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Pathology II Master > Muscle Pathology (AH) > Flashcards

Muscle Pathology (AH) Flashcards

Stars indicate past TQ according to Muzzy

1
Q

Type I mm fibers

A

red -slow twitch - small
more mitochondria
no glycogen - no glycolytic.

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2
Q

Type II mm fibers

A 
White - fast twitch - large - 
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

What spp. get muscular Hyperplasia?

A

Calves and Lambs

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6
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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7
Q

What spp. gets myofibrillar hypoplasia?

A

Pigs

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8
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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9
Q

Lesions of myofibrillar hypoplasia?

A

mm are atrophic
flabby
pale
wet.

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10
Q

Pathogenesis of Polysaccharide storage myopathy in horses?

A

Carbohydrate metabolic disorger –> insufficient energy production (decrease) in mm.

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11
Q

What can occur secondary to Polysaccharide storage myopathy in horses?

A

Acute myoglobinuric nephrosis (Pigment nephrosis) - tubule damage from myoglobin

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12
Q

Etiology of Glycogenoses (glycogen storage Dz)?

A

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

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13
Q

What is Myotonia?

A

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

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14
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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15
Q

HYPP sequelae?

A

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

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16
Q

Although it occurs in all domestic spp., what two species are prone to Arthrogryposis?

A

calves and lambs

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17
Q

What is Arthrogyposis?

A

Muscle hypoplasia due to lack of muscle innervation during gestation.

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18
Q

What do the limbs look like of animals with Arthrogyposis?

A

small limbs with rigid joints –> crooked looking limbs.

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19
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 –> 1. inherited in suffolk lambs,
2. Plant poisoning (lupinus spp.) causes decreased movement in

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20
Q

What is the primary defect associated with Arthrogyposis?

A

Always associated with spinal and brain abnormalities.

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21
Q

What are the categories of mm disturbances of growth?

A 
Atrophy
Hypertrophy
Metaplasia
Infiltration
Muscular Dystrophy
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22
Q

What is mm atrophy?

A

decrease in size of cells that have gained full development

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23
Q

Mm atrophy pathogenesis?

A
  1. Diminished level of work

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

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24
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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25
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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26
Q

Etiology of denervation atrophy?

A

Lack of tonic stimuli due to :

  1. Damage to PNS (trauma, neoplasia, abscesses, pressure by disks) or
  2. Damage to CNS (disk protrusion, chronic meningitis, trauma, metastatic lesions, localized spinal malacia)
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27
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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28
Q

Lesions of denervaiton atrophy?

A

diffuse atrophy involving BOTH type I and II fibers

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29
Q

Etiology of Disuse atrophy?

A

Loss of tonic stimuli (but still intact) secondary to inactivity or limitation of movement (fractures, upper motor neuron damage, recumbency) Usually localized.

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30
Q

Lesions of Disuse atrophy?

A

Mainly involves Type II fibers.

Flabby shruken muscles.

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31
Q

What is the most common form of Atrophy?

A

Atrophy of malnutrition and cachexia.

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32
Q

Etiology of atrophy of malnutrition and cachexia?

A 
malnutrition
starvation
severe helminthosis
chronic debilitating diseases (TB, Johne's Dx)
Neoplasia
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33
Q

Lesions of atrophy of malnutrition an cachexia?

A

type II fibers involved.

Small, thin, dark, sticky, flabby mm.

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34
Q

What type of atrophy is similar to malnutrition and cachexia atrophy?

A

Senile atrophy

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35
Q

Lesions of senile atrophy?

A

Malnutrition + Lipofuscin –> yellow brown color, especially in diaphram.

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36
Q

What causes pressure atrophy?

A

prolonged pressure of muscles from abscesses, tumors, parasitic cysts

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37
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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38
Q

Etiology of hypertrophy?

A
  1. Physiologic - athletic training, pregnant uterus.
  2. Pathologic (left cardiac ventriclular hypertrophy.
  3. Idiopathic (esophagus, ileum - horses).
  4. Iatrogenic - steroids.
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39
Q

Lesions of hypertrophy?

A

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

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40
Q

What is steatosis?

A

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

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41
Q

How does steatosis alter the gross form of the affected muscle?

A

It doesn’t

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42
Q

What spp. is steatosis seen in?

