Muscle (AH) Flashcards
Crossed with class notes, TQs and Muzzy review.
1
Q
Type I mm fibers
A
redslow twitchsmallmore mitochondriano glycogen
2
Q
Type II mm fibers
A
White fast twitchlarge less mitochondria more involved in atrophy II A = oxitative + glycolytic. II B = glycolytic.
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.
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.
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
6
Q
What spp. gets myofibrillar hypoplasia?
A
Pigs
7
Q
Etiology of myofibrillar hypoplasia?( 3)
A
- Hereditary - decreased number of myofibrils in muscle fibers.
- Teratogenic - Toxins (F. graminearum = F-2 toxin = mycotoxicosis) –> depressed growth in utero.
- Choline or methionine deficiency –> decreased Ach synthesis and energy production.
8
Q
Pathogenesis of Polysaccharide storage myopathy in horses?
A
Carbohydrate metabolic disorder –> insufficient energy production –> decrease in mm. –> Acute myoglobinuric nephrosis (pigment nephrosis)
9
Q
Etiology of Glycogenoses (glycogen storage Dz)?
A
Missing or defective enzyme (inherited) –> accumulation of glycogen
10
Q
What is Myotonia?
A
Channelopathy. Inability of myofibers to relax resulting in spasmodic contractions.
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.
12
Q
HYPP sequelae?
A
Laryngeal mm dysfunction. Trembling, weakness, collapse. Metabolic acidosis –> cardiotoxicity and pumonary edema. Can be fatal.
13
Q
What is Arthrogyposis?
A
Muscle hypoplasia due to lack of muscle innervation during gestation.
14
Q
Lesions of Arthrogyposis?
A
Atrophy and dysplasia of muscles Fibrosis → Curvature and rigidity of joints = Crooked limbsPossibly born dead
15
Q
Etiology of Arthrogyposis?
A
Infectious:
- viral (BVD, Akabane)
- vaccinations druing 1st trimester (ruminants) for Rift Vally fever, wesselbron virus, bluetongue. Non-infectious:
- inherited in suffolk lambs
- Plant poisoning (lupinus spp.) causes decreased movement in utero
16
Q
What is the primary defect associated with Arthrogyposis?
A
Always associated with spinal and brain abnormalities.
17
Q
What is mm atrophy?
A
Decrease in size of cells that have gained full development
18
Q
Mm atrophy etiology?
A
- Diminished level of work
2. Removal of source of nutrition or stimulation (more common)
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
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.
21
Q
Give three examples of denervation atrophy syndromes
A
- Equine lyaryngeal hemiplegia (roaring).
- Damage to suprascapular nerve in horses (sweeny).
- Radial or brachial paralysis in dogs associated with trauma.
22
Q
Lesions of denervaiton atrophy?
A
Diffuse atrophy involving BOTH type I and II fibers
23
Q
Lesions of Disuse atrophy?
A
Mainly involves Type II fibers.
Flabby shrunken muscles.
24
Q
What is the most common form of Atrophy?
A
Atrophy of malnutrition and cachexia.
25
Etiology of atrophy of malnutrition and cachexia? (5)
Malnutrition, Starvation, Severe helminthosis, Chronic debilitating diseases (TB, Johne's Dx), Neoplasia
26
Lesions of atrophy of malnutrition an cachexia?
type II fibers involved.
| Small, thin, dark, sticky, flabby mm.
27
Lesions of senile atrophy?
Lipofuscin --> yellow brown color, especially in diaphram.
28
What causes pressure atrophy?
Prolonged pressure of muscles from abscesses, tumors, parasitic cysts
29
What is Hypertrophy?
Incease in size of mm by an increase in fiber size. No new cells, just bigger size.
30
Etiology of hypertrophy?
1. physiologic - athletic training, pregnant uterus.
2. Pathologic (left cardiac ventricular hypertrophy.)
3. Idiopathic (esophagus, ileum - horses).
4. Iatrogenic - steroids.
31
Lesions of hypertrophy?
Dark red. Increase in myofiber diameter. Increased myoglobin. Larger cellular organelles.
32
What is steatosis?
Defective myofiber development --> replacement of muscle tissue by adipose tissue.
33
How do mm affected by severe steatosis appear?
Soapy, marbling appearance. Not clinically significant.
34
What is muscular dystrophy?
Progressive degeneration due to abnormal muscle proteins (ex: dystrophin).
35
Etiology of muscular dystrophy? (2)
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
36
General lesions of muscular dystrophy?
Failed attempts to regenerate --> Fibrosis.
