrosis with extensive calcification making the tissue appear pale and gritty “fish flesh”.
Also hypereosinophilia and loss of striation.
Mostly found in muscle with type I fibers = diaphragm, heart, tongue, intercostal mm.

57
Q

What other selenium/ vit E deficiencies may coexist with WMD?

A

Mulburry heart and heptatitis dietetica

58
Q

Where in the heart are lesions of WMD seen in calves and sheep?

A

RV in sheep, LV in calves

59
Q

Where are lesions of Nutritional myopathy seen?

A

Selective of type I fibers = diaphragm, intercostal, tongue, heart. (diaphram and heart are most severe b/c they can cause death)

60
Q

What is exertional myopathy?

A

Dz resulting in severe muscle degeneration following strenuous exercise.

61
Q

Pathogenesis of Exertional myopathy?

A

Strenuous activity –> utilization of glycogen –> accumulation of lactic acid –> acid denatures protein structure –> loss of water –> interstitial edema –> compressive circulatory disturbances –> ischemia –> Hyaline degeneration and necrosis of sk mm.

62
Q

* TQ Exertional Myopathy Syndromes by Spp.?*

A

Horses - azoturia and tying-up. Cattle - azoturia- like syndrom. Wildlife - capture myopathy

63
Q

By what other names is Azoturia known in horses?

A

Eq. paralytic myogobinuria, Monday morning dz, Sacral paralysis, Exertional rhabdomyolysis.

64
Q

CS of Azoturia?

A

Sudden onset of stiff gate due to mm weakness. Sweating. Death from Cardiac or renal failure. Myoglobinuria. Acidosis.

65
Q

Azoturia etiology?

A

Forced exercise after period of rest w/o feed restriction (#1 cause) Electrolyte imbalances, Se deficiency, polysaccharide dz.

66
Q

Azoturia lesions?

A

Myoglobinuric nephrosis –> DARK BLACK KIDNEYSMuscles:Moist, swollen, dark red, hemorrrhage. Hyaline degeneration and necrosis of sk. Mm. Later: fibrosis, atrophy, mm pallor.

67
Q

Sequelae of Azoturia?

A

Death from cardiac or renal injury. Recovery w/ atrophy. Recovery with mm regeneration.

68
Q

What is the less severe form of Azoturia?

A

Tying-up/setfast/ acute rhabdomyolysis in horses.

69
Q

What form of Azoturia is associated with wild cattle/ zebu?

A

Azoturia-like syndrome. (also in racing greyhounds) Linked to unusual transportation/ confinement –> fighting and struggling.

70
Q

Which form of Exertional Myopathy presents with pronounced Acidosis?

A

Capture Myopathy

71
Q

Lesions of Capture myopathy?

A

Bilateral Symmetry, Pale, swollen, edematous muscles. Hemorrhage Ruptured tendons Myocardial injury (congestive HF).Acidosis

72
Q

Lesions of muscle toxicity?

A

Ill defined pale streaks in skeletal and or myocardium. Sometimes myoglobinuria in presence of extensive necrosis.

73
Q

What are the main Toxins that can cause mm toxicity?

A

Ionophores (monesin salinomycin, narasin, lasalocid), Gossypol -cotton seed. Toxic plants (coffee senna) in horses, cattle, sheep and goats.

74
Q

What spp. is most suseptable to Ionophores? What ionophore in particular?

A

Horses, in particular Monesin.

75
Q

Pathogenesis of Ionophor mm. toxicity?

A

ionophores facilitate moevement of cations –> disruption of normal ionic equalibrium –> Ca2+ overload –> necrosis, death from cardiovascular shock/collapse

76
Q

List all Elecrolyte abnormality myopathies.

A

HYPOKAlemia, HYPERNAtremia, HypoPhosatemia

77
Q

What spp. get Hypokalemia related myopathy?

A

Cattle and Cats

78
Q

What effect on muscle does Hypokalemia have in cattle?

A

Profound weakness and recumbancy

79
Q

Etiology of Hypokalemic myopathy in cattle? (3)

A
  1. Hypokalemia due to Anorexia and Ketosis.2. Glucocorticoids w/ increased mineralcorticoid activity. 3. IV glucose/insulin = increase in cellular K inflow
80
Q

MM Pathologenesis of Hypokalemic myopathy?

