Muscle pathology Flashcards
Changes to muscle can be:
Neurogenic due to dysfunction of the nerve supply
Myogenic a primary change in the myofibre
In what three ways do myocytes respond to injury?
Degeneration
Necrosis
Regeneration
What are some possible causes of injury?
Trauma
Ischaemia
Toxins
Nutritional deficiencies
Infections
Describe degeneration
Changes that may, or may not, cause myofibre death
Potentially reversible
Types
Pigmentation – melanin, myoglobin
Calcification – necrosis, old age
Ossification – non-neoplastic bone/cartilage
True degeneration
Other degenerations
Describe the histopathology of degeneration
Damage to cell membrane
Allows Na+ to enter the cell
Osmosis
Cellular swelling
Describe necrosis
Final stage of irreversible degeneration
Segmented necrosis
Muscle fibres are long and have multiple nuclei
Total necrosis
Extensive infarction, large burns etc
Rare
Describe the histopathology of necrosis
Dark, floccular and granular appearance to the sarcoplasm.
Fragmentation.
Quickly merge into regeneration.
What does the success of regeneration depend on?
Sarcolemmal tube being intact
Basal lamina being intact
Availability of satellite cells
Describe satellite cells
Myosatellite cells’
Precursors to muscle cells
Quiescent but can re-enter cell cycle following injury
Describe atrophy (changes in myofibre size)
Reduction in diameter of muscle / muscle fibre
Myofibrils removed by disintegration
Creates ‘space’ in the sarcolemma around which endomysium contracts
Either:
Denervation
Disuse
Malnutrition / cachexia
Describe denervation atrophy
‘Neurogenic atrophy’
Damage to motor units
If all units affected all fibres atrophy
If only selected units affected mixture of atrophied and normal fibres
Remaining fibres either hypertrophy or undergo disuse atrophy in response
Describe disuse atrophy
Slower form of atrophy
Occurs when muscle stops working
Prolonged recumbency
Fractures
Chronic pain
UMN damage
Type II fibres affected more rapidly
Describe malnutrition/cachexia atrophy
Muscle proteins are metabolised to cover need for nutrients
Gradual
unless associated with febrile disease (cachexia)
Postural muscles unchanged
What can changes in the circulation cause?
Congestion
Ischaemia
Define congestion
Stasis of blood within the vessels
Can resemble haemorrhage at post-mortem
Define ischaemia
Restriction of blood supply
Myocytes most sensitive satellite cells fibroblasts
Due to
Vascular occlusion
External pressure on the muscle
Swelling within a non-expandable compartment
Define contusion
Inflammation and haematoma from blunt, non-penetrating trauma
Define strain
Occur at the myotendinous junction causing haematoma and scare tissue
Define laceration
Direct trauma with a sharp object
Define rupture
Caused by active contraction whilst muscle is passively extended
Define contracture
State of shortening not caused by contraction
What can cause myositis (inflammation)?
Bacterial
Viral
Helminth
Protozoa
Immune-mediated
Idiopathic (unknown cause)
Describe vitamin e/selenium deficiency
White muscle disease
Nutritional myodegeneration
Young, rapidly growing lambs, calves, kids, foals
Cardiac and skeletal muscle
What are the clinical signs of white muscle disease?
Cardiac form can cause sudden death
Skeletal form:
Muscular weakness
Stiffness
Muscle tremors
Trouble standing for long periods of time
+/- recumbency
Describe treatment of white muscle disease
Prognosis for cardiac form is poor
Selenium (parenteral) +/- vitamin E (oral)
Prevention of decubital ulcers
Attention to food / water intake
Antibiotics if secondary infection
E.g. pneumonia, infected ulcers
Describe traumatic - post anaesthesia myopathy
Most common in horses
Prolonged GA in recumbency
Pressure on the muscles
leads to hypoperfusion / ischaemia
Localised or generalised
What are the clinical signs of post-ga myopathy?
Occur within 30-60mins of standing
Muscle can be flaccid or hard
Hot and painful on palpation
Weakness
Restlessness, anxiety etc.
Lateral recumbency triceps, deltoid, hindlimb extensors
Dorsal recumbency longissimus dorsi, gluteal muscles
Describe treatment of post-ga myopathy
Anti-inflammatories
Sedatives
IVFT
+/- slings for support
+/- glucocorticoids
Describe atypical myopathy
Atypical myoglobinuria’
Young horses kept at pasture
Ingestion of sycamore seeds – hypoglycin A (HGA)
Acute rhabdomyolysis
postural, respiratory and cardiac muscles
What are the clinical signs of atypical myopathy?
General weakness
Difficulty in walking and standing
Dyspnoea (difficulty in breathing)
Muscle tremors
Lethargy
Colic signs (but with an appetite)
Brown / dark red urine
Describe diagnosis and treatment of atypical myopathy
Hypoglycin A can be detected in a blood test
Can test seeds, plants etc for the toxin
Treatment
Supportive care Fatal in up to ¾ of horses.
Describe extertional rhabdomyolysis
Rhabdomyolysis – necrosis of the muscle
Associated with exercise, excitement or stress
Also known as:
Tying up
Azoturia
Monday morning disease
What are the clinical signs of exertional rhabdomyolysis?
Regardless of causes, all tend to present in a similar way
Most commonly seen during or after exercise, following a period of rest:
Stiff, stilted gait
Excessive sweating
High respiratory rate
Painful, firm muscles
Myoglobinuria
Describe acute sporadic exertional rhabdomyolysis
Can occur due to:
Overexertion - Exercise above the level of the horses training
Electrolyte imbalance - Na+ / K+ / Ca+ / Mg+ all involved in muscle contraction
Vit E / Selenium deficiency - Damage from free radicals
Diet - High-grain diet
How do you diagnose acute sporadic exertional rhabdomyolysis?
