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Flashcards in Poisons Deck (253)
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1
Q

what resource can be useful when you are dealing with a poisoning case?

A

VPIS - veterinary poisons information service

2
Q

what does VPIS do?

A

available 24/7
has vet helpline to advise on antidotes or management of poisoning
owner support line
tox box services

3
Q

why is a ToxBox so useful?

A

some poisonings are very rare and antidotes not regularly kept in practice

4
Q

how rapid is the onset of symptoms in an intoxication case?

A

acute

5
Q

what can signs of intoxication be referable to?

A

the affected organ system (e.g. liver, kidneys, GI)

6
Q

how does poisoning often occur?

A

inadvertent or accidental

malicious poisoning is rare

7
Q

how may an animal be poisoned accidentally / inadvertently?

A

inappropriate use of human medications by well meaning owner
overdose of prescribed medication
exposure to products in the home environment

8
Q

via what route are most toxins ingested?

A

oral

9
Q

what are the less common routes of toxin ingestion?

A

topical or inhalation (among others)

10
Q

what questions should you ask during phone triage if intoxication is suspected?

A
what
when
what does
(if owner knows)
up to date bodyeight
11
Q

why is an up to date body weight needed?

A

to check if dose ingested is toxic or not

12
Q

what should be done if the suspected intoxicated patient is asymptomatic or has ingested and unknown or low risk product?

A

call VPIS who can offer specific advice

13
Q

what should be done if the suspected intoxicated patient is symptomatic or has ingested known high risk product?

A

requires immediate veterinary attention (even if no signs)

avoid house calls as this only takes up time for treatment

14
Q

what should the owner bring with them when attending the practice with their suspected intoxication patient?

A

product label or photo if possible
a sample of the product if the label is unavailable
an indication of approximate time of toxin ingestion and quantity ingested

15
Q

what should owners do if there is dermal contamination of toxic substance?

A

prevent self-grooming (and so ingestion)

buster collar may be useful

16
Q

what advice should be given to owners before they bring their intoxicated animal into practice?

A

ensure other pets/children to not have access to toxin or anything containing it (e.g. vomit)
do not follow internet remidies

17
Q

what should be done before the intoxicated patient arrives?

A

if dose/toxin/bodyweight already known then contact VPIS or other source for specific up-to date management advice (may already have been done
prepare for triage and initial management

18
Q

what should be done pending owner arrival at the practice with an intoxicated patient if dose/toxin/bodyweight already known?

A

consutl VPIS or other source for specific up-to-date management advice

19
Q

how should you prepare for triage / initial management of intoxicated patients?

A

prepare yourself
inform the vet if not already aware
prep hospital sheet/recording chart
IV catheter and fluid prepped
O2 supply can help in some cases so prepare
diagnostic supplies (e.g. blood tubes and needles)
decontaminents/emetics

20
Q

what should be avoided if anti-coagulant ingestion is suspected?

A

only blood sample from peripheral veins not jugular as pressure bandage is needed

21
Q

what should be involved in the history taken from the owner while their pet is triaged?

A

patient signalment
pre-exisiting medical history (signs day to day and any medication)
current issue
signed consent form

22
Q

how can the history taking be facilitated during triage?

A

delegation / team work

23
Q

what should be asked about the current condition when taking a history from an owner about toxin ingestion?

A

onset and progression of signs

specific information regarding the possible toxin

24
Q

when is a primary survey performed?

A

on all emergancy cases

25
Q

what are the main stages of the primary survey?

A
respiratory
CVS
neurological
urogenital
other
26
Q

what is assessed during the respiratory section of the primary survey?

A
is there apnoea
any URT obstruction
resp distress
cyanosis
abnormal lung sounds
27
Q

what should happen if apnoea is found during the primary survey?

A

commence CPR straight away

28
Q

what is assessed during the cardiovascular section of the primary survey?

