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9- SA- Gastrointestinal and Hepatic Disease > My pet ate something > Flashcards

My pet ate something Flashcards

1
Q

List the basic principles when dealing with known ingestion/exposure to toxin

A

Decontamination
Assessment of effects
Treatment of symptoms

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2
Q

List 3 ways toxins are absorbed

A

eaten- absorbed either across mucous membranes or absorbed across intestinal mucosa
via skin exposure
via inhalation

Many compounds are not inherently toxic until they have been metabolised

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3
Q

what is the window of opportunity with an ingested toxin

A

2-8 hours dogs
2-12 hours cats

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4
Q

can we do decontamination if the toxin is absorbed across the MM

A

no - this is incredibly quick so we often are too late
you can attempt to wash the mouth out but may be pointless

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5
Q

can we do decontamination if the toxin is eaten and absorbed across the GIT

A

yes - we can induce emesis or do gastric decontamination

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6
Q

Describe how we use to make dogs vomit

A

apomorphine

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7
Q

what do we use to make cats vomit

A

alpha-2 agonists e.g. xylazine or medetomidine (decent number won’t vomit)

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8
Q

list 2 situations should we not induce emesis with toxin ingestion

A

Avoid neurologically compromised patients e.g. obtunded due to aspiration risk
avoid caustic substances

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9
Q

why do we not make patients vomit if they have eaten a caustic substance

A

it can cause more of an issue on the way back up
e.g. causing oesophagitis

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10
Q

how to do gastric decontamination

A

flush warmed crystalloid fluid down a tube into the stomach, remove the fluid - repeat

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11
Q

when doing a stomach lavage what do we need to be careful of

A

removing the tube and leaking fluid - aspiration risk

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12
Q

if a toxin has been eaten and the window of opportunity for vomiting has passed, what can we do

A

give activated charoal

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13
Q

how does activated charcoal help in toxic cases

A

it is an incredibly porous substance - this means it is very good at allowing molecules to react and bind - this helps it to remove substances from the GIT before they are absorbed

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14
Q

how can we decontmainate after skin exposure to toxins

A

gently wash the skin with water, activated charcoal or washing up liquid
care when drying- absorption through abrasions
prolonged washing can increase absorption of some chemicals

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15
Q

how can we decontaminate after inhalation of toxins

A

Very rare, but realistically decontamination for your patient is not possible.
appropriate PPE

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16
Q

how can we decontaminate if a toxin is only toxic after metabolism

A

the solution to pollution is dilution
IVFT
lipid infusions

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17
Q

why does fluid therapy help with toxins

A

Increase GFR and promote renal excretion- if renally excreted
Increased organ perfusion and transit of compounds- decreasing opportunity for toxins to damage organs

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18
Q

what fluid rate do we give toxin patients

A

2 x Maintenance in the normally hydrated patient

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19
Q

how do lipid infusions prevent toxicities

A

works well for lipid soluble compounds
lipid soluble toxin is sequesteres into fat and metabolised as part of the fat

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20
Q

what are the side effects of lipid infusions

A

pulmonary lipid embolus - clump of fat gets stuck and leads to lack of perfusion to a section of lung

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21
Q

if we don’t know what toxin was ingested or what that toxin does, what do we do

A

assess all body systems

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22
Q

how do we treat toxin exposures post decontamination attempts

A

symptomatic treatment based on what systems are affected

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23
Q

how do we control seizures

A

diazepam IV - can give 3 doses- should see affect within 10 mins
phenobarbital/levetiracetam IV- if diazepam not working
propofol CRI - causes an induced coma- if the other fail

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24
Q

how can we support the liver after toxin ingestion

A

anti-oxidants

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25
Q

how can we support the kindey after toxin ingestion

A

IVFT (keep up there losses) +/- diuretics depending on urine output (need to be well hydrated- need to be careful)
dialysis if required

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26
Q

what do we give to ventricular tachycardic patients

A

lidocaine

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27
Q

what do we give to supraventricular tachycardic patients

A

beta-blockers
e.g. propranolol

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28
Q

what do we give to bradycardic patients

A

Atropine - should see quick response
may need to readminister because short half-life
if toxin affected vagal tone

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29
Q

how do we maintain a good BP

A

IVFT
vasopressors

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30
Q

what do we give if BP too high

A

anti-hypertensives (e.g. amlodipine)

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31
Q

do we want to stop vomiting in acute phase of toxin ingestion

A

no

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32
Q

what do we give to V/D patients after toxin ingestion

A

IVFT
GIT diet
anti-emetic (e.g. maropitant, metoclopramide, ondansetron) if vomiting won’t stop after prolonged period

