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1
Q

name the dz and its lesions

A

horse mm. azoturia, rhybdomylysis

  • moist, swollen, dark red, hamorrhages
    • hyaline degeneration and necrosis of skeletal mm.
    • later fibrosis,atrophy, muscle pallor
  • myoglobinuric nephrosis >> kidneys: dark-black
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2
Q

expalin the lesion and for what dz it is for

A

myoglobinuric nephrosis in azoturia

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3
Q

Azoturia (equine paralytic myoglobinuria; Monday
morning disease)
– sequelae

A
  • death from cardiac and renal injury
  • recovery and repeated episodes —> muscularatrophy
  • recovery with muscular regeneration
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4
Q

Tying-up (setfast, acute rhabdomyolysis)

A

transient

– less severe form of azoturia

– mild rhabdomyolysis

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5
Q

examples of azoturia in cattle n dogs

A

Zebu type or “wild” cattle more prone
– associated with handling and transportation over long
distances in crowded railway trucks

in dogs (racing greyhounds)

– occurs rarely
– following intense muscular exertion

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6
Q

Capture myopathy

A

wild animals and birds

following capture and/or translocation over long

distances, chase, struggle*

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7
Q

Capture myopathy etiopathogenesis

A

pronounced acidosis

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8
Q

Capture myopathy lesions

A

*bilaterally symmetrical

*pale, edematous muscles

*muscle degeneration, hemorrhage, ruptured tendons

*myocardial injury –> death from congestive heart failure

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9
Q

Toxic Ionophores (monensin, salinomycin, narasin)

A

added to feeds for poultry and ruminants for
antibiotic and growth-enhancing effects

  • equidae, ruminants, dogs, birds
  • susceptibility highest in horses
      – coaccidental feeding within horse feed

  – accidental feeding
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10
Q

Ionophores (monensin, salinomycin, narasin) pathogenesis

A

ionophores facilitate movement of cations (Na+, Ca2+) across CMs leading to disruption of normal ionic
equilibrium

Ca2+ overload causes necrosis of skeletal and cardiac muscle

death from cardiovascular collapse/shock

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11
Q

Toxic Ionophores (monensin, salinomycin, narasin) lesions

A

-monophasic multifocal segmental necrosis

– pallor

– regeneration

– myocardial fibrosis

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12
Q

Toxic Lesions:

A

• segmental necrosis in skeletal and cardiac muscle
± calcification, regeneration, fibrosis

• hemorrhage and myonecrosis

• necrosis restricted to skeletal muscle in
mycotoxicosis

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13
Q

Electrolyte-related myopathies

A

– quarter horses and related breeds

– inherited: autosomal dominant

genetic mutation in sodium channel gene

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14
Q

Hyperkalemic periodic paralysis (HYPP) cs

A

laryngeal muscle dysfunction
• laryngospasms

trembling, weakness, collapse

metabolic acidosis
cardiotoxicity, pulmonary edema

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15
Q

HYPP pathogenesis

A

-delayed inactivaton of sodium channel activity

– uncontrolled sodium influxes into the cell

– altered voltage

– continuous myofiber electrical activity

– uncontrolled twitching

• muscle trembling, weakness and collapse

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16
Q

HYPP gross lesions

A

limited to prominent muscling

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17
Q

HYPP treatment

A

low-potassium diet;

diuresis

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18
Q

cs of Hypokalemia in cattle

A

profound weakness and recumbency

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19
Q

Hypokalemia in cattle etiology

A
  • hypokalemia due to anorexia and ketosis
  • glucocorticoids with high mineralocorticoid activities

• I/V administration of glucose or insulin
– insulin increases the flow of K+into cells

decreased muscle K+

• altered mitochondrial function andvasoconstriction  (ischemia) → myofiber necrosis  – hypokalemia →abnormal cardiac conduction
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20
Q

cs of Hypokalemia in cats

A

generalized weakness with ventriflexion of the neck

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21
Q

hypokalemia mechanism/pathogenesis

A

hyperpolarization of the cell membrane

2° excessive permeability to Na

decrease muscle K+–> interference with muscle cell function –> myofiber necrosis

• abnormal cardiac conduction

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22
Q

Hypokalemia in cats etiology

A

*abnormal skeletal muscle energy metabolism

  • ischemia due to vasoconstriction
  • decreased dietary intake of K+

• increased urinary excretion of K+
following chronic renal disease

  • 2º to GIT disease or inappropriate fluid therapy
  • hyperthyroidism: increases activity of Na-K-ATPase
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23
Q