A
mm colour
CRT
HR
pulse quality
are extremities cold (perfusion check)
BP if possible
29
Q

what should you do if unsure about any respiratory issues (aside from apnoea!!)?

A

provide O2 therapy

30
Q

what is assessed during the neurological section of the primary survey?

A

mentation (dull, stuporous or comatose)
anisocoria
seizures
paresis/paralysis

31
Q

what is assessed during the urogential section of the primary survey?

A

bladder (present and size)
any prolapse
priapism
pregnancy, whelping or dystocia

32
Q

what is assessed after all other systems during the primary survey?

A

hyper/hypothermia
suspected toxicity
pain
obvious trauma or haemorrhage

33
Q

what should be done once the primary survey is completed?

A

treat any abnormalities found

34
Q

how can any issues from the primary survey be addressed?

A

provide O2 and establish airway
address hypoperfusion if any
manage any neurological impairment

35
Q

how can hypoperfusion be addressed?

A

hypovolaemia - IVFT

cardiac rhythm disturbances / myocardial failure - treat as appropriate

36
Q

how is neurological impairment found on the primary survey treated?

A

manage seizures
ensure respiratory function is adequate (may be affected by muscle weakness)
protect against aspiration

37
Q

what happens during the secondary survey?

A

review all areas of primary survey and ensure stabilised

give more in depth exam

38
Q

how is an intoxication diagnosed?

A

history of possible exposure
clinical suspicion
toxin panel analysis is possible also

39
Q

what clinical signs would lead you to suspect toxin exposure?

A

acute onset signs

especially GI, renal and neuromuscular

40
Q

what is the issue with toxin panel analysis?

A

takes time

not often used as clinical diagnosis can be made without

41
Q

what can be used to perform a toxin panel?

A

ingested substance
gastric contents (lavage or vomit)
blood or urine samples

42
Q

when may a toxin panel be used?

A

when required for legal reasons (e.g. owner suspects malicious poisoning)

43
Q

what are the 3 main principles of managing intoxication?

A

remove or eliminate toxin
reduce ongoing absorption
dilution of toxin

44
Q

when is administration of oral products or induction of emesis contraindicated?

A

where there is a risk of aspiration

45
Q

what conditions increase the risk of aspiration?

A

obtundation
seizures
pre-exisiting laryngeal compromise
respiratory distress

46
Q

what can be done to reduce or eliminate a toxin?

A

induce emesis
gastric lavage
cutaneous decontamination
haemodialysis (limited availability)

47
Q

how much of the gastric contents is emptied by emesis?

A

40-60% of gastric contents

48
Q

what can enhance the effectiveness of emesis in clearing toxins from the stomach?

A

feed small meal immediately prior to induction of emesis

49
Q

when is emesis indicated?

A

within 2-3 hours of oral ingestion of a non-corrosive intoxicant

50
Q

when can emesis be possibly effective >3 hours post ingestion?

A

with substances likely to coalesce in the stomach (e.g. chocolate)

51
Q

when is emesis contraindicated?

A

in intoxicant is corrosive or irritant
pre-existing aspiration risk
specifically contraindicated if petroleum distillate is ingested

52
Q

what is the main emetic agent used in dogs?

A

apomorphine

53
Q

via what route is apomorphine given?

A

SC although can be given via other methods if correct solution used

54
Q

how effective is apomorphine in dogs?

A

typically very effective

55
Q

what emetic agent is used in cats?

A

xylazine

56
Q

via what route is xylazine given?

A

IM

57
Q

how effective is xylazine in inducing emesis in cats?

A

works in less than 50% of cats

58
Q

what can be used if xylazine is not available to induce emesis in cats?

A

other alpha 2 agonists

59
Q

what should be used after an alpha 2 agonist is administered and has had emetic effect?

A

appropriate reversal agent

60
Q

what is the main side effect of xylazine?

A

sedation as it is asedative

61
Q

what is found in the home that could be used if the owner is absolutely unable to come to the practice?

