Muscle pathology Flashcards

(56 cards)

1
Q

Changes to muscle can be:

A

Neurogenic  due to dysfunction of the nerve supply

Myogenic  a primary change in the myofibre

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2
Q

In what three ways do myocytes respond to injury?

A

Degeneration

Necrosis

Regeneration

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3
Q

What are some possible causes of injury?

A

Trauma

Ischaemia

Toxins

Nutritional deficiencies

Infections

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4
Q

Describe degeneration

A

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

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5
Q

Describe the histopathology of degeneration

A

Damage to cell membrane

Allows Na+ to enter the cell

Osmosis

Cellular swelling

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6
Q

Describe necrosis

A

Final stage of irreversible degeneration

Segmented necrosis

Muscle fibres are long and have multiple nuclei

Total necrosis

Extensive infarction, large burns etc

Rare

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7
Q

Describe the histopathology of necrosis

A

Dark, floccular and granular appearance to the sarcoplasm.

Fragmentation.

Quickly merge into regeneration.

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8
Q

What does the success of regeneration depend on?

A

Sarcolemmal tube being intact

Basal lamina being intact

Availability of satellite cells

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9
Q

Describe satellite cells

A

Myosatellite cells’

Precursors to muscle cells

Quiescent but can re-enter cell cycle following injury

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10
Q

Describe atrophy (changes in myofibre size)

A

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

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11
Q

Describe denervation atrophy

A

‘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

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12
Q

Describe disuse atrophy

A

Slower form of atrophy

Occurs when muscle stops working

Prolonged recumbency

Fractures

Chronic pain

UMN damage

Type II fibres affected more rapidly

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13
Q

Describe malnutrition/cachexia atrophy

A

Muscle proteins are metabolised to cover need for nutrients

Gradual

unless associated with febrile disease (cachexia)

Postural muscles unchanged

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14
Q

What can changes in the circulation cause?

A

Congestion

Ischaemia

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15
Q

Define congestion

A

Stasis of blood within the vessels

Can resemble haemorrhage at post-mortem

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16
Q

Define ischaemia

A

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

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17
Q

Define contusion

A

Inflammation and haematoma from blunt, non-penetrating trauma

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18
Q

Define strain

A

Occur at the myotendinous junction causing haematoma and scare tissue

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19
Q

Define laceration

A

Direct trauma with a sharp object

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20
Q

Define rupture

A

Caused by active contraction whilst muscle is passively extended

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21
Q

Define contracture

A

State of shortening not caused by contraction

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22
Q

What can cause myositis (inflammation)?

A

Bacterial

Viral

Helminth

Protozoa

Immune-mediated

Idiopathic (unknown cause)

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23
Q

Describe vitamin e/selenium deficiency

A

White muscle disease

Nutritional myodegeneration

Young, rapidly growing lambs, calves, kids, foals

Cardiac and skeletal muscle

24
Q

What are the clinical signs of white muscle disease?

A

Cardiac form can cause sudden death

Skeletal form:

Muscular weakness

Stiffness

Muscle tremors

Trouble standing for long periods of time

+/- recumbency

25
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
26
Describe traumatic - post anaesthesia myopathy
Most common in horses Prolonged GA in recumbency Pressure on the muscles leads to hypoperfusion / ischaemia Localised or generalised
27
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
28
Describe treatment of post-ga myopathy
Anti-inflammatories Sedatives IVFT +/- slings for support +/- glucocorticoids
29
Describe atypical myopathy
Atypical myoglobinuria’ Young horses kept at pasture Ingestion of sycamore seeds – hypoglycin A (HGA) Acute rhabdomyolysis postural, respiratory and cardiac muscles
30
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
31
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.
32
Describe extertional rhabdomyolysis
Rhabdomyolysis – necrosis of the muscle Associated with exercise, excitement or stress Also known as: Tying up Azoturia Monday morning disease
33
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
34
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
35
How do you diagnose acute sporadic exertional rhabdomyolysis?
Clinical signs Muscle enzymes CK - creatinine kinase LDH – lactate dehydrogenase AST – aspartate aminotransferase Muscle biopsy
36
Describe treatment of acute sporadic exertional rhabdomyolysis
Anti-inflammatories Rehydration – IVFT Sedation if required Box rest with hand walking Gradual return to work
37
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
38
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+
39
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
40
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
41
How can you control recurrent exertional rhabdomyolysis?
1. Address exercise regime Daily turnout essential Gradual return to exercise Long warm up / cool down sessions 2. Minimise stress 3. Dietary management Low starch High fat Vit E / selenium
42
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
43
Describe hyperkalemic periodic paralysis
Pure and x-breed quarter horses Hereditary Stallion ‘Impressive’ Sired >102,000 registered QH Males > females < 4 years (2m-15y)
44
What are the clinical signs of hyperkalemic periodic paralysis?
Muscle stiffness Sweating Muscle fasciculations Muscle weakness Tremors Collapse
45
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
46
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
47
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
48
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)
49
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
50
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
51
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
52
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
53
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
54
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
55
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
56
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