A

Decrease in muscle K+ –> altered mitochondrial function and/or vasoconstriction (ischemia) –> myofiber necrosis. Hypokalemia also –> Abnormal cardiac conduction

81
Q

Lesions of hypokalemic myopathy?

A

Ischemic necrosis (from recumbancy), Myofiber necrosisVacuated myofibers.

82
Q

What effect on mm does hypokalemia have in cats?

A

Generalized weakness w/ ventri-flexion of the neck.

83
Q

Pathology of hypokalemia effect on mm in cats?

A

Hyperpolarization of CM –> 2* excess NA permeability –> altered mitochondrial function –> ischemia -> mm necrosis. Also Abnormal cardiac conduction from decreased K+

84
Q

What can hypokalemia eventually lead to in cats?

A

+/- chronic interstitial nephritis.

85
Q

what spp. is prone to hypernatremia?

A

Cats

86
Q

Pathology of Hypernatremia?

A

Increased muscle Na+ –> abnormal energy metabolism. Increased blood Na+ –> vasoconstriction –> ischema. Both lead to transient myofiber necrosis and regeneration.

87
Q

Hypophophatemia is linked to what spp?

A

Cattle

88
Q

CS of Hypophosphatemia related myopathy?

A

Profound mm weakness, neurologic signs, and Hemolytic anemia.

89
Q

What is the major stress induced myopathy?

A

Porcine Stress Syndrom (PSS) (also in dogs and horses)

90
Q

Which mm fibers are effected in PSS?

A

Type II

91
Q

Etiology of PSS?

A

Hereditary enzyme deficiency (Hal gene)–> hypermetabolic syndrome

92
Q

Pathology of PSS?

A

Defect in uptake, storage and release of Ca2+ due to Enzyme deficiency.Excess Ca in cell → hypercontraction, degen, and necrosis of fibers → membrane protein denaturation → mvmt of intracellular water into the interstitium

93
Q

What are the Ischemic injury myopathies?

A

Campartment syndrome and Deep pectoral myopathy

94
Q

How is compartment syndrome characterized?

A

Degeneration and necrosis of mm that are surrounded by heavy aponeurosis (connective tissue). Ex: well conditioned athletes and poultry deep pectoral musculature.

95
Q

What spp. gets Deep Pectoral Myopathy ?

A

Poultry

96
Q

Etiology and Pathogenesis of Deep Pectoral Myopathy?

A

Vigorous flapping of wings –> muscle expansion –> vascular compression –> eschemia –> infarctions

97
Q

What is downer syndrome?

A

ischemic necrosis of ventral and limb muscles following prolonged recumbency. Lesions appear as early as 6-12hrs.

98
Q

What two endocrine disorders cause myopathy?

A

Hypothyroidism, Hypercortisolism

99
Q

What type of atrophy results from endocrine myopathies?

A

Denervation Atrophy

100
Q

Myopathy caused by hypothyroidism lesions?

A

Marked type II atrophy in dogsGeneralized weakness, muscle atrophy (type II fibers), Megaesophagus, *Normal CK and AST.

101
Q

Pathologenesis of hypothyroidism related myopathy?

A
  1. Decrease in thyroid hormone –> decreased mm metabolism –> myofiber wekaness and atrophy. 2. Peripheral neuropathy (axonal degeneration) –> damage to motor nerves –> denervation atrophy
102
Q

How does hypercortisolism related myopathy present?

A

stiff pelvic limbs gait, increased bulk and tone of proximal thigh muscles. (cushingoid pseudomyotonia). And muscle weakness.

103
Q

Path of hypercortisolism related myopathy

A

increased cortisol production –> peripheral neuropathy –> denervation atrophy with regeneration.

104
Q

What is myositis?

A

mm inflammation

105
Q

What causes Hemorragic myositis?

A

Clostridium sp.

106
Q

Common examples of hemorragic myositis caused by Clostridium sp.?

A

Blackleg -ruminants. Gas grangrene - horse. Malignant edema - horses, ruminants and pigs.

107
Q

Pathogenesis of Hemorrhagic myositis?

A

Clostridium sp. –> activation of spores –> proliferation of bacilli –> toxin production –> vascular damage –> edema, hemorrhage, necrosis, myositis and emphysema.

108
Q

What causes suppurative myositis?