A

washing soda 9sodium carbonate)

62
Q

what is gastric lavage?

A

washing out of stomach

63
Q

is gastric lavage commonly used?

A

no

64
Q

when should gastric lavage be considered?

A

known significant toxin ingestion within the last hour or so
and induction of emesis is unsuccessful or contraindicated
and benefits considered to outweigh risks

65
Q

when is gastric lavage unlikely to be of benefit?

A

if emesis (voluntary or involuntary) has already occurred

66
Q

what are the potential complications of gastric lavage?

A

anaesthesia related
aspiration
gastro-oesophageal trauma or perforation

67
Q

how should the patient be prepared for gastric lavage?

A

anaesthetised

intubated with cuffed ET tube

68
Q

what is the issue with cuffing ET tubes in cats?

A

can lead to tracheal necrosis

69
Q

what position should animals be placed in for gastric lavage?

A

lateral recumbancy (left is standard)

70
Q

how should the stomach tube be measured for gastric lavage?

A

nares to last rib

71
Q

what should be done with the stomach tube tip before it is inserted?

A

lubricated

72
Q

how much fluid is used to lavage the stomach?

A

10-30 ml/kg

73
Q

how is gastric lavage performed?

A

10-30ml/kg of warmed water/isotonic saline is instilled into stomach down tube via gravity
then allowed to run out by lowering tube into bucket

74
Q

what can be instilled into the stomach tube following gastric lavage?

A

activated charcoal if indicated

75
Q

how should the stomach tube be removed safely after lavage?

A

kink tube or cover end prior to removal and maintain this until tube is fully removed

76
Q

what should be done after gastric lavage before anaesthetic recovery?

A

suction oropharynx

77
Q

what must have returned prior to extubation after gastric lavage?

A

swallow reflex

78
Q

when is cutaneous decontamination needed?

A

toxin or substance on skin

ingestion occuring via absorption or ingestion after grooming

79
Q

what should you wear when performing cutaneous decontamination?

A

appropriate PPE

80
Q

what should be done with long haired patients during cutaneous decontamination?

A

clip affected regions

81
Q

what should be used to wash the fur/skin during cutaneous decontamination?

A

warm water
mild shampoo / detergent (e.g. baby shampoo)
degreasing agents (e.g. swarfega) if especially greasy

82
Q

what should be avoided when performing cutaneous decontamination?

A

occular contamination and patient grooming post bath

83
Q

how can patient grooming post cutaneous decontamination be prevented?

A

buster collar

84
Q

what should you not do when performing cutaneous decontamination?

A

attempt to neutralise acids or alkali with the opposite

use solvents or alcohol as are likely to spread toxin

85
Q

what is haemodialysis?

A

treatment used as renal replacement (in kidney damage) to filter out nephrotoxins or for solute (toxin) removal

86
Q

is haemodialysis often used?

A

no - only one in UK at RVC

87
Q

what is the weight restriction for haemodialysis?

A

> 2.5kg

88
Q

how can ongoing toxin absorption be reduced?

A
enteric absorbents (activated charcoal)
intralipid (IV)
89
Q

what is the role of enteric absorbents?

A

reduce ongoing absorption and facilitate faecal excretion of toxin by binding it

90
Q

what form is activated charcoal given in?

A

liquid or powder for large surface area

91
Q

how can activated charcoal be administered?

A

mixed with wet food
syringed
stomach tube following gastric lavage

92
Q

is activated charcoal effective for all drugs?

A

no

93
Q

how often should activated charcoal be given for drugs undergoing enterohepatic re-circulation?

A

every 4-8 hours for 2-3 days

94
Q

what drugs is activated charcoal effective for?

A
NSAIDs
salicylates (asprin)
theobromine (chocolate)
mathylxanthines (stimulants)
digoxin
marijuana
95
Q

what may be caused by activated charcoal?

A

GI irritation

96
Q

when is activated charcoal contraindicated?

