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Toxicology > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Method of decontamination (5)

A

Dilution, emesis, gastric lavage, absorbents, cathartics

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2
Q

Indication dilution and what can be used?

A

Ingested an irritant or corosive

2-6ml/kg water or milk

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3
Q

When to induce emesis

A

Within 2-3 hours of ingestion

Can be effective >3 hours if coalesce to form a bezoar e.g. chewable medication, chocolate

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4
Q

Contraindication to emesis (5)

A

Corrosive agent, petroleum distillate (risk of aspiration), coma, seizures, recumbency

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5
Q

Indication gastric lavage

A

When emesis is controintdicated or unsucessful

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6
Q

Name an absorbent

A

Activated charcoal

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7
Q

Name three drugs than under go enterohepatic recirculation

A

Digoxin, NSAID and cannabis

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8
Q

What do absorbents not bind to? (6)

A

Heavy metals, alcohol, fertiliser, nitrates, iodies, clorate

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9
Q

Contra-indication to absorbents, why

A

Caustic material - unlikley to bind and impairs visulaisation of burns/ulcers

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10
Q

What electrolyte abnormality can be associated with activated charcoal

A

Hypernatraemia

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11
Q

Why use activated charcoal with a catthartic

A

Only finds with weak chemical fores, these will break down if the substance resides in the GIT for a prolonger periord&raquo_space;> re-release of the toxins

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12
Q

Three type of cathartics

A

Bulk (psyllium, canned pumpkin)
Osmotic (sorbital frequently added to activated charcoal)
Lubricants (minerral oil - not with activated charcoal)

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13
Q

Antidote to amphetamine

A

Acepromazine

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14
Q

Antidote to amitraz

A

Atimpamazole

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15
Q

Atropine is an antidote for what (2)

A

Carbamates, organophosphates

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16
Q

Antidote for selective serotonin uptake inhibitors

A

5-hydroxtryptophan

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17
Q

Cyprohepadine is a antidote for what?

A

Balcofen

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18
Q

Antidote for ethylene glycol?

A

Ethanol, fomepizole

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19
Q

Flumazenil is an antidote for what?

A

Benzodipazepine

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20
Q

When can intralipid emulsion be useful? (6)

A

Bupivicaine, verampil, propranolol, clompipramine, lidocaine, moxidectin

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21
Q

When can methcarbamol be an antidote? (4)

A

Permethrin, metaldehyde, strychinine, tremorgenic mycotoxins

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22
Q

Antidote for cholecalciferol toxicity

A

Pamidronate

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23
Q

MOA methocarbamol

A

Inhibition of AchE (similar to carbamate)

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24
Q

Types of rodenticides (4)

A

Anticoagulant, neurotoxic, vitamin D3, corrosive to GIT

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25
Q

Action of bromethalin

A

Neurotoxic rodenticide - uncoupling oxidative phosphorylation in the brain and liver mitochronidria leading to decreased ATP (affecting Na/K ATPase pump)
Lipid peroxidation and sodium accumulation in cell –> CNS oedema.

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26
Q

Treatment of bromethalin intoxication

A

Early decontamination, mannitol, supportive care, activated charcoal

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27
Q

MOA phosphide rodenticides

A

Corrosive, direct GIT irritant

Zinc phosphide combines with gastric acid or mositure to form phosphide gas

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28
Q

Treatment of phosphite intoxication

A

emesis, absorbents, well ventilated room

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29
Q

Vitamin K depenent coagulation factors

A

II VII IX and X

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30
Q

Which coagulation factor has the shortest half-life

A

VII

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31
Q

Why are cats sensitive to pyrethrins?

A

Cat’s altered glucuronidation metabollism

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32
Q

Clincial signs of pyrethrin intoxication

A

GI - hypersalivation, v+, nausea
CNS - disorentation, hyperexcitability, seizures
Respiratory - dyspnoea, tachypnoea

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33
Q

Treatment of pyrethrin intoxication (3)

A

Dermal decontamination, mucscle relaxant (methocarbamol), anticonvulsants

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34
Q

MOA carbamates and organophosphates

A

Competetively inhibit AchE&raquo_space; excess Ach accumulation

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35
Q

Clinical signs of organophosphate intoxication

A

Cholinergic crisis - Salivation, lacrimation, urinate, defecation, emesis, bradycardia, bronchoconstriction

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36
Q

MOA amitraz

A

Monoamine oxidase inhibitor and alpha-adrenergic agonist

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37
Q

What do paintballs contain? (4)

A

Contain polyethylene glycol, sorbitol, glycerine and gelatin

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38
Q

Toxicity associated with paintballs, what is therefore contra-indicated

A

Hypernatraemia

Activated charcoal contra-inidcated

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39
Q

What can mouldy food contain

A

Tremorgenic mycotoxins

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40
Q

Adverse effect of 3-6% sodium hypochlorite?

