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Flashcards in Small animal MSK disease 4 Deck (100)
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What does onychosytrophy mean?

Abnormal claw growth


What does onychomadesis mean?

Sloughing of claws


What does onychomalacia mean?

Softening of claws


What does onychorrhexis mean?

Longitudinal splitting of claws


What does onychogryphosis mean?

Hypertrophy and abnormal curvature of claws


What does onychoschizia mean?

Splitting +/- lamination of claws, usually from distal end


Outline the approach to claw/law fold disease in small animals

- History: pattern of claw disease
- General physical examination
- Dermatological examination (lesions elsewhere on body etc.)
- Dermatological tests e.g. cytology, bacterial culture, fungal culture, skin scrapes
- Biopsy may be required


List possible disease of the claws/claw fold of small animals

- Traumatic
- Ingrowing claws
- Infection
- Immune mediated
- Neoplasia
- Nutritional/metabolic
- Idiopathic


Outline the treatment of torn/avulsed claws in small animals

- Remove loose claws with artery forceps
- Keep clean and protected in dressing for 2-3 days, prevent licking
- Systemic antibiotics
- Monitor regrowth for onychodystrophy
- Consider cause for breakage - obesity, poor conformation or bad luck?


When do in-growing claws most commonly occur?

- Dew claws
- Elderly cats
- Cats with polydactyly


Outline the treatment of in-growing claws

- Trim and clean
- Antibiotics if infected


Outline the treatment of bacterial infection of the claws/claw fold in small animals

- Remove loose claw plates (if present) under GA
- Treat with extended course of antibiotics, protect as for traumatic claw


Describe the common appearance of claws/claw fold affected by Malassezia

- Claws may show brown staining as direct result of Malassezia
- Rarely lame


Outline the role and treatment of dermatophytosis in claw/claw fold disease in small animals

- Rare
- Leads to onychodystrophy
- Treat with systemic antifungals until claws are normal (many weeks)


Give examples of immune mediated disease of the claw/claw fold

- Cutaneous lupus
- Vasculitits
- Drug reaction
- Pemphigus foliaceous
- Symmetrical lupoid onychodystrophy


Describe the presentation of symmetrical lupoid onychodystrophy

- Onychomadesis with exudate under claw (secondary infection)
- Often gradual progression over several months to involve multiple/all claws
- Marked pain when slough


Outline the treatment of ILSO

- Remove loose claws
- Treat using oral EFAs, tetracycline, niacinamide, severe cases with glucocorticoids, ciclosporin
- Radical total P3 amputation is unresponsive


Which breed are predisposed to ILSO?



Which breeds are predisposed to squamous cell carcinoma of the claw fold?

Large black dogs e.g. Labradors, Giant Schnauzer


Outline the pathology of SCC of the clawfold in dogs

- +/- multiple digits involved over several years
- Often bone lysis of underlying bone
- 30% metastasise to local LN


Outline the pathology seen with claw fold melanoma in small animals

- Pedal/digital melanomas usually malignant, spread to LNs, lungs esp.
- Stage fully (local LN excision, thoracic radiography, blood screen)
- 50% die from distant mets within a year, must stage before removal


Outline the general treatment for neoplasia of the claw fold in small animals

Amputation of digit at MCP joint


Which muscles are affected by masticatory muscle myositis?

- Temporalis
- Masseter
- Medial and lateral pterygoid
- Rostral portions of digastricus muscles


Which muscles are spared in masticatory muscle myositis?

- Extraocular
- Oesophageal
- Limb muscles


What is trismus?

Restricted jaw movement


Outline the clinical characteristics of the acute phase of masticatory muscle myositis

- Swelling of masticatory muscles
- Restricted jaw movement
- Inability to open jaw, even under GA
- Painful muscles of head and mouth
- Reluctance to eat, depression
- Pyrexia, submandibular, prescapular lymphadenopathy, tonsilitis variably present


Outline the histopathological characteristics of masticatory muscle myositis in the acute phase

- Multifocal and variable degrees of inflammatory cellular infiltration
- Fibrosis not usually observed
- Staining to demonstrate antibody bound to type 2M muscle fibres


Which parameters in biochemistry is commonly raised in the acute phase of MMM?

