path Flashcards
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
2
Q
expalin the lesion and for what dz it is for
A
myoglobinuric nephrosis in azoturia
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
4
Q
Tying-up (setfast, acute rhabdomyolysis)
A
transient
– less severe form of azoturia
– mild rhabdomyolysis
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
6
Q
Capture myopathy
A
wild animals and birds
following capture and/or translocation over long
distances, chase, struggle*
7
Q
Capture myopathy etiopathogenesis
A
pronounced acidosis
8
Q
Capture myopathy lesions
A
*bilaterally symmetrical
*pale, edematous muscles
*muscle degeneration, hemorrhage, ruptured tendons
*myocardial injury –> death from congestive heart failure
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
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
11
Q
Toxic Ionophores (monensin, salinomycin, narasin) lesions
A
-monophasic multifocal segmental necrosis
– pallor
– regeneration
– myocardial fibrosis
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
13
Q
Electrolyte-related myopathies
A
– quarter horses and related breeds
– inherited: autosomal dominant
genetic mutation in sodium channel gene
14
Q
Hyperkalemic periodic paralysis (HYPP) cs
A
laryngeal muscle dysfunction
• laryngospasms
trembling, weakness, collapse
metabolic acidosis
cardiotoxicity, pulmonary edema
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
16
Q
HYPP gross lesions
A
limited to prominent muscling
17
Q
HYPP treatment
A
low-potassium diet;
diuresis
18
Q
cs of Hypokalemia in cattle
A
profound weakness and recumbency
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
20
Q
cs of Hypokalemia in cats
A
generalized weakness with ventriflexion of the neck
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
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
23
Q
Hypokalemia lesions in cats
A
myofiber necrosis
• ± chronic interstitial nephritis
24
Q
myofiber necrosis
• ± chronic interstitial nephritis
A
lesions of hypokalemia in cats
25
Hypernatremia in cats mechanism
1. pathogenesis
2. lesions
increased muscle Na+ →abnormal energy metabolism
increased Na+ in blood → vasoconstriction →ischemia
lesions: myofiber necrosis and regeneration
26
profound muscle weakness, neurologic signs,
hemolytic anemia
Hypophosphatemia in cattle
27
etiology of hypophosphotemia
dietary, vomiting, diarrhea
electrolyte imbalance: hypercortisolism,
renal disease, diuretics
28
lesions of Hypophosphatemia in cattle
myocardial and skeletal muscle necrosis
• ischemic necrosis secondary to recumbency
29
malignant hyperthermia, PSE pork, "herztod", back
muscle necrosis
Porcine stress syndrome (PSS)
inherited
• Landrace, Pietran, Hampshire, Yorkshire, Poland
China
– life-threatening, hypermetabolic syndrome
– also seen in dog, horse
30
Porcine stress syndrome (PSS) pathoetiology
– respiratory and metabolic acidosis
– myoglobinemia, hyperkalemia, high blood lactate
– hyperthermia
– cardiovascular collapse \>\> death
31
causes of Porcine stress syndrome (PSS)
stresses
fighting
exercise
crowding
transport
handling
overheating
slaughter
halothane anesthesia
32
Porcine stress syndrome (PSS) pathogenesis
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
33
Porcine stress syndrome (PSS) lesions
usually type II fibers affected
back muscle necrosis, edema
pale, soft and exudative (PSE)
pulmonary edema, hydrothorax, ascites
34
pale, soft and exudative (PSE)
PSS LESIONS
35
pulmonary edema, hydrothorax, ascites
PSS LESIONS
36
1. DZ
2. LESIONS
3. SPP
4. PATHOGENESIS
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
37
Compartment syndrome PATHOGENESIS
ISCHEMIC MYOPATHY
muscular expansion →vascular compression
ischemia →infarction
38