A

GI irritant

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41
Q

Adverse effects of ultra bleach (5-10% sodium hypochlorite and 0.2-2% sodium hydroxide)

A

Corrosive

42
Q

Toxic ingredient in windshield wiper fluid, metabolism and management

A

Methanol
Metabolised to formaldehyde (with alcohol dehydrogenase) which is rapidly oxidised to formic acid and then metbaolised to CO2 and H2o
Supportive care - decontamination ineffective and activated charcoal contraindicated

43
Q

3 stages of ethylene glycol toxicity

A

Stage 1 - 30 min -12 hr : alcohol poisoning (ataxia, hypersalivation, v+, pu/pd, seizures)
Stage 2 - 12-24 hr: Clinical signs resolve but severe internal injury
Stage 3 12-24 hours (c), 36-72 hours (d): severe AKI secondary to Ca oxalate crystalluria

44
Q

Diagnosis of ethyelene glycol intoxication

A

EG blood test within 24 hours

Venous blood gas - metabolic acidosis with high anion gap

45
Q

Metabolism of propylene glycol

A

Metabolised to D- and L- lactate which can contribute to metabolic acidosis.

46
Q

MOA calcium channel blocker

A

Inhibit transmembrane influx of extracellular calcium through slow or long-lasting L-type ion channels&raquo_space;> decreased myocardial contractility and arterial smooth muscle relaxation&raquo_space;> decrease peripheral resistace, BP and afterload

47
Q

Treatment of CCB overdose (3)

A

Ca gluconate to increase transmembrane flow
Intralipid
High dose insulin therapy (with concurrent dextrose)

48
Q

MOA high dose insulin for CCB intoxication

A

Supression of PDE III&raquo_space;> increased intracellular calcium influx
Mild hypokalaemia causing enhanced myocardial inotropy

49
Q

Characteristics of serotonin toxicity syndrome (6)

A

Muscle rigidity, increased reflexes, tremors, hyperthermia, hypertension and transient blindness.

50
Q

MOA tricyclic antidepressants

A

Inhbit neuronal reuptake of norepinepherine, serotonin and dopamine in the CNS
Also affinity of muscarininc and H1 receptors and can cause Na/K channel blockade of varying degrees

51
Q

MOA benzodiazepines

A

Enhance inhibitory neurotranmitter, GABA

52
Q

Signs of benzodiazepine toxicity

A

CNS depression, ataxia, aggression

53
Q

MOA phenylpropanolamine

A

Alpha adrenergic agonist - increases urethral outflow resistance

54
Q

Adverse effects of phyenylpropanolamine (4) and mechanism

A

Associated with Alpha receptor and B1 receptor stimulation : agitation, mydriasis, hypertension, tachycardia (or bradycardia secondary to hypertension)

55
Q

Management NSAID toxicity

A 
Decontamination
IVFT
Gastroprotectants
Multiple doses activated charcoal (undergoes enterohepatic recirculation)
TPE
56
Q

NSAID toxcity and TPE

A

11/11 dogs survived, 6 had bleeding complications

57
Q

Why is haemodialysis not helpful with NSAID toxicity

A

Highly protein bound

58
Q

Signs of paracetamol toxicity (4)

A

Methemoglobinemia, cyanosis, hepatitoxicosis, hepatic encephalopathy

59
Q

Adverse effect of albuterol intoxication

A

Hypoklaemia

60
Q

MOA albuterol

A

Beta adrenergic agonist

61
Q

MOA balcofen

A

centrally acting skeletal muscle relaxant

62
Q

Class of drug caffine

A

Methylxanthine

63
Q

MOA methylxanthine

A

Non-selective PDE inhibitor

64
Q

Adverse effects diphenhydramine (4)

A

Hyperactivity, tachycardia, vocalisation, hypethermia

65
Q

Prevelence of diphenydramine toxicosis in one study

A

23.5%, 3 dogs died

66
Q

Action amphetamines

A

CNS and CVS stimulants due to release of NE and catecholamines which acts on alpha and beta adrenergic receptors

67
Q

Clinical signs ketamine intoxication - low, high and severe doses

A

Small doses - mild stimulation, halucinations (30-60 mins)
High doses - opsthotonus, mydriasis, ataxia, increased muscle tone
Severe - coma, respiratory depression, hyperthermia, seizures, death

68
Q

MOA gamm hydroxybutanoic acid

A

Synthetic derivative of GABA

69
Q

What is LSD

A

synthetic hallucinogen

70
Q

What types of plants are Calla lilly, pholdendron, peace lilly

A

oxalate containing plants

71
Q

Clinical signs of oxalate containing plant ingestion

A

Calcium oxalate and crystals result in mechanical and inflammatory injury to the skin and mucous membranes
Plant proteolytic enzymes may contribute to local inflammation by promoting release of kinins and histamine.