A

pigs, sheep, cattle

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43
Q

How do mm affected by steatosis appear?

A

soapy, marbling appearance

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44
Q

Is steatosis clinically significant?

A

no, congenital defect with no clinical significance.

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45
Q

What is muscular dystrophy?

A

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

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46
Q

Etiology of muscular dystrophy?

A

Idiopathic (intact innervation, inadequate regeneration, primary myofiber defect)
Hereditary

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47
Q

General lesions of muscular dystrophy?

A

degeneration and failed attempts to regenerate –> fibrosis.

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48
Q

What animals get hereditary muscular dystrophy?

A

Marino sheep.
Dogs - Canine X-linked mm dystrophy.
Labrador retrievers - HMLR (early in life)

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49
Q

Clinical presentation of HMLR?

Lesions?

A

In young dogs.
Bunny hopping.
+/-megaesophagus –> aspiration pneumonia.
Lesions: Type II myofiber deficiency –> decreased mm mass. Segmental necrosis and regeneration.

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50
Q

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

A

Dystrophin deficiency.

Duchenne type

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51
Q

Lesions of ruptured mm?

A

Swollen by edema and hemorrhage.

Tearing of mm.

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52
Q

What specific condition is associated with mm rupture?

Who gets it?

A

Fibotic and ossifying myopathy

torn hamstring in quarter horses

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53
Q

Sequelae of ruptured mm.?

A

Diaphragmatic rupture –> eventration.
Rent in the cascial sheath –> eventration.
In racing greyhounds –> muscle ruptrue during strenuous activity.

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54
Q

Lesions of congestion?

A

swollen red to black.

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55
Q

What is an example of mm congestion?

A

Bovine ruminal tympany (bloat)

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56
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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57
Q

Thrombosis, Embolism, and infarction lesions?

A

hemorrhage and necrosis in infarcted muscle, thrombus

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58
Q

What are the three responses of mm to injury?

A

degeneration, necrosis, regeneration

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59
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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60
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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61
Q

Gross lesions of mm degeneration?

A

Degenerated mm. appear pale.
** 1. Chalky/white = severe calcification.
Red = hemorrhage/ rhabdomyolysis (myoglobin release)**

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62
Q

Micro lesions of mm degeneration?

A
  • **1. Hypereosinophilia (green).
    2. Dystrophic calcification (bluish granules in myofibers w/ von kossa stain).
    3. Vacuoles and loss of striations.
    4. Swelling.
    5. Glassy or hyaline appearance (zenker’s degeneration).
    6. Segmental rupture of fibers.
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63
Q

Types of mm degeneration?

A

Hyaline/waxy = Zenker’s (most common) - irreversible.
Granular.
Vacuolar (hydropic) = increased glycogen.
Fatty.
Lipofuscin (xanthomatosis) = yellow/brown.

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64
Q

When is mm degeneration irreversible?

A

once necrosis ensues

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65
Q

Ddx for degeneration?

A

gross lesion = pallor.

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

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66
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 damage
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67
Q

What causes segmental necrosis?

A

physical insult, toxemia, myopathy, ischemia/infaction, bacterial emboli

68
Q

What causes total necrosis?

A

extensive infarcts, massive trauma, large burns

69
Q

Gross/Micro lesions of necrosis?

A

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

70
Q

What are the main categories of degenerative myopathies?

A

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

71
Q

List all nutritional myopathy syndromes?

A

While muscle Dz, Stiff lamb Dz, Porcine vit E/Se responsive disease complex, Pansteatitis in cats, Brown dog gut, Masticatory myopathy and polymyopathy in foals, muscle necrosis and steatitis in rabbits

72
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

73
Q

What type of mm. is most effected by WMD?

A

Muscles with higher activity (type I) are affected most = diaphragm, intercostals, tongue, heart.

74
Q

Histopathology of WMD?

A

Hypereosinophilia, Calcification, segmental degeneration (zenker’s), proliferation of myostatellite cells, macrophages, fiber framentation(retraction caps) ==> features of necrosis

75
Q

What animals get white muscle disease (WMD) most often?

A

calves and lambs. Also in pigs.

76
Q

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

A

Mulburry heart and heptatitis dietetica

77
Q

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

A

RV in sheep, LV in calves

78
Q

What lesions give Nutritional Myopathy the name WMD?