Hypokalemia lesions in cats

A

myofiber necrosis
• ± chronic interstitial nephritis

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24
Q

myofiber necrosis
• ± chronic interstitial nephritis

A

lesions of hypokalemia in cats

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25
Q

Hypernatremia in cats mechanism

  1. pathogenesis
  2. lesions
A

increased muscle Na+ →abnormal energy metabolism

increased Na+ in blood → vasoconstriction →ischemia

lesions: myofiber necrosis and regeneration

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26
Q

profound muscle weakness, neurologic signs,
hemolytic anemia

A

Hypophosphatemia in cattle

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27
Q

etiology of hypophosphotemia

A

dietary, vomiting, diarrhea

electrolyte imbalance: hypercortisolism,

renal disease, diuretics

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28
Q

lesions of Hypophosphatemia in cattle

A

myocardial and skeletal muscle necrosis

• ischemic necrosis secondary to recumbency

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29
Q

malignant hyperthermia, PSE pork, “herztod”, back
muscle necrosis

A

Porcine stress syndrome (PSS)

inherited
• Landrace, Pietran, Hampshire, Yorkshire, Poland
China

– life-threatening, hypermetabolic syndrome
– also seen in dog, horse

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30
Q

Porcine stress syndrome (PSS) pathoetiology

A

– respiratory and metabolic acidosis

– myoglobinemia, hyperkalemia, high blood lactate

– hyperthermia

– cardiovascular collapse >> death

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31
Q

causes of Porcine stress syndrome (PSS)

A

stresses
 fighting
 exercise
 crowding
 transport
 handling
 overheating
 slaughter
 halothane anesthesia

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32
Q

Porcine stress syndrome (PSS) pathogenesis

A

congenital enzyme deficiency.defect in uptake, storage, and release of Ca2.high intracellular Ca.increased glycolysis

build up of lactate

increased body heat

   hypercontraction and denaturation           →necrosis

movement of intracellular water into interstitium–wet, exudative muscles

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33
Q

Porcine stress syndrome (PSS) lesions

A

usually type II fibers affected

back muscle necrosis, edema

pale, soft and exudative (PSE)

pulmonary edema, hydrothorax, ascites

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34
Q

pale, soft and exudative (PSE)

A

PSS LESIONS

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35
Q

pulmonary edema, hydrothorax, ascites

A

PSS LESIONS

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36
Q
  1. DZ
  2. LESIONS
  3. SPP
  4. PATHOGENESIS
A
  1. PSS
  2. BACK MUSCLE NECROSIS, EDEMA.
  3. SOFT PALE N EXUDATIVE
  4. PULMONARY EDEMA, HYDROTHORAX,ASCITES
    * PIGS
    * POOR INTRACELLULARCAREGULATION
    * INFLUX OF CA INTO THE CELL
    * INCREASED GLYCOLYSIS
    * HYPERCONTRACTABILITY LEADING TO NECROSIS
    * HEAT PRODUCTION
    * INFLUX OF INTRACELLULAR WATER
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37
Q

Compartment syndrome PATHOGENESIS

A

ISCHEMIC MYOPATHY

muscular expansion →vascular compression
ischemia →infarction

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38
Q

Compartment syndrome IN CHICKEN

A

Deep pectoral myopathy
• turkey, chicken
• exertion
↓
• vigorous flapping of
wings
↓
• necrosis of muscles
(supracoracoid)

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39
Q

ischemic necrosis of ventral and limb muscles following prolonged recumbency

  • DZ
  • RECUMBENCY
A

DOWNER’S SYNDROME

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40
Q

Downer syndrome pathogenesis

A

prostration(exhaustion)

  • muscle injury
  • edema
  • compression → venous occlusion
  • ischemia → injury
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41
Q

ischemia/degeneration/fibrosis (pale)
• congestion/hemorrhage /myoglobin (red)

A

LESIONS OFDowner syndrome

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42
Q

Equine post-anesthetic hypotensive myopathy

  1. cs
  2. lesions
  3. sequela
A

occurs in 3-6% of anesthetic cases

– muscle swelling with lameness

– paresis with renal failure and shock

– sequelae: permanent loss of muscle function

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43
Q

Equine post-anesthetic hypotensive myopathy sequelae

A

permanent loss of muscle function

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44
Q

acute degenerative myopathy due to severe trauma to a muscle group

A

Muscle crush syndrome

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45
Q

Muscle crush syndrome PATHOGENESIS N SYNDROME

A

similar to Downer syndrome

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46
Q

vascular occlusion
• ischemia →degeneration and necrosis of muscles

A

Aortic-iliac thromboembolism in cats and horses

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47
Q

CS OF HYPOTHYROIDISM IN MM.

