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MSK2 > Small animal MSK disease 4 > Flashcards

Small animal MSK disease 4 Flashcards

1
Q

What does onychosytrophy mean?

A

Abnormal claw growth

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2
Q

What does onychomadesis mean?

A

Sloughing of claws

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3
Q

What does onychomalacia mean?

A

Softening of claws

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4
Q

What does onychorrhexis mean?

A

Longitudinal splitting of claws

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5
Q

What does onychogryphosis mean?

A

Hypertrophy and abnormal curvature of claws

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6
Q

What does onychoschizia mean?

A

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

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7
Q

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

A
  • 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
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8
Q

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

A
  • Traumatic
  • Ingrowing claws
  • Infection
  • Immune mediated
  • Neoplasia
  • Nutritional/metabolic
  • Idiopathic
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9
Q

Outline the treatment of torn/avulsed claws in small animals

A
  • 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?
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10
Q

When do in-growing claws most commonly occur?

A
  • Dew claws
  • Elderly cats
  • Cats with polydactyly
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11
Q

Outline the treatment of in-growing claws

A
  • Trim and clean

- Antibiotics if infected

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12
Q

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

A
  • Remove loose claw plates (if present) under GA

- Treat with extended course of antibiotics, protect as for traumatic claw

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13
Q

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

A
  • Claws may show brown staining as direct result of Malassezia
  • Rarely lame
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14
Q

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

A
  • Rare
  • Leads to onychodystrophy
  • Treat with systemic antifungals until claws are normal (many weeks)
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15
Q

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

A
  • Cutaneous lupus
  • Vasculitits
  • Drug reaction
  • Pemphigus foliaceous
  • Symmetrical lupoid onychodystrophy
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16
Q

Describe the presentation of symmetrical lupoid onychodystrophy

A
  • Onychomadesis with exudate under claw (secondary infection)
  • Often gradual progression over several months to involve multiple/all claws
  • Marked pain when slough
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17
Q

Outline the treatment of ILSO

A
  • Remove loose claws
  • Treat using oral EFAs, tetracycline, niacinamide, severe cases with glucocorticoids, ciclosporin
  • Radical total P3 amputation is unresponsive
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18
Q

Which breed are predisposed to ILSO?

A

Greyhounds

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19
Q

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

A

Large black dogs e.g. Labradors, Giant Schnauzer

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20
Q

Outline the pathology of SCC of the clawfold in dogs

A
  • +/- multiple digits involved over several years
  • Often bone lysis of underlying bone
  • 30% metastasise to local LN
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21
Q

Outline the pathology seen with claw fold melanoma in small animals

A
  • 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
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22
Q

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

A

Amputation of digit at MCP joint

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23
Q

Which muscles are affected by masticatory muscle myositis?

A
  • Temporalis
  • Masseter
  • Medial and lateral pterygoid
  • Rostral portions of digastricus muscles
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24
Q

Which muscles are spared in masticatory muscle myositis?

A
  • Extraocular
  • Oesophageal
  • Limb muscles
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25
Q

What is trismus?

A

Restricted jaw movement

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26
Q

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

A
  • 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
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27
Q

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

A
  • Multifocal and variable degrees of inflammatory cellular infiltration
  • Fibrosis not usually observed
  • Staining to demonstrate antibody bound to type 2M muscle fibres
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28
Q

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

A

Creatinine kinase, AST

+/- Globulin

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29
Q

Outline the clinical characteristics of the chronic phase of MMM

A
  • Progressive atrophy of the masticatory muscle group
  • Enophthalmos
  • Non-painful
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30
Q

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

A
  • Myofibre loss (atrophy)
  • Interstitial fibrosis may be extensive
  • Regenerative features of muscular fibres can be present
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31
Q

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

A

Creatinine kinase is normal

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32
Q

Outline the diagnosis of masticatory muscle myositis

A

ELISA assay using masticatory muscle myosin as antigen

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33
Q

Outline the pathophysiology of masticatory muscle myositis

A
  • Masticatory muscles contain type 2M fibres, not found in limb muscle
  • Specific autoantibodies against masticatory muscle
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34
Q

Outline the treatment for masticatory muscle myositis

A
  • Corticosteroid therapy
  • Particularly responsive if identified early
  • May add azathioprine
  • Nutritional support if unable to eat
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35
Q

Outline the clinical signs of polymyositis in dogs

A
  • 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
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36
Q