A

where caustic material has been ingested

97
Q

what effect can activated charcoal have on faeces?

A

cause them to go black after 1-2 days and may lead to constipation

98
Q

what is the role of intralipid therapy in treating toxin ingestion?

A

creates ‘lipid sink’ in intravascular space where fat soluble toxins will bind and then can no longer be taken up into organs

99
Q

what is intralipid therapy used for?

A

lipophilic toxins

100
Q

what are the main lipophilic toxins that may be treated with intralipid?

A

macrocyclic lactones
permethrin
LA
calcium channel blockers

101
Q

when is intralipid therapy most often used?

A

where other treatment has failed

102
Q

what are the reported side effects of intralipid therapy?

A

fat embolisation / overload

pancreatitis

103
Q

are side effects of intralipid therapy often seen?

A

no - rare

104
Q

what is involved in the supportive management of intoxication?

A

specific antidote/therapy if available or indicated
supportive/organ specific care as needed (depending on case)
nursing and symptomatic care

105
Q

what is involved in the nursing and symptomatic care of treatment of intoxication?

A
maintain hydration and nutrition
analgesia where required
manage nausea with anti-emetics
correct management of recumbent patients
manage eyes if reduced blink
106
Q

what analgesia is usually given to intoxication cases?

A

opioids

107
Q

how should the recumbent patient be managed?

A
turn regularly (prevent decubital ulcers)
consider urinary management
108
Q

how should patients with a reduced blink be managed?

A

lubrication of eyes every 4-6 hours depending on need

109
Q

why is eye lubrication needed in patients with reduced blink?

A

prevention of corneal drying and ulceration

110
Q

what may be caused by nephrotoxins?

A

acute kidney injury (AKI)

111
Q

what are the main signs of AKI?

A

acute onset azotemia
olig or anuria
less commonly polyuria

112
Q

what are the clinical signs of intoxication with nephrotoxin?

A
sudden onset (within a few hours)
AKI related - inappetance, lethargy, vomiting and diarrhoea
113
Q

how is intoxication with nephrotoxins diagnosed?

A

azotemia with sub-maximally concentrated urine

specific findings

114
Q

what specific findings are there for nephrotoxins?

A

calcium oxalate monohydrate crystals seen with ethylene glycol toxicity

115
Q

what are the common nephrotoxins?

A
NSAIDs
Lillies (cats)
Grapes and raisins (dogs)
ethylene glycol (antifreeze)
vitamin D analogues
116
Q

why can NSAIDs cause nephrotoxicity?

A

COX inhibition meaning that prostaglandins are unable to manage RPF and perform protective GI function.

117
Q

when is NSAID toxicity more profound?

A

if patient is inappetant
dehydrated
hypotensive
due to reduced protection for the stomach and reduced renal plasma flow

118
Q

what parts of the lily are toxic to cats?

A

all parts of the plant and flower

119
Q

why are grapes/raisins toxic?

A

idiosyncratic although dried fruits are worse

120
Q

why are dried fruits more toxic to dogs?

A

more are eaten as smaller and often more palatable

121
Q

what is caused by ethylene glycol?

A

crystals form in the renal tubules

122
Q

what other effects, aside from AKI may be caused by ethylene glycol toxicity?

A

may be hypocalcaemic and have severe tremors or seizures

123
Q

why may patients who have ingested ethylene glycol be hypocalcaemic?

A

due to the formation of crystals

124
Q

what do vitamin D analogues cause?

A

renal calcification

125
Q

what in the blood may indicate ingestion of vitamin D analogues?

A

Ca2+ and phosphate levels will increase

126
Q

where are vitamin D analogues found in the home?

A

psoriasis creams

some house plants

127
Q

what is the effect of renal calcification caused by vitamin D analogues?

A

normal renal byproducts are not removed so build up and lead to AKI

128
Q

how is nephrotoxin ingestion managed?