A
  • generalized weakness
  • atrophy and
  • megaesophagus
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48
Q

PATHOGENESIS OF HYPOTHYROIDISM IN MM.

A

decreased thyroid hormone →affects muscle
metabolism → myofiber weakness and atrophy

  peripheral neuropathy (axonal degeneration) and
 damage to motor nerves → denervation atrophy
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49
Q

LESIONS OF HYPOTHYROIDISM

A

selective atrophy of type II fibers

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50
Q

Hypercortisolism

  1. sc
  2. lesions
  3. pathogenesis
A

– Cushingoid pseudomyotonia

– weakness followed by muscle atrophy (type II fibers)

– increased cortisol production or iatrogenic XS
• peripheral neuropathy →denervation atrophy with
regeneration

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51
Q

LESIONS OF HYPERCORTICOTISM

A
  • muscle atrophy, degeneration and necrosis
  • bilateral adrenocortical hyperplasia
  • +/- tumor (in the pituitary gland or adrenal gland)
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52
Q

myofiber necrosis and regeneration in cats

A

hypernatremia

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53
Q

the type of inflamation caused by bacteria on mm.

A

hemorrhagic

necrotizing

granulomatous

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54
Q

the type of inflammation caused by protozoa on mm.

A

gangrenous

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55
Q

type of inflammation caused by viruses on mm.

A

necrotic

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56
Q

type of inflammation caused by helminths

on mm

A

suppurative

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57
Q

the type of inflammation which is immune mediated

A

granulomatous

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58
Q

type of mm. inflammation which is idipathic

A

eosinophilic

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59
Q

most serious systemic viral infections are capable of
producing

what type of necrosis lesion

A

scattered foci of muscle necrosis

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60
Q

viruses that causes mm. inflamation( necrosis)

A

canine distemper

feline panleukemia

porcine encephal;opathy

hog cholera

FMV

bluetongue

newcastle

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61
Q

inflammatory dz which are immune mediated

  • dog
  • horse
A

dog: masticatory myositis and polymyositis
horse: purpura hemorrhagic

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62
Q

inflammatory dz which is immune mediated

A

iosinophilic myositis in rumminants

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63
Q

Bacterial myositis lesions

A
  1. hemorrhage
  2. supperative
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64
Q

Clostridium sp in ruminants

A

haemorrhagic myositis

blackleg

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65
Q

dz caused by clostridium sp. in horses,ruminants and pigs

A

malignant edema

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66
Q

pathogenesis of clostriium

A

– activation of spores → proliferation of bacilli →toxin
production →vascular damage →edema, hemorrhage,
necrosis, myositis, emphysema

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67
Q

Hemorrhagic myositis

A

blackleg (ruminants); Clostridium chauvoei

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68
Q

lesions of Hemorrhagic myositis

A

usually in the large muscles of pectoral and pelvic
girdles
• heart, tongue, diaphragm masticatory muscles may
also be involved

  • dark red and wet (“wet stage”)
  • black, dry, spongy (“dry stage”)
  • crepitant
  • sweetish to rancid odor
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69
Q

which dz causes this lesions

• dark red and wet (“wet stage”)

A

– blackleg (ruminants); Clostridium chauvoei

Hemorrhagic myositis

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70
Q

which dz causes this lesions

black, dry, spongy (“dry stage”)