Compartment syndrome IN CHICKEN
Deep pectoral myopathy
• turkey, chicken
• exertion
↓
• vigorous flapping of
wings
↓
• necrosis of muscles
(supracoracoid)
39
ischemic necrosis of ventral and limb muscles following prolonged recumbency
* DZ
* RECUMBENCY
DOWNER'S SYNDROME
40
Downer syndrome pathogenesis
prostration(exhaustion)
* muscle injury
* edema
* compression → venous occlusion
* ischemia → injury
41
ischemia/degeneration/fibrosis (pale)
• congestion/hemorrhage /myoglobin (red)
LESIONS OFDowner syndrome
42
Equine post-anesthetic hypotensive myopathy
1. cs
2. lesions
3. sequela
occurs in 3-6% of anesthetic cases
– muscle swelling with lameness
– **_paresis with renal failure and shock_**
– sequelae: permanent loss of muscle function
43
Equine post-anesthetic hypotensive myopathy sequelae
permanent loss of muscle function
44
acute degenerative myopathy due to severe trauma to a muscle group
Muscle crush syndrome
45
Muscle crush syndrome PATHOGENESIS N SYNDROME
similar to Downer syndrome
46
vascular occlusion
• ischemia →degeneration and necrosis of muscles
Aortic-iliac thromboembolism in cats and horses
47
CS OF HYPOTHYROIDISM IN MM.
* generalized weakness
*
* atrophy and
* megaesophagus
48
PATHOGENESIS OF HYPOTHYROIDISM IN MM.
decreased thyroid hormone →affects muscle
metabolism → myofiber weakness and atrophy
```
peripheral neuropathy (axonal degeneration) and
damage to motor nerves → denervation atrophy
```
49
LESIONS OF HYPOTHYROIDISM
selective atrophy of type II fibers
50
Hypercortisolism
1. sc
2. lesions
3. pathogenesis
– Cushingoid pseudomyotonia
– weakness followed by muscle atrophy (type II fibers)
– increased cortisol production or iatrogenic XS
• peripheral neuropathy →denervation atrophy with
regeneration
51
LESIONS OF HYPERCORTICOTISM
* muscle atrophy, degeneration and necrosis
* bilateral adrenocortical hyperplasia
* +/- tumor (in the pituitary gland or adrenal gland)
52
myofiber necrosis and regeneration in cats
hypernatremia
53
the type of inflamation caused by bacteria on mm.
hemorrhagic
necrotizing
granulomatous
54
the type of inflammation caused by protozoa on mm.
gangrenous
55
type of inflammation caused by viruses on mm.
necrotic
56
type of inflammation caused by helminths
on mm
suppurative
57
the type of inflammation which is immune mediated
granulomatous
58
type of mm. inflammation which is idipathic
eosinophilic
59
most serious systemic viral infections are capable of
producing
what type of necrosis lesion
scattered foci of muscle necrosis
60
viruses that causes mm. inflamation( necrosis)
canine distemper
feline panleukemia
porcine encephal;opathy
hog cholera
FMV
bluetongue
newcastle
61
inflammatory dz which are immune mediated
* dog
* horse
dog: masticatory myositis and polymyositis
horse: purpura hemorrhagic
62
inflammatory dz which is immune mediated
iosinophilic myositis in rumminants
63
Bacterial myositis lesions
1. hemorrhage
2. supperative
64
Clostridium sp in ruminants
haemorrhagic myositis
blackleg
65
dz caused by clostridium sp. in horses,ruminants and pigs
malignant edema
66
pathogenesis of clostriium
– activation of spores → proliferation of bacilli →toxin
production →vascular damage →edema, hemorrhage,
necrosis, myositis, emphysema
67
Hemorrhagic myositis
blackleg (ruminants); Clostridium chauvoei
68
lesions of Hemorrhagic myositis
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
69
which dz causes this lesions
• dark red and wet ("wet stage")
– blackleg (ruminants); Clostridium chauvoei
Hemorrhagic myositis
70
which dz causes this lesions
black, dry, spongy ("dry stage")
– blackleg (ruminants); Clostridium chauvoei
Hemorrhagic myositis
71
1. dz
2. lesions
3. type of microb
1. Hemorrhagic myositis
1. – blackleg (ruminants)