A

decontamination

specific antidotes available for some toxins

129
Q

what is involved in GI decontamination of nephrotoxins?

A

induce emesis

give activated charcoal

130
Q

for what nephrotoxin is activated charcoal of no benefit?

A

ethylene glycol

131
Q

when is dermal contamination of a nephrotoxin needed?

A

if lily pollen on skin

132
Q

what nephrotoxins have specific antidotes?

A

NSAIDs

ethylene glycol

133
Q

what is the specific antidote for NSAID toxicity?

A

misoprostal - prostaglandin analogue

134
Q

why must care be taken when administering misoprostal?

A

is abortative in humans

135
Q

what is the specific antidote for ethylene glycol?

A

4-methylpyrazole (in reality often use medical grade ethanol)

136
Q

what is the role of 4-methylpyrazole in treating ethylene glycol toxicity?

A

minimises the production of toxic metabolites

137
Q

what are the nursing considerations for patients with nephrotoxin intoxication?

A
maintain euhydration and euvolaemia
monitor fluid ins and outs and titrate fluid given accordingly
anti-emetics given as often nauseous
opioid analgesia if painful
monitor for and treat hypertension
138
Q

how can the development of food aversions be avoided?

A

control any nausea before feeding

139
Q

what is the prognosis for a patient with nephrotoxin intoxication?

A

variable - depends on the toxin and the extent of the injury
polyuric is better
ethylene glycol is poor

140
Q

what is available for refractory nephrotoxin patients?

A

dialysis

141
Q

what are the clinical signs of neurotoxin ingestion?

A
hyper-excitability 
agitation
muscle tremors
seizures
obtundation or coma
142
Q

what effects can neurotoxins have on the heart?

A

cardiac stimulation (as neurostimulants) leading to tachycardia or arrhythmias

143
Q

what is the risk if a patient with a neurotoxin has muscle tremors?

A

if enough muscle mass is involved they could develop hyperthermia

144
Q

what are the common neurotoxins?

A
theobromine (chocolate)
permethrin (spot on)
Metaldehyde (slug pellets)
tremorogenic mycotoxins
cannabis
145
Q

what signs are commonly caused by theobromine ingestion?

A

cardiac stimulation as well as neuro signs

146
Q

what animals is Permethrin toxic to?

A

cats

147
Q

should Permethrin be used in cat containing households?

A

no as it is so toxic

148
Q

what can metaldehyde intoxication lead to?

A

seizures as it is so toxic

149
Q

where are tremorogenic mycotoxins found?

A

in mould

150
Q

what can cannabis intoxication lead to?

A

ataxia
incontinence
seizures
coma

151
Q

how may cannabis be taken in by an animal?

A

ingestion or inhalation

152
Q

what method of intake makes cannabis toxicity signs worse?

A

ingestion

153
Q

how does theobromide concentration differ between different types of chocolate?

A

the darker the chocolate the more theobromide and so more toxic it is

154
Q

how should neurotoxins be managed?

A

decontamination where possible
muscle relaxants
anti-epileptic therapies
intra-lipid therapy

155
Q

how can GI decontamination of neurotoxins be performed?

A

induce emesis

activated charcoal

156
Q

is induction of emesis often indicated in neurotoxin patients?

A

no - due to gag reflex absence or altered mental status which increases the risk of aspiration pneumonia

157
Q

when is gastric lavage useful for neurotoxin patients?

A

if there has been recent ingestion of high toxicity substance (e.g. metaldehyde) as the benefit will outweigh the risk

158
Q

when may dermal decontamination for a neurotoxin be used?

A

permethrin

159
Q

what muscle relaxants may be used for management of neurotoxins?

A

diazepam

methcarbamol

160
Q

why are muscle relaxants needed in the management of neurotoxins?

A

ongoing seizures or tremors can lead to hyperthermia

161
Q

what should you ensure you have checked if a patient who has ingested a neurotoxin is seizing?

