Tendon, ligament and muscle conditions Flashcards
What are tendons and their functions?
- Insertional points of muscles
- Passively transfer force generated by muscle to bony attachments -> Leads to movement
- Support joints
- Store energy
What are ligaments and their functions?
- Go from bone to bone
- Attach/stabilise bones/joints e.g. cruciate ligaments, collateral ligaments
- Protect tendons
- Proprioception
What is the role of Tenocytes/ligamentocytes?
Responsible for the synthesis, maintenance and degradation of ECM
What are the 4 components of the ECM?
Collagen types, proteoglycans, elastin, water content
Which collagen types make up tendons and ligaments?
- Tendon = 95% collagen type I and 1-5% type III
* Ligament = 90% type I and 10% type III
What is the role of collagen type III?
Acts to crosslink the main collagen fibres which run along the plane of force through a structure
What are the general considerations of tendon/ligament injuries?
- Extrinsic - External trauma e.g. laceration
- Intrinsic - Overload/ degenerative
- Can initially appear as an acute injury but they have a chronic component
- Location/type
What are the possible locations/types of tendon/ligament injuries?
- Intrasynovial/extrasynovial i.e. inside or outside a tendon sheath
- Origin/insertion/mid-body (myo-osseous)/ avulsion fracture
- Extensor versus flexor tendon
What factors are involved in the diagnosis of tendon/ligament injuries?
- History: age, type, previous injury
- Recent exercise e.g. pulled up lame after a jump, or chasing a ball and twisted limb
- Wound/laceration: remember end of tendon may not be at same level as wound due to recoil
- Clinical examination: stance/gait
- Palpation
- Diagnostic imaging
What may be felt on palpation of a tendon/ligament injury?
- Swelling, pain, oedema, effusion
- Range of motion/stability
Ability to extend the tarsus whilst the stifle is flexed in a horse is indicative of what injury?
Peroneus tertius rupture
Using ultrasound in tendon/ligament disorder can allow assessment of what features?
- Change in cross sectional area
- Inflammation: swelling/enlargement of the tissue which will present as a change in the cross sectional area (compare to the other side to see if one is enlarged)
- Fibre echogenicity
- Margination
- Position
- Focal lesion vs generalised changes
- acute vs chronic
- blood flow
What is Fibre echogenicity?
How dark/light the tissue is on the ultrasound machine
- Anechoic/hypoechoic
- Hyperechoic/mineralised
How does inflammation affect margination?
When its inflamed the margins become less clearly defined
Describe the pathophysiology of why intrinsic injuries occur
- Loss of strain energy as heat (hysteresis)
• 43-45C in core of tendon at gallop
• Protein uncoupling -> damage - Although often acute onset, many intrinsic tendon/ligament injuries have an ageing/degenerative component
Describe the 3 repair phases of tendon/ligament injuries (they are slightly overlapping)
- Acute inflammatory response which occurs as soon as the damage does
- Within a couple of days (and lasting a few weeks) is the proliferative phase – migration of cells into the damaged area to start producing normal or repair tissue – want to manipulate this healing process so there isn’t too much scar tissue
- Occurring over weeks/months/years is the tissue remodelling phase
Why is it important that an acute inflammatory response doesn’t last too long?
It can cause damage to the surrounding tissue
What is involved in the tissue remodelling phase?
- Anti-fibrotic cytokines
- ECM and collagen deposition
- Collagen synthesis and degradation
What are the clinical signs of the acute inflammatory phase?