A

Severe calcification following necrosis –> Patchy white streaks with pronouned chalkey whiteness.

79
Q

In pigs, 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)

80
Q

What is exertional myopathy?

A

Dz resulting in severe muscle degeneration following strenuous exercise.

81
Q

Lesions of exertional myopathy?

A

Similar to WMD but affecting type II fibers. Acute degeneration –> rhabomyolysis. Type II fibers affected (glycolytic).

82
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

83
Q

* TQ Exertional Myopathy Syndromes by Spp.?*

A

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

84
Q

By what other names is Azoturia known in horses?

A

Eq. paralytic myogobinuria, Monday morning dz, sacral paralysis, exertional rhabdomyolysis.

85
Q

CS of Azoturia?

A

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

86
Q

Azoturia etiology?

A

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

87
Q

Azoturia lesions?

A

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

88
Q

Sequelae of Azoturia?

A

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

89
Q

What is the less severe form of Azoturia?

A

Tying-up/setfast/ acute rhabdomyolysis in horses.

90
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.

91
Q

Which form of Exertional Myopathy presents with pronounced Acidosis?

A

Capture Myopathy

92
Q

Lesions of Capture myopathy?

A

Bilateral Symetry, Pale, swollen, edematous muscles. Hemorrage, ruptured tendons, myocardial injury (congestive HF)

93
Q

Lesions of muscle toxicity?

A

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

94
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.

95
Q

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

A

Horses, in particular Monesin.

96
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

97
Q

List all Elecrolyte abnormality myopathies.

A

Hyopkalemia, hypernatremia, hypophosphatemia

98
Q

What spp. get Hypokalemia related myopathy?

A

Cattle and Cats

99
Q

What effect on muscle does Hypokalemia have in cattle?

A

Profound weakness and recumbancy

100
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
101
Q

MM Pathologenesis of Hypokalemic myopathy?

A

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

102
Q

Lesions of hypokalemic myopathy?

A

ischemic necrosis (from recumbancy), myofiber necrosis and vacuated myofibers.

103
Q

What effect on mm does hypokalemia have in cats?

A

Generalized weakness w/ ventroflexion of the neck

104
Q

Etiology of hypokalemia in cats

A

Abnormal skeletal mm metabolism. Ischema due to vasoconstriction, decrease in dietary K+ intake. Increased urinary exretion of K+ followeing chronic renal dz. 2* to GIT dz or inappropriate fluid therapy. Hyperthyroidism

105
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+

106
Q

What can hypokalemia eventually lead to in cats?

A

+/- chronic interstitial nephritis.

107
Q

what spp. is prone to hypernatremia?

A

Cats

108
Q

Pathology of Hypernatremia?

A

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

109
Q

Hypophophatemia is linked to what spp?

A

Cattle

110
Q

CS of Hypophosphatemia related myopathy?

A

Profound mm weakness, neurologic signs, and Hemolytic anemia.

111
Q

What is the major stress induced myopathy?

A

Porcine Stress Syndrom (PSS)

112
Q

Besides pigs, what other spp. can get PSS?

A

pigs, dogs, horses can all get PSS

113
Q

Which mm fibers are effected in PSS?

A

Type II

114
Q

Etiology of PSS?

A

Hereditary enzyme deficiency (Hal gene)–> hypermetabolic syndrome

115
Q

Pathology of PSS?

A

Defect in uptake, storage and release of Ca2+ due to Enzyme deficiency –> increase in intracellular Ca2+ via ATPase –> increased glycolysis/ increase in body temp –> Lactate buildup –> denaturing of sarcoplasmic proteins –> movement intracellular H2O

116
Q

What are the Ischemic injury myopathies?

A

Campartment syndrome and Deep pectoral myopathy

117
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.

118
Q

What spp. gets Deep Pectoral Myopathy ?

A

Poultry

119
Q

Etiology and Pathogenesis of Deep Pectoral Myopathy?

A

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

120
Q

What is downer syndrome?

A

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

121
Q

What is Eq. post-anesthetic hypotensive myopathy?

A

Anesthesia induced hypotension –>severity varies from mm swelling with lameness to paresis with renal failure and shock. Sequelae = perm. Loss of mm function.