Creatinine kinase, AST
+/- Globulin


Outline the clinical characteristics of the chronic phase of MMM

- Progressive atrophy of the masticatory muscle group
- Enophthalmos
- Non-painful


Outline the histopathological characteristics of masticatory muscle myositis in the chronic phase

- Myofibre loss (atrophy)
- Interstitial fibrosis may be extensive
- Regenerative features of muscular fibres can be present


How is creatinine kinase affected in the chronic phase of MMM?/

Creatinine kinase is normal


Outline the diagnosis of masticatory muscle myositis

ELISA assay using masticatory muscle myosin as antigen


Outline the pathophysiology of masticatory muscle myositis

- Masticatory muscles contain type 2M fibres, not found in limb muscle
- Specific autoantibodies against masticatory muscle


Outline the treatment for masticatory muscle myositis

- Corticosteroid therapy
- Particularly responsive if identified early
- May add azathioprine
- Nutritional support if unable to eat


Outline the clinical signs of polymyositis in dogs

- Weight loss
- Respiratory signs e.g. coughing
- Generalised weakness
- Stiff, stilted gait
- generalised progressive atrophy of muscles incl. masticatory muscles
- Regurgitation
- Dysphagia
- Weak bark
- Some may be pyrexic


Explain the potential respiratory complications that occur with polymyositis

- Muscle atrophy affecting the oesophagus and pharynx
- Leads to regurgitation and dysphagia
- Can lead to respiratory distress
- May get aspiration pneumonia


Outline the histopathological signs of polymyositis in dogs

- Multifocal necrosis
- Phagocytosis of type 1 and 2 myofibres
- Perivascular lymphocytic and plasmacytic infiltration
- Muscle regeneration and fibrosis
- May appear normal due to multifocal patchy nature of disease


Outline the diagnosis of polymyositis in dogs

- Clinical signs
- Histopathological changes in multiple muscles
- Absence of known infectious case
- Myositis specific autoantibodies found in 2-30% of patients, but not specific to polymyositis -
- CBC, biochem, synovial fluid analysis, urinalysis, serum ANA


Outline the treatment of polymyositis in dogs

- Corticosteroid therapy (response variable)
- Upright feeding if megaoesophagus
- Antibiotics if aspiration pneumonia
- Azathioprine if pred. inadequate


Which tissues, other than the skeletal muscles, may be affected by polymyositis in dogs?

- Myocardium
- Thyroid (thryoiditis)
- Skin
- May be found in connective tissue disease e.g. SLE


What is the cause of acquired myasthenia gravis?

Antibody mediated destruction of Ach- receptors


Outline the clinical signs of myasthenia gravis

- Muscular weakness (may be focal - selective involvement of oesophageal, pharyngeal and facial muscles, or may be diffuse - generalised muscle weakness)
- Intolerance to exercise that improves with rest, to acute tetraplegia
- Aspiration pneumonia


Which condition is commonly associated with acquired myasthenia gravis?



What is the cause of congenital myasthenia gravis?

Deficiency of Ach receptors on postsynaptic membranes


Which breeds are predisposed to congenital myasthenia gravis?

- Springers
- Smooth fox terriers
- Dachshunds


Outline the clinical presentation of congenital myasthenia gravis in dogs

- Onset usually 6-8weeks old
- Generalised muscle weakness associated with age
- Megaoesophagus
- Weakness progressive, leading to tetraplegia and death


Outline the histopathological appearance of muscles in dogs with myasthenia gravis

No changes expected, useful for ruling out other muscular diseases


Outline the diagnosis of myasthenia gravis

- Edrophonium chloride testing (not definitive, but highly suggestive)
- Electrodiagnostic testing (declining amplitude of successive potentials provides presumptive positive for MG)
- Immunological (AchRAb titres - acquired only)
- Intercostal muscle biopsy demonstrating decreased numbers of ACh receptors (congenital)


Outline the difficulties with the treatment of myasthenia gravis in dogs

- May go into spontaneous remission, complicating treatment
- Lots of supportive care required: management of aspiration pneumonia, fluid therapy, nutritional support, respiratory support, modification of GI function
- Early diagnosis important for good clinical outcome


Outline the modification of GI function required in the treatment of MG in dogs

- Increase motility using metaclopramide
- Increase lower oesophgeal sphincter tone with cisapride
- Increase pH of GI contents with cimetidine or ranitidine


Outline the treatment of MG using anticholinesterase agents

- E.g. pyridostigmine bromide, neostigmine bromide
- Enhance neuromuscular transmission
- Dosage adjusted to adverse effects and response to treatment


Outline the treatment of mild/focal MG and moderate generalised MG

- Immunosuppressive therapy
- Low dose pred (0.5mg/kg EOD)
- Others: azathioprine, cyclosporine, cyclophsophamide, mycophenolate mofetil if glucocorticoids contraindicated/adverse effects


List the contraindications for use of glucocorticoids in the treatment of MG in dogs

- Ongoing infections
- Aspiration pneumonia
- Diabetes mellitus
- Severe obesity
- Uncontrolled hypertension
- GI ulcerations


Discuss the prognosis for idiopathic polymyositis

- Outcome dependent on time between onset of clinical signs and diagnosis of disease
- Good if no megaoesophagus, aspiration pneumonia, neoplastic cause
- Spontaneous recovery in some dogs
- Fibrosis: prognosis poor (chronic lesion)


Which breeds are predisposed to idiopathic polymyositis?