Lameness
Pain on palpation
Heat
Swelling
Describe the pathology of the acute inflammatory phase
Haemorrhage Inflammation - Neutrophils - Macrophages and monocytes - Increased blood flow - Oedema - Proteolytic enzymes
What are the treatment principles for the acute inflammatory phase
- Limit inflammation: Cold therapy/ NSAIDs/
(corticosteroids) - Protect limb/reduce further damage/swelling
- Supporting bandage (cast/splint)
- Rest
What are the clinical signs of the reparative/proliferative phase
- Reduction or absence of lameness
- Resolution of signs of inflammation
- Tendon still palpably enlarged and soft
- Signs of re-injury if exercised too early
Describe the pathology of the reparative/proliferative phase
Angiogenesis
Fibroplasia:
++ fibroblasts, collagen III, small collagen fibrils formed
What are the treatment principles for the reparative/proliferative phase
- Promote angiogenesis: tendon splitting, stem cells/platelet-rich plasma
- Minimise formation of excessive scar tissue: stem cells/platelet-rich plasma, physio/ ultrasound therapy
- Early exercise (if lesion filled in) -> positive effect on collagen type I
What are the clinical signs of the Tissue modelling phase
Stiffer/thicker tendon
Describe the pathology of the Tissue modelling phase
Fibrosis
Gradual change from collagen III to I
What are the treatment principles for the Tissue modelling phase
- Increased loading and exercise programme
- Improve fitness
- Monitor progress by repeat ultrasound exam
What are the functions of skeletal, smooth and cardiac muscle?
Skeletal = maintain posture, allow movement Smooth = maintain position of fluids and move fluids Cardiac = movement of blood
Disease of muscles are called?
Myopathies
What are the features of myopathies in skeletal, smooth and cardiac muscle?
Skeletal = weakness or spasm Smooth = retention/incontinence, hypermotility or stasis Cardiac = circulatory failure
What my be found on the clinical exam in a patient with muscle conditions - acute and chronic?
Acute: swelling/pain
Chronic: stiffness, cramping, pain, fasciculations, weakness (differentiate from neurological conditions), atrophy, fibrosis/calcification
Which 2 biochemistry tests can be used to diagnose muscle conditions?
- Serum muscle enzymes (CK/AST/LDH)
- Urine sample
How are serum muscle enzymes used to diagnose muscle conditions?
- CK = creatinine kinase
- AST = Aspartate aminotransferase
- If both of these were raised it would indicate muscle damage
- CK spikes faster and is cleared faster than AST
How is a urine sample used to diagnose muscle conditions?
- Myoglobin = main muscle protein
- Released into the bloodstream when there is damage. If it reaches a particular threshold it spills over into the urine and can be detected
Which muscle conditions can be detected using ultrasound?
Acute: haematoma
Chronic: fibrosis/calcification
What is muscle atrophy?
Reduction in the size of muscles
What are the causes of muscle atrophy?
- Disuse: reversible if function restored
- Denervation
- Cachexia
When is reinnervation of muscles possib;e?
If the nerve sheath is intact
What are some causes of denervation in muscles?
- Trauma e.g. Laryngeal hemiplegia (damage to left recurrent laryngeal nerve), Canine brachial plexus in forelimb avulsion (e.g. RTA)
- Myaesthenia gravis: defect at neuromuscular junction
When is net withdrawal of muscle protein (cachexia) seen?
Pregnancy
Rapid tumour formation
What is hypertrophy?
Increased muscle bulk due to larger fibres and as a result of increased work load
What happens to muscle fibres in hypertrophy?
Undergo longitudinal splitting
Sarcomeres, myofilaments and myofibrils added
What are the three types of muscle degeneration?
- Cellular swelling
- Hyaline degeneration
- Granular degeneration
- increase in severity
Describe cellular swelling
- Minor chemical imbalances within the muscle e.g. Na+/K+ or ATP exhaustion leading to Ca2+ overload in mitochondria
- Moderate swelling but nuclei remain normal
Describe hyaline degeneration
- Affects the sarcoplasm but spares the sarcolemma
* Often seen with nutritional myopathies
Describe granular degeneration
- Severe damage with large basophilic granules of coagulated protein
- Stain positive for calcium (mitochondrial overload)
- Fibrosis or fat replacement
How are calcification and ossification involved in repair?
- Calcification due to irreversibly-damaged tissue
- Ossification where damaged tissue undergoes metaplasia to bone
Each muscle fibres is served by how many capillaries?
3-12
What are the consequences of blockage of the arterial supply to muscles?