122
Q

muscle crush syndrome

A

acute degenerative myopathy caused by severe trauma to a mm group. Similar to downer syndrom in pathogenesis and lesions.

123
Q

What two endocrine disorders cause myopathy?

A

Hypothyroidism, Hypercortisolism

124
Q

What type of atrophy results from endocrine myopathies?

A

Denervation Atrophy

125
Q

How does myopathy caused by hypothyroidism present?

A

generalized weakness, muscle atrophy (type II fibers), megaesophagus, normal CK and AST.

126
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
127
Q

Lesions of hypothryroidism?

A

marked type II atrophy in dogs

128
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.

129
Q

Path of hypercortisolism related myopathy

A

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

130
Q

What is myositis?

A

mm inflammation

131
Q

What types of myositis are there?

A

Infectious - bacterial viral parasitic. Immune-mediated - eosinophilic. Idiopathic.

132
Q

What causes Hemorragic myositis?

A

Clostridium sp.

133
Q

Common examples of hemorragic myositis caused by Clostridium sp.?

A

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

134
Q

Pathogenesis of Hemorrhagic myositis?

A

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

135
Q

What causes suppurative myositis?

A

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

136
Q

What causes granulomatous myositis?

A

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

137
Q

Protozoan parasitic myositis?

A

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

138
Q

Nematode parasitic myositis?

A

Trichinella spiralis (pigs.)

139
Q

Cestode parasitic myositis?

A

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

140
Q

2 Eosinophilic types of myositis?

A

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

141
Q

lesions of eosinophilic myositis?

A

Green!

142
Q

Etiology of eosinophilic myositis?

A

sarcosystosis, immunologic injury - immune reaction to type II muscle fibers. Idiopathic.

143
Q

Immune mediated myosistis examples?

A

Polymyositis of dogs and purpura hemorrhagica in horses

144
Q

Polymyositis of dogs lesions?

A

Lymphoplasmacytic inflammation –> 1. megaesophagus. 2. Atrophy, degeneration, necrosis. 3. infiltraion of lymphocytes and plasma cells.

145
Q

Pupura hemorrhagica in horses etiology?

A

Post-streptococcal infection following strangles –> immune complexes

146
Q

Lesions of purpura hermorrhagica?

A

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

147
Q

What are the three main neoplasias of muscle?

A

Rhabdomyoma, Rhabdomyosarcoma, Botyroid Rhabdomyosarcoma.

148
Q

Etiology/origin of Rhabdomyoma?

A

Congenital. Origin = 66% heart

149
Q

Lesions of Rhabdomyoma?

A

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

150
Q

Rhabdomyosarcoma =?

A

Malignant form of rhabdomyoma

151
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.

152
Q

Botryoid rhabdomyosarcoma is found in what spp?

A

large breed dogs.

153
Q

Origin of BRS?

A

embryonic myoblasts –> urinary trigone –> urinary bladder

154
Q

Disorders of neuromuscular junction?

A

Myasthenia gravis, botulism

155
Q

What is Myasthenia gravis?

A

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

156
Q

Congenital myasthenia gravis etiology?

A

Low # of Ach receptor.

157
Q

Lesions of congenital myasthenia gravis?

A
  1. no change. 2. disuse atrohpy. 3. fibrous.
158
Q

Aquired Myasthenia gravis etiology?

A

Autoimmune - IgG to Ach receptors.

159
Q

Lesions of aquired A MG?

A

muscle weakness –> 2* 1. Megaesophagus –> asperiation pneumonia. 2. Dysphagia. 3. Thymoma

160
Q

Tx of A MG?

A

Anti-Cholinergic drugs (neostigmine) –> dramatic improvement

161
Q

Etiology of Disorders of Tendons?

A

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

162
Q

Perosis of birds is what?

A

displacement of tendons - gastrocnemiusm Due to dietary Mn or Choline deficiency.

163
Q

Tendonitis etiology

A

trauma or penetrating wound.

164
Q

Bowed tendon =?

A

thickened lateral deviation

165
Q

Parasitic tendonitis is caused by what?

A

Onchocerca spp. –> ligamentum nuchae

166
Q

Lesions of parasitic tendonitis?

A

Fibrous nodules = “worm nodules or worms nest”

Pathology II Master (15 decks)

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