37
Clinical presentation of HMLR?
In young dogs. Bunny hopping. +/-megaesophagus --> aspiration pneumonia.
38
What is the defect in dogs with Canine X-linked mm dystrophy?
Dystrophin deficiency. Duchenne type
39
What specific condition is associated with mm rupture?
Fibotic and ossifying myopathy (torn hamstring in quarter horses).
40
Sequelae of ruptured mm.?
Diaphragmatic rupture or rent--> eventration. In racing greyhounds --> muscle ruptrue during strenuous activity.Tearing from slipping cows
41
Lesions of congestion?
swollen, red to black.
42
What is an example of mm congestion?
Bovine ruminal tympany (bloat)
43
Lesions associated with bloat?
Cervical esophagus is red.
Thoracic esophagus is pale (white).
Extensive congestion of cervical region extending to the head. ==> bloat line.
44
Thrombosis, Embolism, and infarction lesions?
hemorrhage and necrosis in infarcted muscle, thrombus
45
What are the three responses of mm to injury?
degeneration, necrosis, regeneration
46
What is true about etiology of degeneration/necrosis?
There is a stereotyped response making it hard to determine etiology.
47
Histopathological interpretation of degeneration/necrosis
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.
48
Gross lesions of mm degeneration?
Degenerated mm. appear pale.
* * 1. Chalky/white = severe calcification.
2. Red = hemorrhage/ rhabdomyolysis (myoglobin release)**
49
Micro lesions of mm degeneration? (6)
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
50
When is mm degeneration irreversible?
once necrosis ensues
51
Ddx for degeneration?
gross lesion = pallor.
| Muscle pallor can also indicate pale muscles of veal calves, enemia, exsanguination, fat.
52
What are the mechanisms of cell injury that lead to necrosis?
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
53
Gross/Micro lesions of necrosis?
Gross: pallor, dry gritty.
Micro: swollen, hypereosinophilic, fragmented sarcoplasm, persistent basal lamina, magrophage invasion, regeneration or fibrosis.
54
What are the main categories of degenerative myopathies?
Nutritional, Exertional, Toxic, Electrolyte, Stress, Ischemic, Endocrine, (Muscular Dystrophy)
55
***TQ What is the pathogenesis of nutritional myopathies?***
Decrease in Se / Vit E--> --> Lipid peroxidation --> damage to CM --> Ca2+ influx --> Mitochondrial damage --> segmental necrosis
56
Lesions of WMD?
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
What other selenium/ vit E deficiencies may coexist with WMD?
Mulburry heart and heptatitis dietetica
58
Where in the heart are lesions of WMD seen in calves and sheep?
*RV in sheep, LV in calves*
59
Where are lesions of Nutritional myopathy seen?
Selective of type I fibers = diaphragm, intercostal, tongue, heart. (diaphram and heart are most severe b/c they can cause death)
60
What is exertional myopathy?
Dz resulting in severe muscle degeneration following strenuous exercise.
61
Pathogenesis of Exertional myopathy?
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
*** TQ Exertional Myopathy Syndromes by Spp.?***
Horses - azoturia and tying-up. Cattle - azoturia- like syndrom. Wildlife - capture myopathy
63
By what other names is Azoturia known in horses?
Eq. paralytic myogobinuria, Monday morning dz, Sacral paralysis, Exertional rhabdomyolysis.
64
CS of Azoturia?
Sudden onset of stiff gate due to mm weakness. Sweating. Death from Cardiac or renal failure. Myoglobinuria. Acidosis.
65
Azoturia etiology?
Forced exercise after period of rest w/o feed restriction (#1 cause) Electrolyte imbalances, Se deficiency, polysaccharide dz.
66
Azoturia lesions?
Myoglobinuric nephrosis --> ***DARK BLACK KIDNEYS***Muscles:Moist, swollen, dark red, hemorrrhage. Hyaline degeneration and necrosis of sk. Mm. Later: fibrosis, atrophy, mm pallor.
67
Sequelae of Azoturia?
Death from cardiac or renal injury. Recovery w/ atrophy. Recovery with mm regeneration.
68
What is the less severe form of Azoturia?
Tying-up/setfast/ acute rhabdomyolysis in horses.
69
What form of Azoturia is associated with wild cattle/ zebu?
Azoturia-like syndrome. (also in racing greyhounds) Linked to unusual transportation/ confinement --> fighting and struggling.
70
Which form of Exertional Myopathy presents with pronounced Acidosis?
Capture Myopathy
71
Lesions of Capture myopathy?