1. wet stage--\>dark red n wet
2. dry stage--\>black,dry spogy
clostridium chauvoei
72
other lesions of black leg
* endocarditis
* fibrinohemorrhagic pleuritis
73
malignant edema causes
– Clostridium septicum,
Clostridium perfringens
74
malignant edema (horses, ruminants, swine) lesions
severe edema
* formation of bubbles of gas
* hemorrhage → dark brown to black muscles
* discoloration of the overlying skin
* coldness of the affected part
75
1. dz
2. etiology
3. cs
malignant edema
clostridium
1. gas gangrene
2. severe edema
3. hemorrhage
4. discoloration of the overlying skin
5. coldness of the affected parts
76
Eosinophilic myositis Etiology
sarcocystosis
• immunologic injury (autoimmune reaction against
type IIc fibers of masticatory muscles)
• idiopathic
77
– Eosinophilic myositis of ruminants
idiopathic
hypersensitivity to Sarcocystis infection?
78
what are the lesions for hypereisinophilic in ruminants
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
– Masticatory muscle myositis (MMM) of dogs
1. what type of dz
2. lesion in dog
1. eisinophilic myositis
2. relapsing eisinophilic myocytic in dog--\>swollen painful jaws
80
– Masticatory muscle myositis (MMM) of dogs is autoimmune against which mm. type
type 2 fibers
81
pathogenesis of Masticatory muscle myositis (MMM) of dogs
antibodies to myosin isoform → myositis
– isoform shares antigenic determinants with
certain bacteria
82
acute myositis
eisinophilic
83
Masticatory muscle myositis (MMM) of dogs
1. acute or chronic
2. spp
3. mm involved
1. acute relapsing myositis
2. most frequent in gsd
3. mainly the mm. of masticatory.other mm.may be involved
84
cs of Masticatory muscle myositis (MMM) of dogs
* 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
Masticatory muscle myositis (MMM) of dogs
• acute stage
mm.are swollen, dark red, doughy or hard with yellow or pale streak of foci
marked eisinophilic infiltration,few plasma cells.
86
Masticatory muscle myositis (MMM) of dogs
chronic stage
atrophy n necrosis is prominent
**numerous plasma cells with fewer eisinophils (notice that with acute,there is more eisinophile bt few plasma cells)**
87
3 Immune-mediated myositis
polymyositis in dog
purpura hemorrhagica in horse
dermatomyositis in dog
88
polymyocytis pathogenesis
involeves mostly mm.
lymphoplasmacytic inflmmation targeted
against myofibers \>\> myofiber necrosis
89
lesions of polymyositis
megaesophagus
atrophy,degeneration,necrosis
infiltration of lymphocytes,plasma cells, occassionally eisinophiles
90
megaesophagus
– atrophy, degeneration, necrosis
– infiltration of lymphocytes, plasma cells,
occasional eosinophil
are lesions of?
polymyositis in dog
91
Purpura hemorrhagica in horses
1. cause
1. post streptococcal infection, associated with strangles
92
cs of purpura hemorrhagica
## Footnote
edema of the head n limbs
leukocytoclastic vasculitis
petechiae
– mucosae, musculature, viscera
• ± glomerulonephritis
93
edema of the head n limbs are lisions for
purpura hemorrhagica
94
Purpura hemorrhagica in horses pathogenesis
immune complexes detected in the sera of horses
with post-strangles purpura hemorrhagica
• immune complexes contain IgA and S. equispecific antigens
95
Dermatomyositis in dogs
1. spp
2. areas affected
1. collies n shelties
2. **_dermatatis:_**face, tip of tail, bony prominences
3. **_myositis : _**masticatory muscles
96
Granulomatous myositis lesions
white firm masses in muscle
* caseous to necrotic centers
* "sulfur granules
97
white firm .caseus to necrotic ;"sulfer granules" masses in mm
granulomatous myositis
98
cuases of granulomatous myositis
tb
higher bacteria
systemic mycosis
metazoan parasites--\>• trichinosis, cysticercosis
Roeckl's granuloma (cattle)
99
wooden tongue is caused by?