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33
Q

treatment for toxin patients with clotting dysfunction

A

vitamin K
plasma (fresh frozen plasma- because got lots of clotting factors in)

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34
Q

how do ibuprofen/ NSAIDs cause toxicity

A

they reduce prostaglandin production (COX inhibitors) - this can damage the kidneys and GIT

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35
Q

List the clinical signs of NSAID toxicity

A

Haemorrhagic vomiting / diarrhoea
AKI

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36
Q

Describe the treatment for NSAID toxicity

A

H2 blockers (ranitidine/ cimetidine)
proton pump inhibitors (omeprazole)
prostaglandin analogue (misoprostol)- not in pregnant animals
intralipid infusion

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37
Q

why is aspirin toxicity different to NSAID toxicity

A

it can have a greater effect on thromboxane which can lead to thrombocytopathy (because it is important for platelet function) on top of the other clinical signs

38
Q

List the clinical signs of asprin toxicity

A

Thrombocytopathy – bleeding e.g. prolonged BMBT
haemorrhagic V+/D+
AKI

39
Q

describe how to treat asprin toxicity

A

Treatment as for NSAIDs.- proton pump inhibitor, prostaglandin analogue, intralipid infusion
Bleeding is unlikely to be significantly associated with death before other damage.

40
Q

how does paracetamol cause toxicity

A

paracetamol is metabolised by the liver - these pathways can become saturated, cytochrome P450 oxidses the excess to NAPQI (BAD)

NAPQI is then detoxified - but these pathways can become exhausted too, PAP can also be produced (ALSO BAD)

NAPQI and PAP cause clinical signs
NAPQI causes hepatic cell necrosis and nephrotoxicity
PAP causes methemoglobinaemia

41
Q

List the clinical signs of paracetamol toxicity

A

Brown mm
jaundice
abdominal pain
lethargy
vomiting
AKI
signs of hypoxia to tissues- arrhythmias, peripheral oedema, resp distress

42
Q

Describe how to treat paracetamol toxicity

A

N-acetyl cysteine (binds to toxic metabolites)
H2 receptor antagonists (rantidine - reduces CP450 oxidation)
ascorbic acid
antioxidants
IVFT
GI support

43
Q

How does chocolate cause toxicity

A

Theobromine and caffeine (Methyl-xanthines) increase catecholamine release
this increases cAMP
which increases intracellular calcium in cardiac and skeletal muscles
it is also inhibits adenosine receptors

44
Q

List the clinical signs of choclate toxicity

A

hyperactivity
V/D
arrythmias
seizures
coma
death

45
Q

Describe the treatment of choclate toxicity

A

symptomatic treeatment
fluids
ECG and monitoring

46
Q

how long do you need to give activated charcoal for following toxin ingestion

A

at least 24 hours

47
Q

how does xylitol cause toxicity

A

it mimics glucose without calorific contribution
stimulates insulin release and is hepatotoxic

48
Q

what is xylitol found in

A

chewing gum - sugar free
some peanut butters (check label)

49
Q

List the clinical signs of xylitol ingestion

A

hypoglucaemia
elevated liver enzymes
weakness
collapse
seizures
coma
death
jaundice

50
Q

Describe treatment of xylitol toxicity

A

IVFT
glucose infusion- oral or IV
- need to avoid causing further insulin spikes
antioxidants

these need constant glucose monitoring (every hour) for 24-48hrs

51
Q

what can pyrethroids be found in

A

insecticides such as ‘raid’ and ant powders
in some old school flea products

52
Q

List the clinical signs of pyrethroid toxicity

A

Primarily act on neural axons (Na channels)
Ataxia
tremours
disorientation
seizures
dyspnoea
respiratory arrest
hypersalivation
vomiting
AKI following rhabdomyolysis from uncontrolled seizuring

53
Q

Describe the treatment for pyrethroid toxicity

A

IVFT
intralipid infusion- as it is highly lipophilic
diazepam for seizures

54
Q

how do cleaning products commonly cause an issue

A

due to surface contact or mucosa contact

55
Q

what is the worrying consequence of ingestion of a caustic agent

A

oesophagitis

56
Q

how does anti-freeze cause toxicity

A

ethylene glycol is metabolised into glycolic acid, glycoaldehyde, oxalic acid
- glycoaldehyde is neurotoxic
- glycolic acid - produces a severe acidosis
- oxalic acid binds calcium leading to calcium oxalate formation in organs

Mortality is high - cats particularly susceptible

57
Q

List the clinical signs of cleaning product toxicity

A

oral pain
dysphagia
regurgitation
vomiting

58
Q

describe how to treat cleaning products toxicity

A

oral water - rinse out mouth as much as can
washing exposed surfaces with water

59
Q

List the clinical signs of anti-freeze toxicity

A

<12 hours- vomiting, lethargy (looking drunk)
12-24 hours - tachyarrythmias, tachypnoea, hypocalcaemia
24-72 hours- AKI and death