Clinical signs
Muscle enzymes
CK - creatinine kinase
LDH – lactate dehydrogenase
AST – aspartate aminotransferase
Muscle biopsy
Describe treatment of acute sporadic exertional rhabdomyolysis
Anti-inflammatories
Rehydration – IVFT
Sedation if required
Box rest with hand walking
Gradual return to work
Describe chronic intermittent exertional rhabdomyolysis
Horses have repeated episodes of ER
Due to abnormal intracellular calcium regulation
Two inherited conditions:
Polysaccharide storage myopathy
Recurrent exertional rhabdomyolysis
Describe polysaccharide storage myopathy
Quarter horses, Draught horses and Warmblood breeds
Inherited enzyme defect
Results in abnormal storage and utilisation of glycogen
1.5 – 4 x normal glycogen levels in muscle
When exercised, cannot generate adequate energy
Reduction in glycolysis ATP
Dysfunction of membrane pumps
Increased intracellular Ca+
Describe diagnosis and treatmentof polysaccharide storage myopathy
Diagnosis is made from muscle biopsy
No cure so long-term management needed
Exercise regime
Consistent turn out and gradual increase in training
Do not stable > 48hrs
Dietary modification
Reduce dietary glucose
Use fat as a means of energy
Describe recurrent exertional rhabdomyolysis
Racing Thoroughbreds, Standardbreds and Arabs
Females
Nervous horses
Defect in regulation of muscle contraction
Expressed when subjected to stress/exercise
Clinical signs the same but occur once the animal becomes fit
Stress or excitement at the time of exercise
How can you control recurrent exertional rhabdomyolysis?
- Address exercise regime
Daily turnout essential
Gradual return to exercise
Long warm up / cool down sessions
- Minimise stress
- Dietary management
Low starch
High fat
Vit E / selenium
What medication can be given for recurrent exertional rhabdomyolysis?
Dantrolene
Reduces calcium release during contraction
Reduces intracellular Ca+
Give 1hr prior to exercise
Phenytoin
Acts on ion channels
Must be withdrawn 7 days prior to racing
Describe hyperkalemic periodic paralysis
Pure and x-breed quarter horses
Hereditary
Stallion ‘Impressive’
Sired >102,000 registered QH
Males > females
< 4 years (2m-15y)
What are the clinical signs of hyperkalemic periodic paralysis?
Muscle stiffness
Sweating
Muscle fasciculations
Muscle weakness
Tremors
Collapse
How do you treat hyperkalemic periodic paralysis?
Exercise in hand/by lunging
Adrenalin helps replace intracellular K+
Feeding grain
Acts as supply of carbohydrates glucose
Glucose stimulates insulin encourages K+ uptake
Diuretics
Acetazolamide
Increase K+ excretion
How can you control hyperkalemic periodic paralysis?
Dietary modification – low potassium (avoid alfalfa, molasses)
Regular exercise
Diuretics can be used long term if required
Affected horses should NOT be bred from
Describe canine exertional myopathy
Similar to ER in horses
Greyhounds, sled dogs etc
Predisposing factors:
Inadequate fitness for level of work
Excitable / tense animal
Hot, humid weather
Excessive bouts of extreme exertion
What are the clinical signs of canine exertional myopathy?
Usually occur within 2-5 days of exercise
Muscle swelling and pain ++
Tremendous thirst
Acute form:
Generalised stiffness
Dragging of pelvic limbs
Distress
Tachypnoea (increased respiratory rate)
How can you treat canine exertional myopathy?
Reduce body temperature – cold packs etc
Intravenous fluid therapy – hydration and electrolyte imbalance
Dantrolene
Pain relief
Muscle relaxants – diazepam
Mild forms – warming of muscles, short lead walks, comfortable bedding
Describe myasthenia gravis
Neuromuscular disorder
Dysfunction of the post-synaptic membrane of the neuromuscular junction
Congenital
Inherited deficiency in acetylcholine receptor
Acquired
Autoimmune
Antibodies bind to the acetylcholine receptors
What are the clinical signs of myathenia gravis?
Focal
40% of affected dogs and 14% of affected cats
Megaoesophagus (regurgitation)
No detectable weakness in rest of body
Generalised
Muscle weakness that worsens with exercise
How do you treat myasthenia gravis?
Anticholinesterase therapy
Reduces destruction of acetylcholine
+/- Immunosuppressive doses of glucocorticoids
If megaoesophagus present
Modify feeding
Feed from a height
Upright position for 10-15 mins post-feeding
Describe swimmer syndrome
Swimmer puppy syndrome / Turtle-pup
Chondrodystrophic breeds and small terriers
and cats!
Myofibril hypoplasia
Inability to walk by 3 weeks of age
Splayed hindlimbs +/- forelimbs
Describe the aetiology of swimmer syndrome
Unknown aetiology.
Possible links to:
Environment
Slippery floors where the newborns are housed in the first few weeks of life
Weight
Weight gain that exceeds the skeletal growth
Neuromuscular disease
Dysfunction, or delay in development, of the neuromuscular system
What are the clinical signs of swimmer syndrome?
By 3 weeks of age:
Inability to stand or walk
Splayed hindlimbs +/- forelimbs
‘Paddling’ motion
Regurgitation
Sores on ventrum
Pectus excavatum - dorsoventral flattening of the chest
How can you manage swimmer syndrome?
Environment
Non-slip, soft flooring
Physiotherapy
Passive ROM
Massage
? Hobbles
Feeding regime
Feed from a height
Keep upright for 15mins after feeding
Nursing care
Cleaning of ventrum
Nutrition