Explain the potential respiratory complications that occur with polymyositis

A
  • Muscle atrophy affecting the oesophagus and pharynx
  • Leads to regurgitation and dysphagia
  • Can lead to respiratory distress
  • May get aspiration pneumonia
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37
Q

Outline the histopathological signs of polymyositis in dogs

A
  • 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
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38
Q

Outline the diagnosis of polymyositis in dogs

A
  • 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
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39
Q

Outline the treatment of polymyositis in dogs

A
  • Corticosteroid therapy (response variable)
  • Upright feeding if megaoesophagus
  • Antibiotics if aspiration pneumonia
  • Azathioprine if pred. inadequate
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40
Q

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

A
  • Myocardium
  • GIT (IBD)
  • Thyroid (thryoiditis)
  • Skin
  • May be found in connective tissue disease e.g. SLE
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41
Q

What is the cause of acquired myasthenia gravis?

A

Antibody mediated destruction of Ach- receptors

42
Q

Outline the clinical signs of myasthenia gravis

A
  • 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
43
Q

Which condition is commonly associated with acquired myasthenia gravis?

A

Thymomas

44
Q

What is the cause of congenital myasthenia gravis?

A

Deficiency of Ach receptors on postsynaptic membranes

45
Q

Which breeds are predisposed to congenital myasthenia gravis?

A
  • JRT
  • Springers
  • Smooth fox terriers
  • Dachshunds
46
Q

Outline the clinical presentation of congenital myasthenia gravis in dogs

A
  • Onset usually 6-8weeks old
  • Generalised muscle weakness associated with age
  • Megaoesophagus
  • Weakness progressive, leading to tetraplegia and death
47
Q

Outline the histopathological appearance of muscles in dogs with myasthenia gravis

A

No changes expected, useful for ruling out other muscular diseases

48
Q

Outline the diagnosis of myasthenia gravis

A
  • 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)
49
Q

Outline the difficulties with the treatment of myasthenia gravis in dogs

A
  • 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
50
Q

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

A
  • Increase motility using metaclopramide
  • Increase lower oesophgeal sphincter tone with cisapride
  • Increase pH of GI contents with cimetidine or ranitidine
51
Q

Outline the treatment of MG using anticholinesterase agents

A
  • E.g. pyridostigmine bromide, neostigmine bromide
  • Enhance neuromuscular transmission
  • Dosage adjusted to adverse effects and response to treatment
52
Q

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

A
  • Immunosuppressive therapy
  • Low dose pred (0.5mg/kg EOD)
  • Others: azathioprine, cyclosporine, cyclophsophamide, mycophenolate mofetil if glucocorticoids contraindicated/adverse effects
53
Q

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

A
  • Ongoing infections
  • Aspiration pneumonia
  • Diabetes mellitus
  • Severe obesity
  • Uncontrolled hypertension
  • GI ulcerations
54
Q

Discuss the prognosis for idiopathic polymyositis

A
  • 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)
55
Q

Which breeds are predisposed to idiopathic polymyositis?

A
  • GSD
  • Boxer
  • Newfoundlands
  • (Also some cats)
56
Q

Discuss the aetiology of polymyositis

A
  • Primary immune mediated
  • Secondary to systemic immune mediated disease (SLE)
  • Protozoal infection (Toxo, neospora)
57
Q

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

A
  • Serum creatinine kinase

- Serum AST

58
Q

Discuss the aetiology of infectious myositis

A
  • Infection with T. gondii alone, or with myelitis, meningitis or polyradiculoneuritis
  • N. caninum
59
Q

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

A

Progressive rigid HL hyperextension

60
Q

Describe the clinical presentation of infectious myositis in dogs and cats

A
  • Muscle pain, swelling or atrophy
  • Weakness
  • T gondii in cats: signs relate more to CNS, respiratory or GI
61
Q

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

A

Spontaneous activity in affected muscles

62
Q

Identify the diagnostic procedures required for infectious myositis

A
  • CBC and biochem (elevated CK and AST)
  • Serum titres for organism
  • EMG
  • Muscle biopsy
  • Immunohistochemical staining
  • PCR and CSF fluid analysis
63
Q

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

A
  • Mononuclear inflammatory reaction
  • Identification of organisms
  • Segmental myofibre necrosis
  • Intracytoplasmic protozoal cysts
64
Q

Outline the treatment for Toxoplasma in dogs

A
  • Oral clindamycin

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

65
Q

What is used in the treatment of Neospora in cats?

