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NEU2 > Neurological diseases of small animals 3 > Flashcards

Neurological diseases of small animals 3 Flashcards

Toxicities, pain

1
Q

List commo neuroinhibitory toxins

A
  • Venom (not found in UK)
  • Macadamia nuts
  • Metronidazole
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2
Q

What is the first line of treatment with all causes of intoxication?

A

Decontamination

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3
Q

List the methods for decontamination of gastrointestinally absorbed toxins

A
  • Emesis
  • Gastric lavage
  • Activated charcoal
  • Colonic lavage and cathartics
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4
Q

Outline the use of emesis as a method of decontamination of toxins

A
  • Within 2 hours of ingestion
  • In alert patients only in order to prevent aspiration pneumonia
  • LImits absorption
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5
Q

Outline the use of gastric lavage as a method of decontamination of toxins

A
  • Within 2 hours of ingestion
  • Can be used in subdued/comatose animals
  • Must be under GA
  • Extreme care to protect airways using cuffed ET tube
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6
Q

Outline the use of activated charcoal as a method of decontamination of toxins

A
  • 1-5g/kg every 6-8 hours for up to 24 hours

- In alert patients only

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7
Q

Outline the method of decontamination of cutaneous toxins

A
  • Bath, for stable patients

- Washing up liquids may be best as are effective against greasy substances which are absorbed best through the siin

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8
Q

What method is used for the decontamination of inhaled toxins?

A

Ventilation, mechanical in severe cases

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9
Q

Outline the use of lipid infusions as a method of decontamination of toxins

A
  • Lipid infusion (intralipid) if exposure to lipophilic substances
  • Acts as lipid sink
  • Bolus of 2mg/kg followed by CRI of 4mg/kg/hr for 4 hours
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10
Q

Describe the clinical signs of ivermectin and macrolide parasiticide toxicity

A
  • Ataxia
  • Lethargy
  • Tremors
  • Mydriasis
  • Blindness
  • Hypersalication
  • Disorientation
  • Seizures rare)
  • In minority of cases: weakness, stupor, coma, respiratory failure
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11
Q

Outline the management of ivermectin and macrolide parasiticide toxicity

A
  • Emesis
  • Activated charcoal
  • Lipid infusion
  • Supportive treatment (temperature)
  • Phenobarbital for seizure control or propofol CRI if not responding
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12
Q

Discuss the prognosis for ivermectin/macrolide parasiticide toxicities

A
  • Dose related
  • Can be guarded
  • Long recovery due to long half life (can have significant financial impact)
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13
Q

How does metaldehyde intoxication occur?

A

Found in slug and snail baits, contain beetroot derivatives so smell and taste appealing

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14
Q

Describe the mechanism of action of metaldehydes leading to toxicity

A
  • Reduces levels of GABA, reducing inhibition and increasing excitation
  • Reduce levels of noradrenaline and serotonin, leading to behavioural effects
  • Pro-convulsive effects
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15
Q

What are the lethal doses of metaldehyde in cats and dogs?

A

LD50 100mg/kg in dogs, 207mg/kg in cats PO

- Difficult to know how much ingested as is sprinkled on the ground

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16
Q

Describe the clinical signs of metaldehyde toxicity

A
  • Anxiety
  • Muscle tremors
  • Fasciculations
  • Ataxia
  • Seizures common
  • Minority: tachypnoea, tachycardia, hyperthermia
  • Muscle involvement can lead to heat stroke
  • Vomiting and diarrhoea with highly indicative green-blue colour
  • NB often late presentation
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17
Q

Describe the management of metaldehyde toxicity

A
  • Emesis or gastric lavage if not yet seizuring
  • Activated charcoal
  • Benzodiazepine/phenobarbital for muscle tremors/seizures
  • Propofol infusion in refractor seizures
  • Monitor body temp, cool if needed
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18
Q

Outline the prognosis for metaldehyde toxicity

A

Good if prompt intervention

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19
Q

How does methylxanthine toxicity occur?