60
Q

can you test for ethylene glycol ingestion

A

there are tests but they are not great, some anti-freeze has fluorescein in so you can test the paws and mouth for its presence (with Woods lamp)

61
Q

what is the prognosis like for animals after ingesting anti-freeze

A

poor

62
Q

can we treat anti-freeze toxicity

A

may be able to slow production of toxic metabolites by diluting with alcohol dehydrogenase for 3 days (basically vodka diluted with saline (20%), dialysis can help the outcome

63
Q

what is ethically wrong with anti-freeze toxicity treatment

A

we are providing 3 days worth of alcohol to an animal
don’t know if worked at 7 day mark

64
Q

how does warfarin cause toxicity

A

it inhibits vitamin K epoxide reductase - this inhibits vitamin K synthesis which inhibits the production of clotting factors

65
Q

List the clinical signs warfarin toxicity

A

coagulopathies 36-72 hours post-ingestion

66
Q

Describe how can we diagnose warfarin toxicity

A

PT prolonged
aPTT prolonged
caviatatory bleeds

Petechiae are unlikely to be present

67
Q

Describe warfarin toxicity treatment

A

vitamin K injections and oral- up to 8 weeks (expensive)
fresh frozen plasma transfusion in severe cases

68
Q

what is the toxic substance in raisins/grapes/sultanas/currants

A

unknown but thought to be tartaric acid

69
Q

List the clinical signs of raisin/ grape toxicity

A

V+/D+
AKI- but unknown at what dose this will occur

70
Q

What is the toxic dose of raisin/ grapes/ sultanas/ currants

A

no known toxic dose- so any exposure should be considered serious

71
Q

Describe the treatment for raisin/ grape toxicity

A

IVFT- 48-72hrs is recommended because unknown toxic dose (expensive)
emetic
dialysis

Most dogs will be fine but some get AKI

72
Q

List the clinical signs of cocaine toxicity

A

hyperactive
hyperthermia
tachyarrythmias
vomiting
ataxia
seizures

73
Q

Describe treatment of cocaine toxicity

A

IVFT
cooling- depends on degree of hyperthermia you see
antidysrhymia drugs
seizure medication, etc

74
Q

List the clincial signs marijuana toxicity

A

vomiting
‘paranoia’
ataxia
depression
coma
urinary incontinence

75
Q

Describe treatment of marijuana toxicity

A

urinary catheter
IVFT
intralipid - may take a while to recover

76
Q

List clinical signs of opiate toxicity

A

depression
lethargy
vomiting
constipation
hypoventilation

77
Q

Describe treatment for opiate toxicity

A

IVFT
oxygen
naloxone reversal
may need ventilation

78
Q

List the clinical signs of ketamine toxicity

A

ataxia
hallucinations
aggression
cataplexy
loss of patent airway

79
Q

Describe treatment of ketamine toxicity

A

IVFT
intubation
ventilation

80
Q

What is the toxic substance in lillies

A

Toxic substance not known (probably a steroidal glycoalkaloid

81
Q

clinical signs of lily ingestion in cats

A

AKI

82
Q

clinical signs of lily ingestion in dogs

A

GI signs

83
Q

What part of a lily is toxic

A

Any part of the plant is toxic – including the stamen and pollen – which cats will play with because they are ‘floppy’

84
Q

Describe treatment for lily ingestion

A

decontamination of fur
IVFT
treatment per AKI

85
Q

How much Onions, Garlic, Leeks, Chives need to be ingested to be toxic

A

large quantities
cats may be more sensitive

86
Q

how do onions/garlic/leeks/chives cause toxicity

A

sulphur containing compounds can cause haemolysis or heinz-body anaemia

87
Q

List the clinical signs of onion/garlic/leek/chive ingestion

A

V+/D+
tachycardia
tachypnoea
pale MM (anaemia)

88
Q

Describe how to treat Onions, Garlic, Leeks, Chives toxicity

A

general principles
keep an eye on PCV- transfusion if severe

89
Q

why can mouldy foodds be toxic

A

fungal metabolites are neurotoxic

90
Q

List the clinical signs of mould ingestion

A

muscle tremors
hyperaesthesia
seizure
coma
death

91
Q

treatment for mould ingestion

A

IVFT
Diazepam is ineffective for muscle tremors- methocarbamol instead
intralipid infusion

92
Q

if in doubt about a toxin, who do you call

A

VPIS

9- SA- Gastrointestinal and Hepatic Disease (14 decks)

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