A

– blackleg (ruminants); Clostridium chauvoei

Hemorrhagic myositis

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71
Q
  1. dz
  2. lesions
  3. type of microb
A
  1. Hemorrhagic myositis
  2. – blackleg (ruminants)
  3. wet stage–>dark red n wet
  4. dry stage–>black,dry spogy

clostridium chauvoei

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72
Q

other lesions of black leg

A
  • endocarditis
  • fibrinohemorrhagic pleuritis
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73
Q

malignant edema causes

A

– Clostridium septicum,

Clostridium perfringens

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74
Q

malignant edema (horses, ruminants, swine) lesions

A

severe edema

  • formation of bubbles of gas
  • hemorrhage → dark brown to black muscles
  • discoloration of the overlying skin
  • coldness of the affected part
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75
Q
  1. dz
  2. etiology
  3. cs
A

malignant edema

clostridium

  1. gas gangrene
  2. severe edema
  3. hemorrhage
  4. discoloration of the overlying skin
  5. coldness of the affected parts
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76
Q

Eosinophilic myositis Etiology

A

sarcocystosis

• immunologic injury (autoimmune reaction against
type IIc fibers of masticatory muscles)

• idiopathic

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77
Q

– Eosinophilic myositis of ruminants

A

idiopathic

hypersensitivity to Sarcocystis infection?

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78
Q

what are the lesions for hypereisinophilic in ruminants

A

focal necrosis

+eisinophilic infiltration

– well-demarcated green foci
» eosinophils impart the green color to muscle
» green color fades to “off-white” on exposure
to air

with chronicity
» focal necrosis and fibroplasia
» eosinophilic granulomas

79
Q

– Masticatory muscle myositis (MMM) of dogs

  1. what type of dz
  2. lesion in dog
A
  1. eisinophilic myositis
  2. relapsing eisinophilic myocytic in dog–>swollen painful jaws
80
Q

– Masticatory muscle myositis (MMM) of dogs is autoimmune against which mm. type

A

type 2 fibers

81
Q

pathogenesis of Masticatory muscle myositis (MMM) of dogs

A

antibodies to myosin isoform → myositis

– isoform shares antigenic determinants with
certain bacteria

82
Q

acute myositis

A

eisinophilic

83
Q

Masticatory muscle myositis (MMM) of dogs

  1. acute or chronic
  2. spp
  3. mm involved
A
  1. acute relapsing myositis
  2. most frequent in gsd
  3. mainly the mm. of masticatory.other mm.may be involved
84
Q

cs of Masticatory muscle myositis (MMM) of dogs

A
  • recurrent attack of pain
  • mandibular immobility
  • +/-swelling of the affected mm. (temporal,masseter, zygomatic)
  • mouth is held partial open
  • animal eats with pain
  • attacks lasts from 1 to 3 weeks
  • after attack the mm. become more atrophied
85
Q

Masticatory muscle myositis (MMM) of dogs

• acute stage

A

mm.are swollen, dark red, doughy or hard with yellow or pale streak of foci

marked eisinophilic infiltration,few plasma cells.

86
Q

Masticatory muscle myositis (MMM) of dogs

chronic stage

A

atrophy n necrosis is prominent

numerous plasma cells with fewer eisinophils (notice that with acute,there is more eisinophile bt few plasma cells)

87
Q

3 Immune-mediated myositis

A

polymyositis in dog

purpura hemorrhagica in horse

dermatomyositis in dog

88
Q

polymyocytis pathogenesis

A

involeves mostly mm.

lymphoplasmacytic inflmmation targeted
against myofibers >> myofiber necrosis

89
Q

lesions of polymyositis

A

megaesophagus

atrophy,degeneration,necrosis

infiltration of lymphocytes,plasma cells, occassionally eisinophiles

90
Q

megaesophagus

– atrophy, degeneration, necrosis

– infiltration of lymphocytes, plasma cells,
occasional eosinophil

are lesions of?

A

polymyositis in dog

91
Q

Purpura hemorrhagica in horses

  1. cause
A
  1. post streptococcal infection, associated with strangles
92
Q

cs of purpura hemorrhagica

A

edema of the head n limbs

leukocytoclastic vasculitis

petechiae
– mucosae, musculature, viscera
• ± glomerulonephritis

93
Q

edema of the head n limbs are lisions for

A

purpura hemorrhagica

94
Q

Purpura hemorrhagica in horses pathogenesis

A

immune complexes detected in the sera of horses
with post-strangles purpura hemorrhagica

• immune complexes contain IgA and S. equispecific antigens

95
Q

Dermatomyositis in dogs

  1. spp
  2. areas affected
A
  1. collies n shelties
  2. dermatatis:face, tip of tail, bony prominences
  3. _myositis : _masticatory muscles
96
Q