A

Pyogenic bacteria: -T. pyogenes, Strep spp., Staph spp., Corynebacterium. Psuedotuberculosis in horses.

109
Q

What causes granulomatous myositis?

A

Actinobacillus lingieresii - wooden tongue (pale granulomas). Actinomyces bovis –> Lumpy jaw (caseous granulomas)

110
Q

Protozoan parasitic myositis?

A

Sarcosystis spp (horse, cattle, sheep, camilids, pigs) Neospora caaninum (dogs, fetal cattle.)

111
Q

Nematode parasitic myositis?

A

Trichinella spiralis (pigs.)

112
Q

Cestode parasitic myositis?

A

Cysticercus spp (cattle, sheep, goats, pigs) - large visible cysts

113
Q

2 Eosinophilic types of myositis?

A

Eosinophilic myositis of ruminants, Masticatory muscle myositis of dogs (GSD)

114
Q

lesions of eosinophilic myositis?

A

Green! May turn to off white when exposed to air.

115
Q

Etiology of eosinophilic myositis?

A

Sarcosystosis, Immunologic injury - immune reaction to type II muscle fibers. Idiopathic.

116
Q

Immune mediated myosistis examples?

A

Polymyositis of dogs and purpura hemorrhagica in horses

117
Q

Polymyositis of dogs lesions?

A

Lymphoplasmacytic inflammation –> 1. Megaesophagus. 2. Atrophy, degeneration, necrosis.

118
Q

Pupura hemorrhagica in horses etiology?

A

Post-streptococcal infection following strangles –> immune complexes

119
Q

Lesions of purpura hermorrhagica?

A

Edema of the head and limbs. Leukocytoclastic vaculitis. Petechiae +/- glomerulonephritis.

120
Q

What are the three main neoplasias of muscle?

A

Rhabdomyoma, Rhabdomyosarcoma, Botyroid Rhabdomyosarcoma.

121
Q

Etiology/origin of Rhabdomyoma?

A

Congenital. Origin = 66% heart

122
Q

Lesions of Rhabdomyoma?

A

Large pedunculated mass made up of cells that resemble skeletal mm (cross striations) found embeded in heart. Benign

123
Q

Rhabdomyosarcoma =?

A

Malignant form of rhabdomyoma

124
Q

Rhabdomyosarcoma gross pathology?

A

Tumors are poorly encapsulated spherical nodules formed by pink/grey tissue. Metastasis to lung, spleen, lymph nodes and kidneys are common.

125
Q

Botryoid rhabdomyosarcoma is found in what spp?

A

large breed dogs.

126
Q

Origin of BRS?

A

embryonic myoblasts –> urinary trigone –> urinary bladder

127
Q

Disorders of neuromuscular junction?

A

Myasthenia gravis, botulism

128
Q

What is Myasthenia gravis?

A

weakness and severe muscle fatigue from mildest exercise due to reduction of Ach receptors

129
Q

Congenital myasthenia gravis etiology?

A

Low # of Ach receptor.

130
Q

Lesions of congenital myasthenia gravis?

A
  1. no change. 2. disuse atrophy. 3. fibrous.
131
Q

Aquired Myasthenia gravis etiology?

A

Autoimmune - IgG to Ach receptors.

132
Q

Lesions of aquired A MG?

A

Muscle weakness –> 2* Dz:1. Megaesophagus –> asperiation pneumonia. 2. Dysphagia. 3. Thymoma

133
Q

Tx of A MG?

A

Anti-Cholinergic drugs (neostigmine) –> dramatic improvement

134
Q

Etiology of Disorders of Tendons?

A

Congenital anomalies (contracted tendons), Physical injury (Perosis of bird), Inflammation (tendonitis, parasitic.)

135
Q

Perosis of birds is what?

A

Displacement of tendons - gastrocnemius m. Due to dietary Mn or Choline deficiency.

136
Q

Tendonitis etiology

A

trauma or penetrating wound.

137
Q

Bowed tendon =?

A

Thickened lateral deviation of tendon

138
Q

Parasitic tendonitis is caused by what?

A

Onchocerca spp. –> ligamentum nuchae

139
Q

Lesions of parasitic tendonitis?

A

Fibrous nodules = “worm nodules or worms nest”

Pathology II Master (15 decks)

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