A

Ingestion of caffeine, theobromine (chocolate), theophylline

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20
Q

Describe the mechanism of action of methyxanthine toxicity

A
  • Elevation of intracellular cAMP, leading to increased intracellular Ca++ and increased neuromuscular excitability and inotropic effect
  • Competitive inhibition of adenosine receptors leading CNS stimulation (A1 and A2 present in brain, regulat heart beat, release of dopamine and glutamate, adenosine increases heart rate and stimulation of the brain)
  • Acts on autonomic nervous system
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21
Q

What doses of caffeine and theobromine are likely to lead to mild clinical signs and seizures?

A
  • Mild: 20mg/kg
  • Seizures: 60mg/kg
  • Cocoa percentage on packet can help work out how many mg
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22
Q

Describe the clinical signs of methylxanthine toxicity

A
  • Usually 1-2 hours after ingestion
  • Restlessness, hyperactivity
  • V/D
  • Tachycardia/tachypnoea
  • Polyuria
  • Muscle twitching
  • Seizures (tonic or tetanic)
  • Hyperthermia
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23
Q

Describe the management of methylxanthine toxicity

A
  • Emesis/activated charcoal
  • Control of ventricular arrhythmias (lidocaine, procainamide, Ca channel blockers, beta blockers)
  • Control muscle tremors/seizures with BZD/phenobarb/propofol if refractory
  • Control temperature
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24
Q

Outline the prognosis for methylxanthine toxicity

A
  • Dose dependent

- Good if early treatment

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25
Q

How does organophosphate and carbamate toxicity occur?

A

Ingestion or dermal contact, commonly used in agriculture, domestic garden use and external parasite control

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26
Q

Describe the mechanism of action of organophosphates and carbamates leading to toxicity

A

Inhibit action of acetylcholinesterase so Ach accumulates in synaptic space leading to continued muscle contraction (Na+ continues to pass through the channels that are opened by ACh)

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27
Q

What are the 3 syndromes of organophosphate/carbamate toxicity?

A
  • Acute
  • Intermediate
  • Delayed (neuropathy)
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28
Q

What are the 4 groups of clinical signs seen in acute OP/carbamate toxicity?

A
  • Muscarinic (autonomic Ach receptors)
  • Nicotininc (peripheral NS Ach receptors)
  • CNS signs
  • Heat stroke as a result of muscular thermogenesis
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29
Q

Describe the muscarinic clinical signs of acute OP/carbamate toxicity

A
  • Hypersalivation
  • Lacrimation
  • Urination
  • Defaecation
  • Vomiting
  • Miosis
  • Bradycardia
  • Bronchospasm
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30
Q

Describe the nicotinic clinical signs of acute OP/carbamate toxicity

A
  • Muscle fasciculations, twitches, tremors

- Dealy neuromusclar signs due to damage to receptors from over stimulation leading to weakness and paralysis

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31
Q

Describe the CNS signs of acute OP/carbamate toxicity

A
  • Anxiety
  • Ataxia
  • seizure
  • Obtundation (reduced alertness)
  • Coma
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32
Q

Describe the intermediate syndrome of OP/carbamate toxicity

A
  • 7-96hours
  • Severe neuromuscular signs
  • Weakness
  • Neck ventroflexion
  • Generalised FL weakness
  • Hypoventilation (intercostal muscles may be affected)
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33
Q

Describe the delayed syndrome of OP/carbamate toxicity

A
  • 1-4 weeks after exposure
  • Anorexia, lethargy, pevic limb paresis
  • Hyperaesthesia
  • Neck ventroflexion (cat)
  • Uncommon
  • Presents as LMN weakness
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34
Q

Describe the diagnosis of OP/carbamate toxicity

A
  • Known exposure
  • Whole blood (heparin) cholinesterase activity <20-25% of normal
  • Gastric content
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35
Q

Describe the management of OP/carbamate toxicity

A
  • Skin decontamination if topical
  • EMesis or activated charcoal if ingestion
  • Atropine 0.02mg/kg IV for muscarinic signs
  • Pralidoxine (2-PAM) 10-20mg/kg SC, IM or IV (care, may worsen clinical signs)
  • Supportive care, esp. temperature
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36
Q

Outline the prognosis for OP/carbamate toxicity

A
  • Good if patient survives

- Quick intervention at presentation of initial toxicity needed

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37
Q

How may permethrin toxicity occur?