Granulomatous myositis lesions

A

white firm masses in muscle

  • caseous to necrotic centers
  • “sulfur granules
97
Q

white firm .caseus to necrotic ;”sulfer granules” masses in mm

A

granulomatous myositis

98
Q

cuases of granulomatous myositis

A

tb

higher bacteria

systemic mycosis

metazoan parasites–>• trichinosis, cysticercosis

Roeckl’s granuloma (cattle)

99
Q

wooden tongue is caused by?

and name the type of dz

A

Actinobacillus lignieresii causes

granulomatous myositis

100
Q

granulomatous myositis

Actinomycosis bovis causes

A

lumpy jaw

101
Q

granulomatous macosis

botryomycosis; horses and pigs is caused by

A

Staphylococcus aureus

102
Q

Viral myositis lesions

A

small poorly defined foci or streaks

• infarcts secondary to vasculitis
– e.g., bluetongue in sheep

• multifocal necrosis due to direct effect of virus on
myofibers
– enteroviruses, FMD virus

103
Q

Inflammatory myopathies
 Parasitic

A

uncommon in domestic animals
– high incidence in fish

– nematodes

     • most important is Trichinella spiralis in pigs
      • Ancylostoma caninum larva migrans --\> myositis
     • Toxocara canis --\> focal granulomatous myositis
     • Dirofilaria immitis --\> thromboembolsim --\>
       infarction
104
Q

trichinosis; Trichinella spiralis

A

the only nematode to enter cells as a part of its
life cycle
– 2 major biological phases
» enteric and visceral
– adult life of the parasite is spent in the intestine
of many species of carnivores
– females deposit larvae directly into lymphatics
» then to bloodstream → myocytes

105
Q

– trichinosis; Trichinella spiralis lesions

A

muscle cells undergo striking transformation
when invaded by larvae
» myofibrils within affected myocytes becomes disoriented

» myofilaments are detached and frayed at the
Z line
» most organelles degenerate and disappear
(especially the mitochondria and lysosomes)

106
Q

» myofibrils within affected myocytes become
disoriented
» myofilaments are detached and frayed at the
Z line
» most organelles degenerate and disappear
(especially the mitochondria and lysosomes)

A

trichinella spiralis in mm.

107
Q

–trichinosis; Tric hinella spiralislesions (cont..)

A

by day 21 PI, after infection, the cytoplasm of
transformed cells is filled with large arrays of
smooth endoplasmic reticulum

the larvae exist free in the cytoplasm and the
host cell secretes the acidic
mucopolysaccharides which form the dense
hyaline cyst wall

108
Q

cysticercus

  1. name the 2 parasides
  2. where they are found
  3. lesions
A

Taenia solium and Taenia saginata

– in heart, masseter, tongue

small, white or gray cysts

109
Q

small, white or gray cysts

A

cysticercus

110
Q

Inflammatory myopathies

protozoa

  1. in cats
  2. in dogs
  3. lesions
A

toxoplasma gondi in cats

neosporium caninuum in ogs

segmental necrosis to necrotising myositis

111
Q

segmental necrosis to necrotising myositis is due to which parasites

A

protozoa

dogs. neoporium caninuun
cats: t. gondi

112
Q

sarcosistosis

protozoa

A

– invasion of striated muscles of mammals, birds
and reptiles with Sarcocystis sp.

– parasites invade muscle fibers and grow to form
elongated spindle-shaped structures

113
Q

enlongated spindle shaped structures in mm.

A

sarcosistosis

114
Q

“white dots”
or “streaks” in affected muscle

A

sarcosistosis

115
Q

Sarcocystosis
– tissues most commonly affected

A

» skeletal muscles in general, tongue, heart,
esophagus and diaphragm

116
Q

Rhabdomyoma

primary neoplasia

  1. lesions
  2. organ affecte
A

benign

  • congenital
  • cow, sheep, pig
  • origin: heart (66%)
  • large pedunculated mass in the heart
  • cross-striation
117
Q

Rhabdomyosarcoma

primary

  1. nt reported in which animal?
  2. lesions
A

malignant
• distant metastasis
– lung, spleen, lymph nodes, kidneys
• cow, sheep, dog, horse; not reported in pigs
• poorly encapsulated spherical nodules
– formed by pink/grey tissue

