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Musculoskeletal dysfunction > Muscle pathology > Flashcards

Muscle pathology Flashcards

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
Q

Describe treatment of white muscle disease

A

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
Q

Describe traumatic - post anaesthesia myopathy

A

Most common in horses

Prolonged GA in recumbency

Pressure on the muscles

leads to hypoperfusion / ischaemia

Localised or generalised

27
Q

What are the clinical signs of post-ga myopathy?

A

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
Q

Describe treatment of post-ga myopathy

A

Anti-inflammatories

Sedatives

IVFT

+/- slings for support

+/- glucocorticoids

29
Q

Describe atypical myopathy

A

Atypical myoglobinuria’

Young horses kept at pasture

Ingestion of sycamore seeds – hypoglycin A (HGA)

Acute rhabdomyolysis

postural, respiratory and cardiac muscles
30
Q

What are the clinical signs of atypical myopathy?

A

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
Q

Describe diagnosis and treatment of atypical myopathy

A

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
Q

Describe extertional rhabdomyolysis

A

Rhabdomyolysis – necrosis of the muscle

Associated with exercise, excitement or stress

Also known as:

Tying up

Azoturia

Monday morning disease

33
Q

What are the clinical signs of exertional rhabdomyolysis?

A

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
Q

Describe acute sporadic exertional rhabdomyolysis

A

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
Q

How do you diagnose acute sporadic exertional rhabdomyolysis?

A

Clinical signs

Muscle enzymes

CK - creatinine kinase

LDH – lactate dehydrogenase

AST – aspartate aminotransferase

Muscle biopsy

36
Q

Describe treatment of acute sporadic exertional rhabdomyolysis

A

Anti-inflammatories

Rehydration – IVFT

Sedation if required

Box rest with hand walking

Gradual return to work

37
Q

Describe chronic intermittent exertional rhabdomyolysis

A

Horses have repeated episodes of ER

Due to abnormal intracellular calcium regulation

Two inherited conditions:

Polysaccharide storage myopathy

Recurrent exertional rhabdomyolysis

38
Q

Describe polysaccharide storage myopathy

A

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
Q

Describe diagnosis and treatmentof polysaccharide storage myopathy

A

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
Q

Describe recurrent exertional rhabdomyolysis

A

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
Q

How can you control recurrent exertional rhabdomyolysis?

A
  1. Address exercise regime

Daily turnout essential

Gradual return to exercise

Long warm up / cool down sessions

  1. Minimise stress
  2. Dietary management

Low starch

High fat

Vit E / selenium

42
Q

What medication can be given for recurrent exertional rhabdomyolysis?

A

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
Q

Describe hyperkalemic periodic paralysis

A

Pure and x-breed quarter horses

Hereditary

Stallion ‘Impressive’

Sired >102,000 registered QH

Males > females

< 4 years (2m-15y)

44
Q

What are the clinical signs of hyperkalemic periodic paralysis?

A

Muscle stiffness

Sweating

Muscle fasciculations

Muscle weakness

Tremors

Collapse

45
Q

How do you treat hyperkalemic periodic paralysis?

A

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
Q

How can you control hyperkalemic periodic paralysis?

A

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
Q

Describe canine exertional myopathy

A

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
Q

What are the clinical signs of canine exertional myopathy?

A

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
Q

How can you treat canine exertional myopathy?

A

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
Q

Describe myasthenia gravis

A

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
Q

What are the clinical signs of myathenia gravis?

A

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
Q

How do you treat myasthenia gravis?

A

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
Q

Describe swimmer syndrome

A

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
Q

Describe the aetiology of swimmer syndrome

A

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
Q

What are the clinical signs of swimmer syndrome?

A

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
Q

How can you manage swimmer syndrome?

A

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

Musculoskeletal dysfunction (12 decks)

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