A
  • Commonly found in medicated shampoo, spot on flea treatments, flea collars, environmental insecticidal treatments
  • Common in cats due to inappropriate flea treatment product use
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38
Q

Why are cats more susceptible for permethrin toxicity?

A

Deficiency in hepatic glucoronidatin

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39
Q

Describe the mechanism of action of permethrin toxicity

A
  • Slows opening and closing of voltage sensitive Na+ channels
  • Results in prolonged depolarisation
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40
Q

Describe the clinical presentation of permethrin toxicity

A
  • 3hrs to 3 days post exposure
  • Muscle fasciculations
  • Ears twitching
  • Tremors
  • Ataxia
  • Seizures, hyperthermia, hyperaesthesia
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41
Q

Describe the management of permethrin toxicity

A
  • Decontamination of skin if dermal exposure (washing up liquid)
  • Control temperature (hyperthermia form muscle fasciculations, hypothermia from bath which will extend half life of permethrin)
  • BZD, phenobarb for tremors/seizures
  • IV lipids to act as lipid sink
42
Q

Outline the prognosis for permethrin toxicity

A
  • Usually good if treatment/decontamination started promptly

- Recovery takes 2-7 days

43
Q

Explain how mycotoxin toxicity occurs

A

e.g Penitrem A and Roquefortine

Ingestion for mouldy foods e.g. nuts, soft cheese, garbage, compost

44
Q

Outline the mechanism of action of mycotoxins-

A

Unknown, likely inhibition of glycine function or release in the CNS

45
Q

Describe the clinical signs of mycotoxin toxicity

A
  • 30 min to several hours post ingestion
  • Hyperaesthesia
  • Restlessness
  • Vomiting
  • Salivation
  • Muscle tremors
  • Seizures
  • Status epilepticus (dose dependent)
  • Heat stroke
46
Q

Describe the diagnosis of mycotoxin toxicity

A
  • History
  • Mass spectroscopy
  • Chromatography
  • Culture of vomitus
  • May be able to identify specific mould toxin
47
Q

Describe the management of mycotoxin toxicity

A
  • Emesis, gastric lavage, activated charcoal (for 24 hours to reduce enterohepatic recirculation of the toxin0
  • BZD/phenobarb
  • GA for refractory tremors
  • Supportive care incl, temperature management
48
Q

Describe the prognosis for mycotoxin toxicity

A

Generally good, improvements in 1 to 5 days

49
Q

Explain how strychnine toxicity may occur

A
  • Used as a pesticidal for small mammals
  • Restricted access in EU countries as plant pesticide, becoming less common
  • Inhalation or ingestion
50
Q

Describe the mechanism of action of strychnine toxicity

A
  • Blocks action of glycine (inhibitory neurotransmitter)
  • Prevents release fo glycine from Renshaw cells in spinal cord
  • CNS and LMN lack of glycine causes contraction of muscles
51
Q

Describe the clinical signs of strychnine toxicity

A
  • Onset 10-120 mins from exposure
  • Progressive and severe muscle spasm and extensor rigidity (saw horse and risus sardonicus-rictus grin)
  • convulsions
  • Heat stroke
  • Paralysis of diaphragm leading to hypoventilation )(potentially fatal)
  • Pain
52
Q

Outline the diagnosis of strychnine toxicity

A
  • History

- Analysis of gastric content, esp. if suspicious of malicious exposure

53
Q

Outline the management of strychine toxicity

A
  • Emesis (not if clinical signs already present)
  • Gastric lavage under GA
  • Activated charcoal
  • Muscle spasm and convulsions must be controlled by BZDs/phenobar/CRU propofol (24-72 hours)
  • Mechanical ventilation may be necessary
54
Q