- Partial blockage of distal aorta/iliacs can cause an ischaemic paralysis
e. g. aortic-iliac thrombosis in horses and saddle thrombi in cats with left sided cardiomyopathy
What are the consequences of blockage of the venous supply from muscles?
- Blockage of large veins leading to congestion with leakage of blood to muscles with eventual muscle necrosis and fibrosis
- Feature of prolonged recumbency in large animals
How is Selenium/ Vitamin E used in the body?
As a part of the anti-oxidant system
What are the consequences of Selenium/ Vitamin E deficiency?
If the anti-oxidant system is inefficient then there is damage to the cells within the body (particularly muscle cells) – white muscle disease
Which animals are most commonly affected by Selenium/ Vitamin E deficiency?
Calves less than 6 months old
Beef calves from dams overwintered on poor rations
What are the clinical signs of Selenium/ Vitamin E deficiency?
- Muscle weakness/ stiffness, recumbency, dyspnoea (intercostals mm)
- Arrhythmias/ murmurs when myocardium is affected
- Myoglobinuria; Elevated CK, AST values
- Serum/ whole blood levels of Selenium
How is Selenium/ Vitamin E deficiency treated?
Parenteral administration of selenium/ Vitamin E
Describe the features of stiff-lamb disease
- 2-4 week old lambs (up to 1yr)
- Similar aetiology to white muscle disease (poor rations for ewe)
- Neck and tongue muscles (young lambs) or shoulder, thigh, back and intercostal muscles (older lambs)
- Similar appearance to calves but calcification often more pronounced
How is stiff-lamb disease treated?
Parenteral administration of selenium/ Vitamin E
Describe acute exercise-induced Exertional rhabdomyolysis (ER) in the horse
- Unfit horses; “tying-up”; “colic-signs” - Laminitis would be the 3rd differential for a painful, recumbent horse
- Stiffness to severe pain/recumbency
- Commonly gluteals, semitendinosus/ semimembranosus; biceps femoris (quadriceps, back)
How is acute exercise-induced Exertional rhabdomyolysis (ER) in the horse diagnosed?
Clinical exam; muscle enzymes; myoglobinuria
How is acute exercise-induced Exertional rhabdomyolysis (ER) in the horse treated?
Pain relief; fluid therapy; acepromazine (anxiolytic/vasodilation)
Describe chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse
- 5% of TB racehorses; stress/nervous
- Poor performance/ stiffness/ ”cramps”
How is chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse diagnosed?
History; muscle enzymes; muscle biopsy (non-specific)
How is chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse treated?
Warm-up; avoid stress and high energy feeds
Describe the features and clinical signs of eosinophilic myositis
- Large breed dogs e.g. GSDs
- Acute recurrent pain and mandibular immobility: immune mediated condition
- Bilaterally enlarged temporal/masticatory muscles
- High percentage of eosinophils in the blood
Describe the features of eosinophilic myositis on histology
Central necrotic area with dead eosinophils and sarcoplasmic clumping; numerous eosinophils in periphery, some giant cells and inwardly radiating fibroblasts
How is eosinophilic myositis treated?
Corticosteroids
Name 2 bacterial conditions that affect muscles
- Blackleg
- Malignant oedema
Name 3 parasitic causes of muscle conditions
- Trichonellosis (Trichenella spiralis in pigs)
- Cysticercosis (Cysticercus ovis in sheep)
- Toxoplasmal myositis
- Sarcocysts (Sarcocytis tenella in sheep)
Describe the features of toxic-atypical myoglobinuria
- Atypical myoglobinuria in the horse
- Horses at pasture
- Unknown cause
- Associated with sudden change in weather conditions
What are the clinical signs of toxic-atypical myoglobinuria?
- Acute onset, rapid and frequently fatal
- Muscle weakness/recumbency
- Increased CK/AST and myoglobinuria
What will be seen in the PM of a horse with toxic-atypical myoglobinuria?
Widespread myonecrosis (skeletal and cardiac muscle)