72
Q

Management of oxalate plant ingestion

A

Decontamination - rinse mouth with water or milk

73
Q

Signs of liliaceae (Eater lilly/tiger lilly) intoxication (3)

A

First phase: GIT within minutes to hours
Second phase - oliguric/anuric renal failure CNS depression
36% develop neureo signs - ataxia, depression, tremors

74
Q

Toxic dose of lilly ingestion

A

<1 leaf

75
Q

Management of lilly ingestion

A

decontamination, intensive IVFT

76
Q

Active component of canabis

A

delta-tetrahydrocannabinol which interact with cannabinoid type 1 receptors

77
Q

Clinical signs of canabis intoxication

A

CNS depression, mydriasis, hyperesthesia, ptyalism, tremors

78
Q

Will emetics work with canabis ingestion

A

No, strong anti-emetic properties

79
Q

Toxin associated with rhododendrums and MOA

A

Grananotoxin - binds Na channels and maintains excitable membranes in a state of depolarisation

80
Q

Clinical signs of rhododendrum intoxication

A

Abdominal pain, tenesmus, CNS depression, skeletal muscle weakness, pulmonary oedema, arrythmia, hypotension

81
Q

Toxin associated with castor bean

A

Ricin - inactivates RNA, inhibiting protein synthesis

82
Q

Clinical signs associated wiht iris or tulip intoxication

A

Gastrointestinal irritant - potent emetic (interaction NK-1)

83
Q

Toxicity associated with macadamia nuts

A

Acute toxic syndrome with in 1-2 hours characterised by weakness, CNS depression, vomiting, ataxia, tremors

84
Q

Toxicity associated wiht onion, garlic, chives

A

Sulphoxides broken down to N-propyl disulphide&raquo_space; oxidate damage to haemoglobin and erythrocyte membranes&raquo_space;> methemoglobin, heinz bodies and eccentrocytes (intravascular haemolysis)

85
Q

What treatment can be given for heinz body anaemia and methemoglobinemia associated with onion/garlic intoxication

A

ascorbic acid

86
Q

Toxicity associated with raisins and grapes

A

AKI +/- vestibilar/forebrain signs (not associated with azotaemia)

87
Q

Prognosis raisin/grape toxocity

A

53% survived

88
Q

MOA of nicotine

A

Cholinergic (nicotine) receptor agonist - stimulant at low doses and depressent at high doses

89
Q

What toxic componentsdo E-cigarettes contain

A

Nicotine along with glycerol, propylene glycol and ethylene glycol

90
Q

Management nicotine intoxication

A

Gastric decontamination, symptomatic care, atropine if bradycardia, activated charcoal q6-8 hr post ingestion transdermal patches (delayed nictotine relase may occur)

91
Q

Types of pit vipers (2)

A

Rattlesnakes, copperheads

92
Q

Purpose of toxin from pit vipers

A

Neurotoxin to immobilise prey

93
Q

Clinical signs of pit viper bite

A

Local - bleeding, swelling, ecchymosis, erythema, sloughing
60% develop hypocoagulablity - correlates with plt not TEG
Systemically pain, weakness, nausea, muscle fasiculations

94
Q

MOA coral snake venom

A

Neurotoxic - non-depolarising post synpatic neuromuscular blockade with little tissue reaction

95
Q

Clinical sign of coral snake envenomation

A

Ascending flacid paralysis

96
Q

Management coral snake envenomation (4)

A

Assisted ventilation
Elastic compression bandage around bitten limb
Antivenom
Supportive care

97
Q

MOA brown spider venom

A

Single bite can be fatal
Sphingomyelinase D binds to cell membranes and induces leukocyte infiltration
Induces rapid coagulation and occlusion of small capillaries causing tissue necrosis

98
Q

Clinical signs of brown spider bite

A

Local - pruritus, oedema (bulls-eye lesion) and sorness (vasoconstriction and ischemia)
systemic (less common) - Coombs negative IMHA, DIC

99
Q

Management brown spide bite

A

Supportive care local and systemically

100
Q

MOA black widow spider venom

A

Promotes calcium-independent release of Ach and NA and inhibits reuptake

101
Q

Clinical signs of black widow spider bite

A

Pain, abdominal rigitidy, systemic hypertension

102
Q

Signs of european adder bite

A

57% ventricular arrythmia (increased cTnI)

Toxicology (1 decks)

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