Describe the prognosis for strychnine toxicity

A
  • Fair to good
  • Very painful
  • Intervene early and small amount ingested then stand a fair chance
55
Q

Describe the mechanism of action of lead toxicity

A
  • Bind to sulfhydryl groups
  • Interferes with haem synthesis, leading to RBC fragility, basophilic stippling within erythrocytes
  • Neurotoxicity likely linked to interference with action of GABA, capillary damage, neuronal necrosis, inhibition of Ca2+, interference with dopamine uptake
56
Q

Describe the clinical signs of lead toxicity

A
  • Systemic: V+, anorexia, abdo pain, lethargy, PUPD
  • Neuro: behavioural changes (may be presented as forebrain disease), ataxia, head pressing, blindness, tremors, polyneuropathy, seizures
  • Signs can be intermittent and depend on exposure.amount ingested
57
Q

Outline the diagnosis of lead toxicity

A
  • History
  • Presence of nucleated RBC and basophilic stippling
  • Blood lead: >0.35ppm, Urine lead >0.75ppm
58
Q

Describe the management of lead toxicity

A
  • Decontamination: emesis, removal of lead fb, magnesium sulphate 200-500mg/kg PO (cathartic, reduces absorption)
  • Chelation therapy
  • Seizure control with BZD
  • Mannitol to reduce ICP
59
Q

Explain why lead toxicity may raise the ICP

A

Chronic lead exposure can lead to neuronal damage, which leads to oedema, causing elevated ICP

60
Q

Describe the chelation therapies that can be used for lead toxicity

A
  • Succimer 10mg/kg q8hrs for 10 days
  • Calcium EDTA 27mg/kg q6hrs SC injection (must be diluted as can cause renal tubular necrosis)
  • D-penicillamine 10-15mg/kg/day for 1 week
61
Q

Describe the prognosis for lead toxicity

A

Variable, generally goo if undergoing chelating therapy

62
Q

Describe the clinical signs of macadamia nut toxicity

A
  • 12-24 hours after ingestion
  • Pelvic limb weakness
  • Stiffness
  • Paresis
  • Muscle tremors
  • Vomiting
  • Hyperthermia
63
Q

Describe the management of macadamia nut toxicity

A
  • Emesis within 2-4 hours
  • Supportive care (fluidotherapy, antiemetics, control temp)
  • Methocarbacom to reduce muscle tremors
64
Q

Explain how metronidazole toxicity may occur

A
  • Commonly used antibacterial and antiprotozoal

- Some may receive long or repeated courses of emtronidazole

65
Q

Describe the mechanism of action of metronidazole as a neurotoxin

A
  • Not fully understood
  • Purkinje cell loss
  • Axonal degeneration in vestibular tracts
66
Q

What is the toxic dose of metronidazole?

A

60mg/kg/day, some individual susceptibility involved and if given for a few months 40mg/kg/day may be enough

67
Q

Describe the clinical presentation of metronidazole toxicity

A
  • Ataxia
  • Vestibular signs
  • Tremors
  • Seizures
  • Peripheral neuropathies
  • Often present as vetsibulocerebellar (bilateral)
  • reluctance to start movement
  • Hypermetria
  • Usually bright and alert, eating and drinking
  • Tetraparetic
68
Q

Describe the management of metronidazole toxicity

A
  • Discontinue metronidazole
  • Supportive care relating to motility mostly
  • Diazepam 0.2-0.5mg/kg PO for 3 days accelerates recovery (appears to have antagonistic/displacing effect on metronidazole)
69
Q

What would be the most likely differential for a dog presented with short and fast forelimb movement and long and slow hindlimb movement?

A

CCSM - caudal cervical spondylomyopathy

70
Q

What are the main causes of “Wobbler” in dogs and horses?