- Boxer
- Newfoundlands
- (Also some cats)


Discuss the aetiology of polymyositis

- Primary immune mediated
- Secondary to systemic immune mediated disease (SLE)
- Protozoal infection (Toxo, neospora)


Which parameters are likely to be raised on biochemistry in an animals with polymyositis?

- Serum creatinine kinase
- Serum AST


Discuss the aetiology of infectious myositis

- Infection with T. gondii alone, or with myelitis, meningitis or polyradiculoneuritis
- N. caninum


Describe the typical appearance of infectious myositis resulting from N. caninum

Progressive rigid HL hyperextension


Describe the clinical presentation of infectious myositis in dogs and cats

- Muscle pain, swelling or atrophy
- Weakness
- T gondii in cats: signs relate more to CNS, respiratory or GI


What would be expected on EMG in a case of infectious myositis?

Spontaneous activity in affected muscles


Identify the diagnostic procedures required for infectious myositis

- CBC and biochem (elevated CK and AST)
- Serum titres for organism
- Muscle biopsy
- Immunohistochemical staining
- PCR and CSF fluid analysis


Describe the histopathological appearance of muscle in a case of infectious myositis

- Mononuclear inflammatory reaction
- Identification of organisms
- Segmental myofibre necrosis
- Intracytoplasmic protozoal cysts


Outline the treatment for Toxoplasma in dogs

- Oral clindamycin
- Successful for 14d, but recommended course of 4-6 weeks


What is used in the treatment of Neospora in cats?

- Clindamycin


Discuss the prognosis of infectious myositis in dogs and cats

- Therapy started early in order to be effective
- Prognosis poor in chronic cases


Discuss the prognosis of masticatory myositis

- Aggressive treatment gives good prognosis
- Chronic fibrosis has adverse effect on outcome in some cases
- Risk of relapse


Which breed is predisposed to centronuclear myopathy?

Labrador retrievers


Outline the aetiology of centronuclear myopathy

- Inherited autosomal recessive
- Aka: Hereditary Labrador retriever myopathy (HLRM), autosomal recessive muscular dystrophy, type 2 myofibre deficiency


Describe the clinical presentation of centronuclear myopathy

- Normal at birth, signs 2-11MO
- Muscular weakness within 6 MO
- Awkward gait, exercise intolerance, muscular atrophy without myalgia 3-5MO
- Low head carriage, short strided, stilted gait, back arched, bunny hopping, marked muscle atrophy esp. proximal limbs and muscles of mastication
- Neurological examination normal except patellar and triceps hypo/areflexia
- Megaoesophagus
- Signs stabilise after 12 months if mildly affected


Under what conditions are the clinical signs of centronuclear myopathy exacerbated?

- Stress
- Exercise
- Excitement
- Cold temperatures


What tests are used in the diagnosis of centronuclear myopathy?

- Blood biochemistry
- Histopathology
- DNA/genetic testing


Describe the histopathological appearance of muscle in a case of centronuclear myopathy

- Mild to marked variation in fibre size
- Atrophic type 1 and type 2 myofibres
- replacement of tepe 2 myofibres by type 1 fibres
- Marked increase in centralisation of nuclei within muscle cells
- No inflammation
- Clusters of fibres showing atrophy or hypertrophy


What would be expected on biochemistry in a case of centronuclear myopathy?

Normal, may have moderately elevated serum CK


What would be expected on EMG in a case of centronuclear myopathy?

Spontaneous electrical activity and bizarre high-frequency discharges


What is the treatment for centronuclear myopathy?

NO treatment, usually does not progress more after 6-12MO, mildly affected can function as pets


Which animals may be affected by steroid myopathy?