A
  • Clindamycin

- TMPS

66
Q

Discuss the prognosis of infectious myositis in dogs and cats

A
  • Therapy started early in order to be effective

- Prognosis poor in chronic cases

67
Q

Discuss the prognosis of masticatory myositis

A
  • Aggressive treatment gives good prognosis
  • Chronic fibrosis has adverse effect on outcome in some cases
  • Risk of relapse
68
Q

Which breed is predisposed to centronuclear myopathy?

A

Labrador retrievers

69
Q

Outline the aetiology of centronuclear myopathy

A
  • Inherited autosomal recessive

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

70
Q

Describe the clinical presentation of centronuclear myopathy

A
  • 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
71
Q

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

A
  • Stress
  • Exercise
  • Excitement
  • Cold temperatures
72
Q

What tests are used in the diagnosis of centronuclear myopathy?

A
  • Blood biochemistry
  • EMG
  • Histopathology
  • DNA/genetic testing
73
Q

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

A
  • 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
74
Q

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

A

Normal, may have moderately elevated serum CK

75
Q

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

A

Spontaneous electrical activity and bizarre high-frequency discharges

76
Q

What is the treatment for centronuclear myopathy?

A

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

77
Q

Which animals may be affected by steroid myopathy?

A
  • Dogs with HAC

- Dogs and cats with exogenous steroid treatment

78
Q

Describe the clinical presentation for a case of steroid myopathy

A
  • Muscle weakness and atrophy

- Atrophy may be more pronounced in muscles of mastication

79
Q

Outline the diagnosis of steroid myopathy

A
  • 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
80
Q

Outline the treatment of steroid myopathy

A
  • Supplementation with L-carnitine, coenzyme Q10, riboflavin may improve muscular strenght
  • control of excess glucocorticoids (stop/reduce)
  • Trilostane if HAC
81
Q

Which animals are usually affected by hypokalaemic myopathy?

A

Cats mainly

82
Q

Discuss the aetiology of hypokalaemic myopathy in cats

A
  • 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
83
Q

Outline the clinical presentation of hypokalaemic myopathy

A
  • 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
84
Q

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

A
  • Serum CK activity increased
  • Serum potassium decreased
  • Serum urea and creatinine increased if renal dysfunction
85
Q

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

A

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

86
Q

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

A

Increased fractional urinary excretion of K

87
Q

Which diagnostic tests are used to identify hypokalaemic myopathy?

A
  • Blood biochem
  • Urinalysis
  • EMG
  • +/- muscle histopathology
88
Q

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

A
  • Freqyent positive sharp waves
  • Fibrillation potentials
  • Occasional bizarre high frequency discharges with normal nerve conduction velocities
89
Q

Describe the muscle histopatholgy in a case of hypokalaemic myopathy

A
  • May be normal

- Or may have variable muscular necrosis and regeneration

90
Q

Outline the treatment of hypokalaemic myopathy in cats

A
  • 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
91
Q

Discuss the prognosis of hypokalaemic myopathy

A

Generally good if underlying problem addressed

92
Q

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

A
  • Cats: cardiomyopathy, or protein losing nephropathy

- Dogs: hypercoagulabiltiy disorders

93
Q

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

A

Ischaemic neuromyopathy

94
Q

Outline the treatment for aortic thromboembolism/ischaemic neuromyopathy

A
  • Analgesia
  • +/- anticoagulants e.g. sodium heparin, enoxaparin, dalteparin sodium
  • Treatment of underlying disease
  • No safe specific treatment available
95
Q

List the negative prognostic indicators for aortic thromboembolism in cats

A
  • Hypothermia
  • Cardiomyopathy
  • Hyperphasophataemia
  • Progressive hyperaemia
  • Azotaemia
  • Bradycardia
  • Persistent lack of motor function
  • Progressive limb injury
  • Severe LA enlargement
  • Presence of intracardiac thrombi
  • DIC
  • History of previous thromboembolism
96
Q

Outline the diagnostic tests in dogs for suspected aortic thromboembolism

A

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

97
Q

Which breeds are predisposed to extraocular myositis?

A
  • Labs, Golden retrievers

- Females more than males

98
Q

Outline the aetiolofy of extraocular myositis

A
  • Immune mediated

- Confined to extraocular muscles

99
Q

Outline the clinical presentation of extraocular myositis

A
  • Acute: bilateral exophthalmos and eyelid retraction, chemosis, no TEL prolapse
  • Vision may be impaired
  • Chronic: restrictive strabismus
100
Q

List the tests used in the diagnosis of extraocular myositis

A
  • Blood biochemistry
  • Orbital sonography/MRI
  • Biopsy

MSK2 (29 decks)

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