Bilateral Symmetry, Pale, swollen, edematous muscles. Hemorrhage Ruptured tendons Myocardial injury (congestive HF).Acidosis
72
Lesions of muscle toxicity?
Ill defined pale streaks in skeletal and or myocardium. Sometimes myoglobinuria in presence of extensive necrosis.
73
What are the main Toxins that can cause mm toxicity?
Ionophores (monesin salinomycin, narasin, lasalocid), Gossypol -cotton seed. Toxic plants (coffee senna) in horses, cattle, sheep and goats.
74
What spp. is most suseptable to Ionophores? What ionophore in particular?
Horses, in particular Monesin.
75
Pathogenesis of Ionophor mm. toxicity?
ionophores facilitate moevement of cations --> disruption of normal ionic equalibrium --> Ca2+ overload --> necrosis, death from cardiovascular shock/collapse
76
List all Elecrolyte abnormality myopathies.
HYPOKAlemia, HYPERNAtremia, HypoPhosatemia
77
What spp. get Hypokalemia related myopathy?
Cattle and Cats
78
What effect on muscle does Hypokalemia have in cattle?
Profound weakness and recumbancy
79
Etiology of Hypokalemic myopathy in cattle? (3)
1. Hypokalemia due to Anorexia and Ketosis.2. Glucocorticoids w/ increased mineralcorticoid activity. 3. IV glucose/insulin = increase in cellular K inflow
80
MM Pathologenesis of Hypokalemic myopathy?
Decrease in muscle K+ --> altered mitochondrial function and/or vasoconstriction (ischemia) --> myofiber necrosis. Hypokalemia also --> Abnormal cardiac conduction
81
Lesions of hypokalemic myopathy?
Ischemic necrosis (from recumbancy), Myofiber necrosisVacuated myofibers.
82
What effect on mm does hypokalemia have in cats?
Generalized weakness w/ ventri-flexion of the neck.
83
Pathology of hypokalemia effect on mm in cats?
Hyperpolarization of CM --> 2* excess NA permeability --> altered mitochondrial function --> ischemia -> mm necrosis. Also Abnormal cardiac conduction from decreased K+
84
What can hypokalemia eventually lead to in cats?
+/- chronic interstitial nephritis.
85
what spp. is prone to hypernatremia?
Cats
86
Pathology of Hypernatremia?
Increased muscle Na+ --> abnormal energy metabolism. Increased blood Na+ --> vasoconstriction --> ischema. Both lead to transient myofiber necrosis and regeneration.
87
Hypophophatemia is linked to what spp?
Cattle
88
****CS of Hypophosphatemia related myopathy?****
Profound mm weakness, neurologic signs*, and Hemolytic anemia*.
89
What is the major stress induced myopathy?
Porcine Stress Syndrom (PSS) (also in dogs and horses)
90
Which mm fibers are effected in PSS?
Type II
91
Etiology of PSS?
Hereditary enzyme deficiency (Hal gene)--> hypermetabolic syndrome
92
Pathology of PSS?
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
What are the Ischemic injury myopathies?
Campartment syndrome and Deep pectoral myopathy
94
How is compartment syndrome characterized?
Degeneration and necrosis of mm that are surrounded by heavy aponeurosis (connective tissue). Ex: well conditioned athletes and poultry deep pectoral musculature.
95
What spp. gets Deep Pectoral Myopathy ?
Poultry
96
Etiology and Pathogenesis of Deep Pectoral Myopathy?
Vigorous flapping of wings --> muscle expansion --> vascular compression --> eschemia --> infarctions
97
What is downer syndrome?
ischemic necrosis of ventral and limb muscles following prolonged recumbency. Lesions appear as early as 6-12hrs.
98
What two endocrine disorders cause myopathy?
Hypothyroidism, Hypercortisolism
99
What type of atrophy results from endocrine myopathies?
Denervation Atrophy
100
Myopathy caused by hypothyroidism lesions?
Marked type II atrophy in dogsGeneralized weakness, muscle atrophy (type II fibers), Megaesophagus, *Normal CK and AST.
101
Pathologenesis of hypothyroidism related myopathy?
1. Decrease in thyroid hormone --> decreased mm metabolism --> myofiber wekaness and atrophy. 2. Peripheral neuropathy (axonal degeneration) --> damage to motor nerves --> *denervation atrophy*
102
How does hypercortisolism related myopathy present?
stiff pelvic limbs gait, increased bulk and tone of proximal thigh muscles. (cushingoid pseudomyotonia). And muscle weakness.