118
Q

which neoplasia has poorly encapsulated nodules

A

rhabdomyosarcoma

119
Q

Botryoid rhabdomyosarcomas

  1. spp n age affected
  2. shape
  3. where it arises
A
  1. young (< 18 months) large breed dogs especially St.
    Bernard
  2. botryoid: shaped like a bunch of grapes
  3. arise from sites with no striated muscle
    • kidney, urinary bladder (trigone, urethra)
120
Q

Myasthenia gravis

  1. spp
  2. cs
  3. cause
  4. breeds
A
  1. dogs n cats
  2. mm. weakness n fatique
  3. – deficiency of acetylcholine receptors
    – congenital or acquired
  4. reported in Jack Russell terriers, springer spaniels, and smooth fox terriers(congenital)
121
Q

myasthenia gravis

  1. differentiate congenital vs acquired
  2. which one is autoimmune
A

Ach receptor mulfxn in acquired–> autoimmune

congenital–>less Ach released—>no autoimmune

122
Q

Acquired myasthenia gravis associated lesions:

A

megaesophagus
• dysphagia
• secondary aspiration pneumonia
• thymoma

123
Q

Botulism

  1. pathogenesis
A

toxins produced by Clostridium botulinum
• ingested from feed or produced in the gut
– toxins bind irreversibly to the presynaptic nerve
terminals, preventing release of acetylcholine

124
Q

Botulism lesions

A

profound generalized flaccid paralysis

– dysphagia, tongue weakness, aspiration pneumonia

– recumbency –> ischemia and focal necrosis

125
Q

Displacement – perosis of birds

A

dietary deficiency of Mn or choline
• lateral displacement of gastrocnemius tendon
• collapse of hock

126
Q

Tendonitis – “bowed tendon” in chicken is caused by

A

viral arthritis (reovirus)

127
Q

tenosynovitis in chicken is caused by

A

trauma, penetrating wound

• distension of tendon sheath by exudate
– serous, fibrinous or purulent

128
Q

Onchocerca spp.

Parasitic diseases of tendons

A

adults live in tendons, tendon sheaths, or
connective tissues of the brisket, abdominal wall
or ligamentum nuchae

– liberate microfilariae over long periods

129
Q

fibrous nodules (“worm nodule” or “worm nest”)

A

Onchocerca spp

130
Q

lesions of oonchoceca spp

A

fibrous nodules (“worm nodule” or “worm nest”)
– brisket
– external surfaces of hind limbs
– ligamentum nuchae

131
Q

Endochondral ossification sequence of
events

A
  1. –mineralization of the physis
  2. apoptosis of chondrocytes
  3. ** vascular** invasion of cartilage
132
Q

Deficiency of mineralized bone dz

A

Osteoporosis

Rickets

Osteomalacia

Fibrous osteodystrophy

Drug-induced osteodystrophy

Hypovitaminosis C

133
Q

Osteoporosis (atrophy) is characterized by

A

a decrease in bone mass (osteopenia)

  • enlargement of bone spaces
  • increased fragility of affected bones

the remaining bone is normally mineralized

134
Q

etiolgy of esteoperosis

A

• imbalance between bone formation and resorption in
favor of resorption

135
Q

mm.are swollen, dark red, doughy or hard with yellow or pale streak of foci

A

acute eosinophilic muscle myositis

136
Q

which dz causes laryngospasms

A

HYPP

137
Q

Affected mm atropic, flabby, pale & wet

A

myofibrilar hypoplasia (splay leg)

138
Q

causes of splay leg(myofibrilar hypoplasia)

A
  1. heditory
  2. teratogenic–>exposure to chlorine or methenione def.
139
Q

Carb metabolic disorder > insufficient energy production

A

Polysaccharide Storage Myopathy

140
Q

lesions of Polysaccharide Storage Myopathy

A

Mm pale pink or diffusely red;

acute myoglobinuric nephrosis (pigment nephrosis);

↓mm mass;

severe acute to subacute myofibril necrosis

141
Q

Mm pale pink or diffusely red; acute myoglobinuric nephrosis (pigment nephrosis); ↓mm mass; severe acute to subacute myofibril necrosis