and name the type of dz
Actinobacillus lignieresii causes
granulomatous myositis
100
granulomatous myositis
Actinomycosis bovis causes
lumpy jaw
101
granulomatous macosis
botryomycosis; horses and pigs is caused by
Staphylococcus aureus
102
Viral myositis lesions
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
Inflammatory myopathies
Parasitic
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
trichinosis; Trichinella spiralis
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
– trichinosis; Trichinella spiralis lesions
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
» 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)
trichinella spiralis in mm.
107
–trichinosis; Tric hinella spiralislesions (cont..)
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
cysticercus
1. name the 2 parasides
2. where they are found
3. lesions
Taenia solium and Taenia saginata
– in heart, masseter, tongue
small, white or gray cysts
109
small, white or gray cysts
cysticercus
110
Inflammatory myopathies
protozoa
1. in cats
2. in dogs
3. lesions
toxoplasma gondi in cats
neosporium caninuum in ogs
segmental necrosis to necrotising myositis
111
segmental necrosis to necrotising myositis is due to which parasites
protozoa
dogs. neoporium caninuun
cats: t. gondi
112
sarcosistosis
protozoa
– 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
enlongated spindle shaped structures in mm.
sarcosistosis
114
"white dots"
or "streaks" in affected muscle
sarcosistosis
115
Sarcocystosis
– tissues most commonly affected
» skeletal muscles in general, tongue, heart,
esophagus and diaphragm
116
Rhabdomyoma
primary neoplasia
1. lesions
2. organ affecte
benign
* congenital
* cow, sheep, pig
* origin: heart (66%)
* large pedunculated mass in the heart
* cross-striation
117
Rhabdomyosarcoma
primary
1. nt reported in which animal?
2. lesions
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
which neoplasia has poorly encapsulated nodules
rhabdomyosarcoma
119
Botryoid rhabdomyosarcomas
1. spp n age affected
2. shape
3. where it arises
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
Myasthenia gravis
1. spp
2. cs
3. cause
4. breeds
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
myasthenia gravis
1. differentiate congenital vs acquired
2. which one is autoimmune
Ach receptor mulfxn in acquired--\> autoimmune
congenital--\>less Ach released---\>no autoimmune
122
Acquired myasthenia gravis associated lesions:
megaesophagus
• dysphagia
• secondary aspiration pneumonia
• thymoma
123
Botulism
1. pathogenesis
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
Botulism lesions
profound generalized flaccid paralysis
– dysphagia, tongue weakness, aspiration pneumonia
– recumbency --\> ischemia and focal necrosis
125
Displacement – perosis of birds
dietary deficiency of Mn or choline
• lateral displacement of gastrocnemius tendon
• collapse of hock
126
Tendonitis – “bowed tendon” in chicken is caused by
viral arthritis (reovirus)
127
tenosynovitis in chicken is caused by
trauma, penetrating wound
• distension of tendon sheath by exudate
– serous, fibrinous or purulent
128
Onchocerca spp.