103
Path of hypercortisolism related myopathy
increased cortisol production --> peripheral neuropathy --> *denervation atrophy with regeneration*.
104
What is myositis?
mm inflammation
105
What causes Hemorragic myositis?
Clostridium sp.
106
Common examples of hemorragic myositis caused by Clostridium sp.?
Blackleg -ruminants. Gas grangrene - horse. Malignant edema - horses, ruminants and pigs.
107
Pathogenesis of Hemorrhagic myositis?
Clostridium sp. --> activation of spores --> proliferation of bacilli --> toxin production --> vascular damage --> edema, hemorrhage, necrosis, myositis and emphysema.
108
What causes suppurative myositis?
Pyogenic bacteria: -T. pyogenes, Strep spp., Staph spp., Corynebacterium. Psuedotuberculosis in horses.
109
What causes granulomatous myositis?
Actinobacillus lingieresii - wooden tongue (pale granulomas). Actinomyces bovis --> Lumpy jaw (caseous granulomas)
110
Protozoan parasitic myositis?
Sarcosystis spp (horse, cattle, sheep, camilids, pigs) Neospora caaninum (dogs, fetal cattle.)
111
Nematode parasitic myositis?
Trichinella spiralis (pigs.)
112
Cestode parasitic myositis?
Cysticercus spp (cattle, sheep, goats, pigs) - large visible cysts
113
2 Eosinophilic types of myositis?
Eosinophilic myositis of ruminants, Masticatory muscle myositis of dogs (GSD)
114
lesions of eosinophilic myositis?
***Green!*** May turn to off white when exposed to air.
115
Etiology of eosinophilic myositis?
Sarcosystosis, Immunologic injury - immune reaction to type II muscle fibers. Idiopathic.
116
Immune mediated myosistis examples?
Polymyositis of dogs and purpura hemorrhagica in horses
117
Polymyositis of dogs lesions?
*Lymphoplasmacytic inflammation* --> 1. Megaesophagus. 2. Atrophy, degeneration, necrosis.
118
Pupura hemorrhagica in horses etiology?
Post-streptococcal infection following strangles --> immune complexes
119
Lesions of purpura hermorrhagica?
Edema of the head and limbs. Leukocytoclastic vaculitis. Petechiae +/- glomerulonephritis.
120
What are the three main neoplasias of muscle?
Rhabdomyoma, Rhabdomyosarcoma, Botyroid Rhabdomyosarcoma.
121
Etiology/origin of Rhabdomyoma?
Congenital. Origin = 66% heart
122
Lesions of Rhabdomyoma?
Large pedunculated mass made up of cells that resemble skeletal mm (cross striations) found embeded in heart. Benign
123
Rhabdomyosarcoma =?
Malignant form of rhabdomyoma
124
Rhabdomyosarcoma gross pathology?
Tumors are poorly encapsulated spherical nodules formed by pink/grey tissue. Metastasis to lung, spleen, lymph nodes and kidneys are common.
125
Botryoid rhabdomyosarcoma is found in what spp?
large breed dogs.
126
Origin of BRS?
embryonic myoblasts --> urinary trigone --> urinary bladder
127
Disorders of neuromuscular junction?
Myasthenia gravis, botulism
128
What is Myasthenia gravis?
weakness and severe muscle fatigue from mildest exercise due to reduction of Ach receptors
129
Congenital myasthenia gravis etiology?
Low # of Ach receptor.
130
Lesions of congenital myasthenia gravis?
1. no change. 2. disuse atrophy. 3. fibrous.
131
Aquired Myasthenia gravis etiology?
Autoimmune - IgG to Ach receptors.
132
Lesions of aquired A MG?
Muscle weakness --> 2* Dz:1. Megaesophagus --> asperiation pneumonia. 2. Dysphagia. 3. Thymoma
133
Tx of A MG?
Anti-Cholinergic drugs (neostigmine) --> dramatic improvement
134
Etiology of Disorders of Tendons?
Congenital anomalies (contracted tendons), Physical injury (Perosis of bird), Inflammation (tendonitis, parasitic.)
135
Perosis of birds is what?
Displacement of tendons - gastrocnemius m. Due to dietary Mn or Choline deficiency.
136
Tendonitis etiology
trauma or penetrating wound.
137
Bowed tendon =?
Thickened lateral deviation of tendon
138
Parasitic tendonitis is caused by what?
Onchocerca spp. --> ligamentum nuchae
139
Lesions of parasitic tendonitis?
Fibrous nodules = "worm nodules or worms nest"