A

polysaccharide storage myopathy

142
Q

: recurrent exertional rhabdomyolysis, stiff gait, symmetric mm atropy, weakness (bilat pelvic limb or generalized

A

polysaccharide storage myopathy`

143
Q

what are the cs of polysaccharide storage myopathy

A

: recurrent exertional rhabdomyolysis,

stiff gait,

symmetric mm atropy,

weakness (bilat pelvic limb or generalized

144
Q

Accum of excess glycogen due to metab defect (or missing enzyme)

A

Glycogenoses (glycogen storage dz

145
Q

: mm weakness & incoordination

A

glycogenosis

146
Q

microscopic lesions of glycogenosis

A

glycogen storage in neurons, hepatocytes cardiac & skeletal mm

147
Q

Defective Cl channel activity > ↓Cl conductance and ionic instability of sarcolemma > continuous abnormal mm activity

A

Myotonia (channelopathies)

148
Q

: limited to prominan muscling

A

myotonia

149
Q

cs of myotonia

A

Sustained involuntary contraction of mm > spontaneous myotonia, generalized stiffness, exercise intolerance

150
Q

which equine muscular dz is associated with post anesthetic recumbency

A

HYPP

151
Q

arthrogryposis( crocked limbs” or congenital articular rigidity (CAR))

causes

A

inflas (egWesselsbron virus,

Bluetongue given during 1st trimester of pregnancy);

in utero viral infs (BVD, Akabane virus); Inherited?;

Plant poisoning;

admin of parbendazole (sheep) in 1st trimester

152
Q

Arthrogryposis (“crooked limbs” or congenital articular rigidity (CAR)) cs

A

decrease mm. ineversation

hypoplasia—>deformity of limbs

153
Q

Arthrogryposis (“crooked limbs” or congenital articular rigidity (CAR)) lesions

A

Cuvtaure & rigidity of joints;

atropy & dysplasia of mm (limb mm);

still born; hydrops amnii > dystocia; fibrosis > joint fixation; torticollis, scoliosis, kyphosis, distorted joints; congenital hernias (rare)

154
Q

still born; hydrops amnii > dystocia; fibrosis > joint fixation; torticollis, scoliosis, kyphosis, distorted joints; congenital hernias (rare)

A

arthrogroposis

155
Q

list different types of mm.atrophy

A

1) Denervation atrophy
2) Disuse atrophy
3) Malnutrition atrophy
4) Senile atrophy
5) Pressure atrophy

156
Q

what causes denervation atrophy in

  1. CNS
  2. PNS
A

damage to the CNS : disk potrution, chronic meningitis, trauma, metastatic lesions, localized spinal malacia

Damage to PNS: trauma, neoplasia, abscesses, pressure by discs

157
Q

causes of disuse atrophy

A

↓movement (fractures, rupture of tendons, joint immobility, ↓use (b/c pain), UMN damage, recumbancy

158
Q

causes of malnutrition atrophy

A

malnutrition,

starvation,

emaciation,

severe helminthiosis,

chronic inflammatory dz

, neoplasia & senility

159
Q

causes of Senile atrophy

A

sim to atropy of cachexia

160
Q

causes of Pressure atrophy

A

prolonged pressure on mm due to abscesses, tumors, parasitic cysts

161
Q

flabby & shrunken mm; type II fibers 1ᵒ involved (lesions localized to affected mm gps

A

disuse atrophy

162
Q

yellowish-brown to dk brown (due to lipofuscin 1° in diaphragm) mm.

A

pressure atrophy

163
Q

laryngeal hemiplasia (roarers) or damage to L recurrent laryngeal n.;

Sweeny (atrophy of supraspinatus mm.b/c damage to suprascapular n.; mm atrophy (dogs) w/ radial or brachial paralysis (trauma)

are all examples of

A

denervation atrophy

164
Q

Firm, gritty, white, boney plates in mm

A

metaplasia

165
Q

Inadequacy of regen in myofibril; degen changes > ↓mm fibers > eventually replaced by fat * fibrous CT

A

mm.dystrophy

166
Q

pathogenensis of mm. dystrophy

A

X-linked (dogs):myofibrer degen & necrosis; attempts at regen; ↓mm mass; replacement by fat; fibrosis

b)deficiency of type II fibers > atrophy +/-megaesophagus > aspiration pneumonia, segmental necrosis & regen

167
Q

lesions of mm.dystrophy

A

atrophy +/-megaesophagus > aspiration pneumonia, segmental necrosis & regen

pallor, firmness, atrophy, fibrosis

168
Q

cs of mm.dystrophy

A

)mm weakness, bunny hopping, exercise intolerance, collapse
c)neuro-mm weakness, stiff gait, exercise intolerance

169
Q

Glistening, chalky-white, opaque foci in mm;ngritty on cutting

A

calcium overload necrosis

170
Q

differentials for a black mm.