A
  • Horses: cervical vertebral malformation

- Dogs: CCSM caudal cervical spondylomyopathy

71
Q

List the differentials for a 5yo FN dog presented with sudden onset cervical pain and low head carriage

A
  • Cervical muscle myositis
  • Spondylosis
  • Neoplastic e.g. fibrosarc, soft tissue sarc, osteosarc
  • SRMA (steroid responsive meningitis arteritis)
  • Focal GME
  • Trauma
  • SRMA most likely
72
Q

Outline your approach to a 5yo FN dog presented with sudden onset cervical pain and low head carriage

A
  • Full systemic exam to rule out systemic disease incl. blood biochem and haematology
  • Advanced imaging (MRI)
  • CSF tap
73
Q

List your differentials for a 5mo FN dog with one month progressive ataxia, proprioceptive deficits on all limbs, worse on HL, no systemic illness noted and litter mates normal

A
  • Chronic degenerative radiculomyelopathy (unlikely, usually onset 6-9yo)
  • Cervical vertebral malformation
  • Cataplexy (but no litter mates affected)
  • Cervical spondylomyelopathy
  • Hypoglycaemia
  • Nutritional
  • Neoplasm unlikely due to age
  • Neospora
  • Meningitis
  • Toxicity
74
Q

List your differentials for a 3yo dog presented with tetraparesis following traumatic episode at exercise 5 days prior and anaesthesia for radiography. Dull mental state and behaviour, non-ambulatory, tetraplegia, proprioceptive deficiets in all limbs, cervical pain, low tail carriage

A
  • Generalised GME
  • Trauma to cervical spine/fracture
  • IVDD
  • Neoplasia
  • Ischaemic episode
  • Radiographic positioning exacerbating traumatic lesions/IVDD
  • Ischaemic myelopathy
75
Q

Give your most likely lesion localisation and your differentials for a 1yo FN chihuahua presented with sudden onset tetraplegia overnight. Proprioceptive deficits in all limbs, recumbent, cervical pain, reduced visual placing

A
  • Cervical lesion C1-5 (sensation and reflexes present)
  • Neoplasia
  • Ischaemic myelopathy
  • Trauma
  • IVDD
  • Acute onset focal GME
76
Q

Give your lesion localisation and most likely differentials for a 5yo ME dachsie presented with sudden onset tetraparesis at exercise, ambulatory, ataxia, facial asymmetry, anisocoria (L

A
  • Brainstem lesion (affecting facial nerve which comes out of brainstem)
  • Trauma
  • Neoplasia
  • Peripheral Horner’s with concurrent cervical disease
  • Ischaemic episode
  • Focal GME
  • FCE in the brainstem
77
Q

Give your lesion localisation and most likely differentials for a boxer presented with asymmetric tetraparesis (worse on left), absent proprioception in all 4 limbs, normal mentation, splayed legs, normal reflexes in HL reduced reflexes in thoracic limbs, normal palpebral but no menace response, facial sensation present, nystagmus. Panniculus present, no cervical pain

A
  • C6-T2 lesion
  • degenerative myelopathy
  • IVDD (less likely, bu chonic protrusions can cause less pain)
  • Cervical spondylomyelitis
  • Neoplastic
  • Discospondylitis
  • Most likely are inflammatory, neoplastic and degenerative causes
78
Q

What is chronic pain?

A

Maladaptive, extends beyond the time for healing

79
Q

Define pain

A

The conscious recognition of nociceptive stimuli

80
Q

What are the 2 key ascending pathways of pain?

A

Spinocervicothalamic tract and spinoreticular tract

81
Q

What is the function of the spinocervicothalamic tract in pain? How is it tested?

A

Touch and superficial pain with high degree of somatotropy, test by light quick pinch of the skin

82
Q

Describe the anatomy of the spinocervicothalamic tract

A
  • Located in lateral funiculus
  • Primary afferent synapses with secondary afferent into spinocervicothalamic tract
  • Ascend to C1 and C2 where they cross and synapse in lateral cervical nucleus
  • Project through brainstem to thalamus and cortex
83
Q

What is the function of the spinoreticular tract?