A

ensure no hypoglycaemia or hypocalcaemia and if present, treat

162
Q

why is intra-lipid therapy often used for neurotoxins?

A

many neurotoxins are lipid soluble

163
Q

what are the main nursing considerations for patients with neurotoxin intoxication?

A

assess ambulatory capacity
monitor for and manage muscle tremors and seizures and associated hyperthermia
monitor respiratory function if a neuromuscular toxin has been ingested
monitor gag reflex to see if feeding or oral medication is appropriate
IVFT, nutrition where appropriate

164
Q

what are the main areas to be managed if a patient is non-ambulatory?

A
decubital ulcers are a risk - regular turning, padded bedding
toileting considerations (catheter or manual expression)
165
Q

how should respiratory function of neurotoxin patients be monitored?

A

monitor resp pattern and EtCO2 using capnography

166
Q

what are the common hepatotoxins?

A
xylitol (artificial sweetener)
Mushrooms
blue green algae
aflatoxins (food contamination)
drugs
167
Q

what drugs can be hepatotoxic?

A
phenobarbitone
paracetamol
azathioprine
doxycycline
lomustine (CCNU)
168
Q

what are the main supportive measures for hepatotoxins?

A

antioxidant support
treat encephalopathy if present
treat hypoglycaemia if present
treat coagulopathies if presnet

169
Q

what antioxidant support can be given to hepatotoxic intoxication patients?

A

SAMe/silybin

NAC

170
Q

what support can be given to encephalopathic hepatotoxic intoxication patients?

A

lactulose orally or via enema

ensure electrolytes are normal (especially K+) as this exacerbates signs

171
Q

what do encephalopathy and hypoglycaemia indicate?

A

extreme liver dysfunction

172
Q

what support can be given to hypoglycaemic hepatotoxic intoxication patients?

A

supplementation of glucose

173
Q

what support can be given to coagulopathic hepatotoxic intoxication patients?

A

consider plasma

174
Q

how can you tell if a patient is coagulopathic?

A

PT / aPTT prolonged

clinically bleeding

175
Q

what is the effect of xylitol in the body?

A

stimulates endogenous insulin release

hepatotoxic

176
Q

what does endogenous insulin release due to xylitol lead to?

A
hypoglycaemia within 2 hours
lethargy
weakness
ataxia
collapse
seizures
(as muscles and brain deprived of oxygen)
177
Q

how should xylitol intoxication be managed?

A

GI decontamination

management of hypoglycaemia

178
Q

how is GI decontamination performed in patients who have ingested xylitol?

A

emesis
activated charcoal
(assuming not contraindicated)

179
Q

how is hypoglycaemia managed?

A

IV supplementation

feeding

180
Q

what IV glucose supplementation is used in an emergency?

A

bolus (i.e seizing)

181
Q

what IV glucose supplementation is used if it is not an emergency?

A

CRI of 1.25-5% infusion

182
Q

how can feeding be used to manage hypoglycaemia?

A

little and often
high fibre
complex carbs

183
Q

what should be avoided when feeding the hypoglycaemic patient?

A

simple sugars

184
Q

where are clotting factors activated in the body?

A

in liver

185
Q

what clotting factors are activated within the liver?

A

II
VII
IX
X

186
Q

how are clotting factors activated?

A

oxidation of vitamin K which makes the clotting factors become carboxylated

187
Q

how do anticoagulant rodenticides work?

A

interfere with the enzyme vitamin k-epoxide reductase which reactivates vitamin K

188
Q

how long does it take for symptoms of anticoagulant rodenticide ingestion to present?

A

2-5 days

189
Q

is indirect anticoagulant rodenticide toxicity common?

A

no - dog/cat would have to consume over half their body weight in poisoned rats for there to be any effect

190
Q

what are the main reasons patients present with anticoagulant rodenticide ingestion?

A

witnessed ingestion and so pre-symptomatic

symptomatic - severe coagulopathy

191
Q

what is the presentation of symptomatic anticoagulant rodenticide intoxication?