A

hemorrhages

melanosis

171
Q

causes of brown coloration in mm.

A

aging–>episodes of starvatin \caxemia

xanthomatosis–>aging, cachexia, hypovitaminosis E

172
Q

pathogenesis of brown mm.

A

lipofuscine ans lipofuscine like pigments accumulates in mm.

173
Q

causes of white mm. dz(nutritional myopathy)

A

Se/vit E def.

174
Q

apthogenesis for Nutritional myopathy (White mm dz)

A

Def in Se or Vit E > free radical formation > attack lipid membranes > lipid peroxides > destroy CMs > Ca influx > segmental necrosis

175
Q

Bilat, symmetrical lesions;

segmental necrosis,

calcification, regen;

Pigs: selective necrosis of type I fibers (diaphragm, intercostals, tongue, heart);

mm are pale w/ white streaks or pronounced chalky whiteness (Ca deposits); L ventricle in claves & R in sheep

A

white mm. dz

176
Q

mulbery heart dz

A

Porcine Vit E/Se responsive dz complex

177
Q

: deposition of ceroid-like pigment in sm. Mm (spleen, SI)

A

Brown dog gut

178
Q

calcified lesions in masticatory & tongue mm

A

Masticatory myopathy & polymyopathy (foals):

death from aspiration pneumonia

179
Q

lesions o MM necrosis & steatitis (rabbits)

A

necrosis in skeletal and heart mm

180
Q

cauuse of Azoturia (Equine paralytic myoglobinuria; Monday morning dz; Sacral paralysis; Exertional rhabdomyolysis)

A

Electorlyte abnormalities (Na, K, Ca);

Se def;

forced exercise after a period of rest and food restriction;

polysaccharide dz?

181
Q

Mm swelling w/lameness; paresis w/ renal failure & shock

A

Equine post-anesthetic hypotensive myopathy

182
Q

stiff; stilted pelvic limb gait w/ ↑bulk & tone or prox thigh mm; mm weakness

A

hyperadrenocorticotism

183
Q

well demarcated green foci

A

eosinophilic myositis

184
Q

leukocytoclastic vasculitis

A

purpura hemorrhagica

think about the bv inflamation.

185
Q

Multifocal necrosis of myofibers w/ focal interstitial & perivascular infiltrate of lymphocytes, macrophages and a few neuts

A

Porcine encephalomyelitis

186
Q

Heart & skeletal mm may have yellow streaks and grey foci of segmental myofiber necrosis w/ lymphocytic & neutrophilic infilt

A

foot n mouth

187
Q

Nonpurulent myositis in fetus

A

akabane dz

188
Q

Myofibers w/n affected mm become disoriented; myofilaments detach and fray at Z line; most organelles degen and disappear (esp mitochondria and lysosomes)

A

nematodes

189
Q

Sm white or grey cysts containing clear fluid and larva

Histo: min inflammatory response (few lymphocytes and/or eosinophils); dead larva become clacified

A

cestoides

190
Q

segmental necrosis to necrotizing myositis

b) gps of organisms surrounded by thick cyst of both paracytic and host origin; in many hosts can only observe parasites microscopically; in sheep, cattle, pigs and ducks cysts are white dots or streaks in affected mm
c) necrosis, myositis

A

protozoa

191
Q

large pedunculated mass in heart

A

rhabdomyoma

192
Q

Poorly encapsulated spherical nodules of pink/grey tissue

A

Rhabdomyosarcoma (1° neoplasm)

193
Q

shaped like a bunch of grapes
Histo: variable, w/ or w/o striation or giant cells

A

Botryoid rhabdomyosarcomas

Young <18 mos lg breed dogs (esp St Bernard); occurs in sites w/ no striated mm (urinary bladder, urethra); infiltrative and metastasis

194
Q
A

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