A

Deep pain and visceral sensations, poor somatotropy, intersegmental reflexes

84
Q

Describe the anatomy of the spinoreticular tract

A
  • Primary afferents enter cord and diverge cranially and caudally and spreads over several segments
  • Second order afferents in dorsal horn (therefore diffuse and bilateral)
85
Q

What activates the emotional response to pain?

A

The limbic system

86
Q

Explain the gate theory of pain

A
  • CNS can control nociception
  • Activity in large non-nociceptive fibres can modify perception of activity in small nociceptive fibres and descending activity can also inhibit it
  • Small fibres control large fibre signals in spinal cord
87
Q

Explain the use fo methadone in chronic pain patients

A
  • Pure mu agonist and acts on NMDA receptor and affects serotonin reuptake
  • Interferes with sensation of pain as NMDA is wind up receptor in chronic pain
88
Q

List the main medical analgesia options

A
  • Opioids
  • NSAIDs
  • Alpha-2 agonists
  • NMDA receotor antogonists
  • Nitrous oxide
  • Local anaesthetics
  • Paracetamol, steroids, amantidine, tramadol, gabapentin, tapentadol, pregabalin, TCAs, SSRIs, methocarbamol
89
Q

Discuss the use of opioids as analgesics

A
  • ACute pain phase
  • Side effects prohibit chronic use
  • Tolerance can develop
  • May develop opioid induced pain hypersensitivity so pain becomes uncontrollable with chronic use
90
Q

Discuss the use of NSAIDs in analgesia

A
  • Care re. contraindications

- Welfare perspective requires use

91
Q

When are alpha-2 agonists indicated as analgesics?

A

Peri-operatively only, not suitable for chronic pain treatment

92
Q

Give an example and indication for the use of NMDA receptor agonists as analgesics

A
  • Ketamine

- Chronic pain

93
Q

Discuss the use of nitrous oxide as an analgesic

A
  • Less used now for intraoperative

- Some benefits for chronic pain as well as antidepressant effects

94
Q

Discuss the use of local anaesthetics in analgesia

A
  • Good intra-operatively

- Reduces risk of chronic pain by reducing hypersensitivity

95
Q

Describe the use of liposome encapsulated opioids

A
  • Allows reservoir of drugs to be stored within layers of liposomal membranes
  • Drugs released from liposome in a number of ways that may be categorised as either release through passicve efflux or liposome degeneration
  • Fewer adverse effects, no risk to in contact people, lower opportunity for abuse if administered by vet
96
Q

Explain the process of release of opioids from liposome encapsulated opioids

A
  • Degradation of liposome structure via lipases present in tissue fluid and uptake by phagocytic cells
  • Liposome degradation is affected by lipid composition, physical characteristics, method of manufacture
97
Q

Give examples of novel delivery systems for analgesics

A
  • Polymer gels and buprenorphine SR
  • Liposome encapsulated opioids
  • Pro-drugs
98
Q

OUtline the holistic approach to the treatment of chronic pain

A
  • Weight control, exercise, physical therapies, acupuncture
  • Functional foods, neutraceuticals, DMOADs
  • Licensed pharmacotherapy (NSAIDs, PLT, paracetmol)
  • Un-licensed pharmacotherapy e.g. amantadine, tramadol, gabapentin, methocarbamol, trazadone
99
Q

What is the main use of amantadine in vet med?

A

Multimodal analgesic for alleviation of refractory osteoarthritis pain in dogs

100
Q

Identify “other” chronic pain treatments that can be used in vet med

A
  • Stem cells
  • Physical therapies
  • Complementary therapies
  • Nerve growth factor therapies
  • EP4 Rc antagonists
  • Autoimmune therapies
  • Therapies targeting descending controls
  • Euthanasia

NEU2 (23 decks)

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