A

haemoabdomen/haemothorax
collapse
hypovolaemic
+/- anaemia

192
Q

why does anticoagulant rodenticide toxicity present as a severe coagulopathy?

A

due to lack of clotting factors

193
Q

how should pre-symptomatic witnessed ingestion of anticoagulant rodenticides be treated?

A

GI decontamination - emesis and activated charcoal

measure clotting times at admission and 48 hours post decontamination

194
Q

what is diagnosis of anticoagulant rodenticide intoxication based on?

A

prolonged PT +/- aPTT

195
Q

when should clotting times of asymptomatic anticoagulant rodenticide intoxication be taken?

A

at admission and 48 hours after decontamination

196
Q

what will indicate if GI contamination has been effective in preventing anticoagulant rodenticide intoxication?

A

normal clotting times 48hrs post treatment

197
Q

what must happen if clotting times are abnormal when tested?

A

treatment required

198
Q

how is asymptomatic anticoagulant rodenticide intoxication treated?

A

vitamin K therapy - 4 weeks

199
Q

what should be repeated after vitamin K treatment?

A

PT/aPTT testing

200
Q

when must symptomatic cases of anticoagulant rodenticide intoxication be seen?

A

urgently by vet

201
Q

what must be considered when handling and performing diagnostic tests on anticoagulant rodenticide intoxication patients?

A

care with handling and blood sampling as they have coagulopathy
no jugular vein samples

202
Q

is decontamination indicated in symptomatic anticoagulant rodenticide intoxication cases?

A

no as 2-3 days will have passed

203
Q

how is symptomatic anticoagulant rodenticide intoxication treated?

A

vitamin K1 therapy
plasma if life threatening bleeding
RBC if needed

204
Q

how can vitamin K1 therapy be administered?

A

oral

SC

205
Q

how long does vitamin K1 therapy take to work?

A

12 hours

206
Q

why may plasma be needed in symptomatic anticoagulant rodenticide intoxication patients that have serious bleeding?

A

rapid replacement of clotting factors

207
Q

in what species is paracetamol toxicity more of a problem?

A

cats

208
Q

can paracetamol toxicity occur in dogs?

A

yes but is also used therapeutically so is related to overdose

209
Q

what do cats with paracetamol toxicity present with?

A

methaemoglobinaemia as main issue

210
Q

what do dogs with paracetamol toxicity present with?

A

hepatic injury is main issue

211
Q

what state must the iron in haem be in to bind oxygen?

A

Fe2+

212
Q

what is the effect of RBC oxidative damage on haem?

A

leads to creation of Fe3+ which leads to methaemoglobin and an inability to bind oxygen

213
Q

what is the main clinical sign of methaemoglobinaemia?

A

discolouration of MM

usually chocolate coloured but may be dark/dusky cyanotic

214
Q

how is methaemoglobinaemia diagnosed?

A

drop of blood onto tissue

if >10% MetHb there is noticeable brown discolouration

215
Q

how does non-methaemoglobinaemia blood appear when exposed to air (oxygen)?

A

bright red

216
Q

why are cats so susceptible to paracetamol toxicity?

A

they lack pathways required for the metabolism of paracetamol and therefore accumulate highly oxidative metabolites

217
Q

what signs do patients with methaemoglobinaemia present with?

A

signs of shock (tachycardia, tachypnoea)
cardio respiratory distress
neurological signs due to reduced O2 supply to the brain
facial and limb oedema (cats only)

218
Q

what is the main effect of methaemoglobinaemia?

A

reduced delivery of O2 to tissues

219
Q

how is paracetamol toxicity treated?

A
induced emesis (if ingestion was <1hr ago and no contraindications)
activated charcoal
antioxidants
220
Q

when is emesis indicated for paracetamol toxicity?

A

if ingestion <1 hr ago and no contraindications

221
Q

what antioxidants may be given to paracetamol toxicity patients?