- Dogs with HAC
- Dogs and cats with exogenous steroid treatment


Describe the clinical presentation for a case of steroid myopathy

- Muscle weakness and atrophy
- Atrophy may be more pronounced in muscles of mastication


Outline the diagnosis of steroid myopathy

- History of exogenous steroids/HAC
- Clinical findings consistent with steroid excess e.g. PUPD, alopecia, pendulous abdomen, thin skin
- Muscle biopsy showing non-specific changes e.g. type 2 myofibre atrophy, focal necrosis, fibre size variation


Outline the treatment of steroid myopathy

- Supplementation with L-carnitine, coenzyme Q10, riboflavin may improve muscular strenght
- control of excess glucocorticoids (stop/reduce)
- Trilostane if HAC


Which animals are usually affected by hypokalaemic myopathy?

Cats mainly


Discuss the aetiology of hypokalaemic myopathy in cats

- Chronic renal failure, acidifying diets, poor dietary inake of K
- PUPD secondary to hyperT
- Anorexia
- Burmese kittens
- Primary hyperaldosteronism due to functional adrenal neoplasia (Conn's syndrome)
- Iatrogenic IV fluids without K supplementation, diuresis with frusemide


Outline the clinical presentation of hypokalaemic myopathy

- Generalised, dramatic muscle weakness
- Ventroflexion of the neck
- Stiff, stilted gait
- Reluctance to move
- Excessive dorsal scapular movement during walking
- Exertional tremor
- Collapse
- Muscle pain
- Neurologically normal otherwise
- May be episodic signs


What findings would be expected on biochemistry in a case of hypokalaemic myopathy?

- Serum CK activity increased
- Serum potassium decreased
- Serum urea and creatinine increased if renal dysfunction


Explain why detection of underlying renal dysfunction may be difficult in a case of hypokalaemic myopathy

Hypokalaemia decreased renal blood flow and GFR, interfering with urine concentrating mechanisms


What findings would be expected on urinalysis in a case of hypokalaemic myopathy?

Increased fractional urinary excretion of K


Which diagnostic tests are used to identify hypokalaemic myopathy?

- Blood biochem
- Urinalysis
- +/- muscle histopathology


What would be expected on EMG in a case of hypokalaemic myopathy?

- Freqyent positive sharp waves
- Fibrillation potentials
- Occasional bizarre high frequency discharges with normal nerve conduction velocities


Describe the muscle histopatholgy in a case of hypokalaemic myopathy

- May be normal
- Or may have variable muscular necrosis and regeneration


Outline the treatment of hypokalaemic myopathy in cats

- Parenteral/oral potassium supp. (potassium gluconate oral for mildly affected, 2.5-5mEq/cat BID for 2 days)
- In severe cases: parenteral LRS IV/subcut, supplemented with at least 80mEq/L of potassium chloride
- IV supp. of K should not exceed 0.5mEq/kg/h
- Long term supp. with potassium gluconate may be required
- periodic monitoring of serum potassium to adjust dose


Discuss the prognosis of hypokalaemic myopathy

Generally good if underlying problem addressed


What are the common underlying cases of ischaemic neuromyopathy in dogs and cats?

- Cats: cardiomyopathy, or protein losing nephropathy
- Dogs: hypercoagulabiltiy disorders


What is caudal aortic thromboembolism leading to paralysis in cats an example of?

Ischaemic neuromyopathy


Outline the treatment for aortic thromboembolism/ischaemic neuromyopathy

- Analgesia
- +/- anticoagulants e.g. sodium heparin, enoxaparin, dalteparin sodium
- Treatment of underlying disease
- No safe specific treatment available


List the negative prognostic indicators for aortic thromboembolism in cats

- Hypothermia
- Cardiomyopathy
- Hyperphasophataemia
- Progressive hyperaemia
- Azotaemia
- Bradycardia
- Persistent lack of motor function
- Progressive limb injury
- Severe LA enlargement
- Presence of intracardiac thrombi
- History of previous thromboembolism


Outline the diagnostic tests in dogs for suspected aortic thromboembolism

Should be evaluated for nephrotic syndrome, hyperadrenocorticism, heartworm, neoplasia, endocarditis


Which breeds are predisposed to extraocular myositis?

- Labs, Golden retrievers
- Females more than males


Outline the aetiolofy of extraocular myositis

- Immune mediated
- Confined to extraocular muscles


Outline the clinical presentation of extraocular myositis

- Acute: bilateral exophthalmos and eyelid retraction, chemosis, no TEL prolapse
- Vision may be impaired
- Chronic: restrictive strabismus


List the tests used in the diagnosis of extraocular myositis

- Blood biochemistry
- Orbital sonography/MRI
- Biopsy