Parasitic diseases of tendons
adults live in tendons, tendon sheaths, or
connective tissues of the brisket, abdominal wall
or ligamentum nuchae
– liberate microfilariae over long periods
129
fibrous nodules (“worm nodule” or “worm nest”)
Onchocerca spp
130
lesions of oonchoceca spp
fibrous nodules (“worm nodule” or “worm nest”)
– brisket
– external surfaces of hind limbs
– ligamentum nuchae
131
Endochondral ossification sequence of
events
1. **–mineralization** of the physis
2. **apoptosis** of chondrocytes
3. ** vascular** invasion of cartilage
132
Deficiency of mineralized bone dz
Osteoporosis
Rickets
Osteomalacia
Fibrous osteodystrophy
Drug-induced osteodystrophy
Hypovitaminosis C
133
Osteoporosis (atrophy) is characterized by
a decrease in bone mass (osteopenia)
* enlargement of bone spaces
* increased fragility of affected bones
the remaining bone is normally mineralized
134
etiolgy of esteoperosis
• imbalance between bone formation and resorption in
favor of resorption
135
mm.are swollen, dark red, doughy or hard with yellow or pale streak of foci
## Footnote
acute eosinophilic muscle myositis
136
which dz causes laryngospasms
HYPP
137
Affected mm atropic, flabby, pale & wet
myofibrilar hypoplasia (splay leg)
138
causes of splay leg(myofibrilar hypoplasia)
1. heditory
2. teratogenic--\>exposure to chlorine or methenione def.
139
Carb metabolic disorder \> insufficient energy production
Polysaccharide Storage Myopathy
140
lesions of Polysaccharide Storage Myopathy
Mm pale pink or diffusely red;
acute myoglobinuric nephrosis (pigment nephrosis);
↓mm mass;
severe acute to subacute myofibril necrosis
141
Mm pale pink or diffusely red; acute myoglobinuric nephrosis (pigment nephrosis); ↓mm mass; severe acute to subacute myofibril necrosis
polysaccharide storage myopathy
142
: recurrent exertional rhabdomyolysis, stiff gait, symmetric mm atropy, weakness (bilat pelvic limb or generalized
polysaccharide storage myopathy`
143
what are the cs of polysaccharide storage myopathy
: recurrent exertional rhabdomyolysis,
stiff gait,
symmetric mm atropy,
weakness (bilat pelvic limb or generalized
144
Accum of excess glycogen due to metab defect (or missing enzyme)
Glycogenoses (glycogen storage dz
145
: mm weakness & incoordination
glycogenosis
146
microscopic lesions of glycogenosis
glycogen storage in neurons, hepatocytes cardiac & skeletal mm
147
Defective Cl channel activity \> ↓Cl conductance and ionic instability of sarcolemma \> continuous abnormal mm activity
Myotonia (channelopathies)
148
: limited to prominan muscling
myotonia
149
cs of myotonia
Sustained involuntary contraction of mm \> spontaneous myotonia, generalized stiffness, exercise intolerance
150
which equine muscular dz is associated with post anesthetic recumbency
HYPP
151
arthrogryposis( crocked limbs” or congenital articular rigidity (CAR))
causes
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
Arthrogryposis (“crooked limbs” or congenital articular rigidity (CAR)) cs
decrease mm. ineversation
hypoplasia---\>deformity of limbs
153
Arthrogryposis (“crooked limbs” or congenital articular rigidity (CAR)) lesions
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
still born; hydrops amnii \> dystocia; fibrosis \> joint fixation; torticollis, scoliosis, kyphosis, distorted joints; congenital hernias (rare)
arthrogroposis
155
list different types of mm.atrophy
1) Denervation atrophy
2) Disuse atrophy
3) Malnutrition atrophy
4) Senile atrophy
5) Pressure atrophy
156
what causes denervation atrophy in
1. CNS
2. PNS
_damage to the CNS_ : disk potrution, chronic meningitis, trauma, metastatic lesions, localized spinal malacia
_Damage to PNS_: trauma, neoplasia, abscesses, pressure by discs
157
causes of disuse atrophy
↓movement (fractures, rupture of tendons, joint immobility, ↓use (b/c pain), UMN damage, recumbancy
158
causes of malnutrition atrophy
malnutrition,
starvation,
emaciation,
severe helminthiosis,
chronic inflammatory dz
, neoplasia & senility
159
causes of Senile atrophy
sim to atropy of cachexia
160
causes of Pressure atrophy
prolonged pressure on mm due to abscesses, tumors, parasitic cysts
161
flabby & shrunken mm; type II fibers 1ᵒ involved (lesions localized to affected mm gps
disuse atrophy
162
yellowish-brown to dk brown (due to lipofuscin 1° in diaphragm) mm.