A

N-acetylcysteine (preferred)

vitamin C and SAMe (less effective)

222
Q

how is N-acetylcysteine administered to paracetamol toxicity patients?

A

slow IV injection

223
Q

why must you take care when placing an IV catheter to give N-acetylcysteine?

A

can lead to phlebitis if extravasates

224
Q

what is the prognosis of paracetamol toxicity?

A

guarded prognosis as highly toxic

225
Q

what is the only UK venomous snake?

A

adder (protected species)

226
Q

where are adders found?

A

moorlands, heaths, sands, peripheral woodlands

227
Q

when are adders typically encountered?

A

the summer by inquisitive dogs

228
Q

what are the effects of adder venom?

A

cytotoxic
cytolytic
can cause direct cardiovascular effects if it enters systemic circulation

229
Q

when do clinical signs of adder bites usually present?

A

within 2 hours

230
Q

what are the clinical signs of adder bites?

A

swelling local to bite +/- severe bruising
altered mentation (depressed) due to pain
panting
pyrexia
may have cardiac arrhythmias

231
Q

how should adder bites be treated?

A
keep dog quiet and calm
leave bite area alone
give anti-venom
analgesia (opioids)
IVFT
232
Q

what does of antivenom is needed for adder bites?

A

single dose per bite

233
Q

when is antivenom recommended for adder bites?

A

facial bites and patients with systemic signs

234
Q

are steroids indicated for adder bites?

A

no

235
Q

are antibiotics needed for adder bites?

A

no unless there is clear evidence of concurrent infection (which is rare)

236
Q

what is the prognosis of an adder bite?

A

reasonably good with treatment

237
Q

why is it important to leave the adder bite area on the patient alone?

A

prevents any venom reaching systemic circulation

238
Q

what irritants or caustic substances may animals ingest?

A
alkali
batteries
Benzalkonium chloride
Petrolleum distillate
washing tablets
239
Q

what are the clinical signs of irritant/caustic ingestion?

A

varies depending on location of burns / irritation

may be oral, oesophageal, gastric or dermal ulceration

240
Q

what are the signs of oral ulceration following irritant/caustic ingestion?

A

pain
hypersalivation
anorexia

241
Q

what are the signs of oesophageal ulceration following irritant/caustic ingestion?

A

regurgitation

242
Q

what are the signs of gastric ulceration following irritant/caustic ingestion?

A

vomiting

243
Q

what are the signs of irritant/caustic contact with the skin?

A

dermal alopecia
burns
ulceration

244
Q

is gut decontamination indicated for irritant/caustic ingestion?

A

no

245
Q

how should irritant/caustic ingestion / exposure be treated?

A

if battery, radiograph to assess location and if it is intact
dermal decontamination with warm water if recent dermal exposure
analgesia (opioids)
maintain hydration with IVFT
tube feeding often needed to bypass ulcerated areas
trail soft foods to see if animal will eat

246
Q

what should be done if an animal has ingested a battery?

A

radiograph to assess location (obstruction risk) and if it is intact as this will alter treatment plan

247
Q

what may happen if animals consume the contraceptive pill?

A

possible V/D

may interrupt oestrus if contain progesterone

248
Q

is treatment required for ingestion of the contraceptive pill?

A

no

249
Q

is treatment required for ingestion of silica gel?

A

no - in this case do not eat warning just means it is a non-food item

250
Q

is treatment required for catnip exposure?

A

no - cats may appear stimulated or that they are hallucinating but is is euphoria releated

251
Q

is treatment required for ingestion of novelty luminous items?

A

may need other oral fluid or food to take away the taste but other than that none needed

252
Q

what is usually found within novelty luminous items?

A

dibutyl phthalate (low toxicity)

253
Q

what can be caused by ingesting novelty luminous items?

A

hypersalivation and occasional vomiting / hyperactivity

Decks in X Clinical Veterinary Nursing Theory Class (70):