pressure atrophy
163
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
denervation atrophy
164
Firm, gritty, white, boney plates in mm
metaplasia
165
Inadequacy of regen in myofibril; degen changes \> ↓mm fibers \> eventually replaced by fat \* fibrous CT
mm.dystrophy
166
pathogenensis of mm. dystrophy
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
lesions of mm.dystrophy
atrophy +/-megaesophagus \> aspiration pneumonia, segmental necrosis & regen
pallor, firmness, atrophy, fibrosis
168
cs of mm.dystrophy
)mm weakness, bunny hopping, exercise intolerance, collapse
c)neuro-mm weakness, stiff gait, exercise intolerance
169
Glistening, chalky-white, opaque foci in mm;ngritty on cutting
calcium overload necrosis
170
differentials for a black mm.
hemorrhages
melanosis
171
causes of brown coloration in mm.
aging--\>episodes of starvatin \caxemia
xanthomatosis--\>aging, cachexia, hypovitaminosis E
172
pathogenesis of brown mm.
lipofuscine ans lipofuscine like pigments accumulates in mm.
173
causes of white mm. dz(nutritional myopathy)
Se/vit E def.
174
apthogenesis for Nutritional myopathy (White mm dz)
Def in Se or Vit E \> free radical formation \> attack lipid membranes \> lipid peroxides \> destroy CMs \> Ca influx \> segmental necrosis
175
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
white mm. dz
176
mulbery heart dz
Porcine Vit E/Se responsive dz complex
177
: deposition of ceroid-like pigment in sm. Mm (spleen, SI)
Brown dog gut
178
calcified lesions in masticatory & tongue mm
Masticatory myopathy & polymyopathy (foals):
death from aspiration pneumonia
179
lesions o MM necrosis & steatitis (rabbits)
necrosis in skeletal and heart mm
180
cauuse of Azoturia (Equine paralytic myoglobinuria; Monday morning dz; Sacral paralysis; Exertional rhabdomyolysis)
Electorlyte abnormalities (Na, K, Ca);
Se def;
forced exercise after a period of rest and food restriction;
polysaccharide dz?
181
Mm swelling w/lameness; paresis w/ renal failure & shock
Equine post-anesthetic hypotensive myopathy
182
stiff; stilted pelvic limb gait w/ ↑bulk & tone or prox thigh mm; mm weakness
hyperadrenocorticotism
183
well demarcated green foci
eosinophilic myositis
184
leukocytoclastic vasculitis
purpura hemorrhagica
think about the bv inflamation.
185
Multifocal necrosis of myofibers w/ focal interstitial & perivascular infiltrate of lymphocytes, macrophages and a few neuts
Porcine encephalomyelitis
186
Heart & skeletal mm may have yellow streaks and grey foci of segmental myofiber necrosis w/ lymphocytic & neutrophilic infilt
foot n mouth
187
Nonpurulent myositis in fetus
akabane dz
188
Myofibers w/n affected mm become disoriented; myofilaments detach and fray at Z line; most organelles degen and disappear (esp mitochondria and lysosomes)
nematodes
189
Sm white or grey cysts containing clear fluid and larva
Histo: min inflammatory response (few lymphocytes and/or eosinophils); dead larva become clacified
cestoides
190
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
protozoa
191
large pedunculated mass in heart
rhabdomyoma
192
Poorly encapsulated spherical nodules of pink/grey tissue
Rhabdomyosarcoma (1° neoplasm)
193
shaped like a bunch of grapes
Histo: variable, w/ or w/o striation or giant cells
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
