Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

acute care > toxicology > Flashcards

toxicology Flashcards

1
Q

what are the common toxidromes?

A

anticholinergic, cholinergic, opiate, sympathomimetic and sedative - hypnotic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are features of anticholinergic toxicity?

A

tachycardia, pyrexia, dry mouth, mydriasis
(enlarged pupils) and flushing. hallucinations, seizures and
conscious level reduced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

causes of anticholinergic toxidrome?

A

Antihistamines,
antipsychotics,
tricyclic antidepressants,
atropine (deadly nightshade, belladonna)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

features of cholinergic toxidrome?

A

increased salivation, lacrimation, urination, diarrhoea and vomiting;
the most common cause of mortality for patients with the cholinergic toxidrome is
bradycardia and bronchorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

causes of cholinergic toxidrome?

A

Organophosphate
pesticides, sarin gas,
physostigmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

features of opioid toxidrome?

A

depression of conscious level, reduced RR, bradycardia and hypotension. Typically the pupils are grossly constricted, often described as pinpoint.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

causes of opioid toxidrome?

A

Heroin, morphine,
codeine,
dihydrocodiene,
tramadol, methadone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

features of sympathomimetic toxidrome?

A

excited state with dilated pupils, tachycardia, hypertension,
hyperpyrexia. They may progress to have seizures or reduced conscious level and can develop brady or tachyarrythmias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

causes of sympathomimetic toxidrome?

A

Ecstasy, cocaine,
amphetamines,
cathinones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

features of sedative - hypnotic toxidrome?

A

BP - down
HR - down
RR - down
temp - down
pulls - generally smaller

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

causes of sedative-hypnotic toxidrome?

A

Benzodiazepines,
zopiclone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how do you remember anticholingeric toxidrome?

A

Hot as a hare
o Dry as a bone
o Red as a beet
o Mad as a hatter
o Blind as a bat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cholingeric pneumonic for main features?

A

DUMBELLS – Diarrhoea, Urination, Miosis (small pupils), Bradycardia, Emesis,
Lacrimation, Lethargy and Salivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how do you decontaminate skin?

A

copious irrigation, lavage and dilution with large volumes of water

PPE and ideally a closed drainage system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when is activated charcoal given?
dose?

A

within 1 hour of ingestion
the usual adult dose is 50g or 1g/kg for children.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does activated charcoal work?

A

The activated charcoal adsorbs toxin that is present in the stomach,
preventing systemic absorption. It may be of benefit to take charcoal after 1 hour if
the substance taken is a sustained release medicine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when is charcoal contraindicated?

A

if the time lapsed since ingestion is greater than 1 hour, if
the patient’s airway is not protected - either by intact protective reflexes or a cuffed
endotracheal tube, if the ingested substance is not bound by charcoal, or if an oral
antidote has been given.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what substances not adsorbed by activated charcoal?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

antidote for paracetamol?

A

N-acetyl cysteine, methionine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

antidote for tricyclics?

A

Sodium bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

antidote for BB?

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

antidote for Ethylene glycol and methanol

A

Ethanol, fomepizole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

antidote for cyanide?

A

Dicobalt edentate, hydroxycobalamin,
nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

antidote for iron salts?

A

Desferrioxamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

antidote for opiods?

A

naloxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

antidote for organsphospahtes?

A

Atropine, pralidoxime mesylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what can you do to increase elimination of toxins?

A

Urinary alkalinisation
o Haemodialysis
o Haemofiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what do you treat with urinary alkalinisation?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what can you treat with haemodialysis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what do you treat with haemofiltration?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the toxic metabolite in paracetamol?

A

N-acetyl-p-benzoquinoneimine (NAPQI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what predisposes to paracetamol toxicity?

A

> 75 mg/kg

Glutathione deficiency

Enhanced cytochrome p450 system. commonly caused by i.Prescription drugs i.e. carbamazepine, phenytoin,
phenobarbitone, primidone, rifampicin.
ii. Herbal remedies i.e. St Johns Wort.
iii. Alcohol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

common symptoms of paracetamol toxicity?

A

Common symptoms of significant poisoning are nausea, vomiting and abdominal
pain.

34
Q

diagnosis of paracetamol overdose?

A

bloods at least 4hrs post ingestion, at 4 hrs or asap
LFT’s, U&E’s and INR are useful tests for recognising hepatorenal toxicity and
failure.

35
Q

what do you give if pt presents within 1 hr of paracetamol overdose?

A

Paracetamol is adsorbed by activated charcoal, this should be offered if the patient
presents within 1 hour of overdose. (50g for adults or 1g/kg for children)

36
Q

how do you deliver N-acetyl-cysteine?

A

IV infuseion over 12 hrs or 21 hrs

effective if given within 8hrs ingestion

37
Q

what levels of aspiring cause toxicity?

A

125mg/kg = mild
> 250mg/kg = moderate
> 500mg/kg = severe

38
Q

what is seen in salicycle acid toxicity?

A

a respiratory alkalosis and metabolic acidosis.

Respiratory alkalosis is caused by direct stimulation of the central respiratory centres
causing increased respiration and ventilation.
Metabolic acidosis is caused by a disruption of Krebs Cycle causing lactic acidosis
and the presence of salicylic acid itself resulting in an increased anion gap acidosis.

39
Q

presentation of salicylate poisoning?

A
40
Q

diagnosis of salicylate poisoning?

A

Salicylate levels should be checked at least 2 hours post ingestion if the patient is
symptomatic or after 4 hours if they are asymptomatic.

ABGs
check paracetamol levels too

41
Q

how to treat salicylate poisoning?

A
42
Q

features of opiate toxicity?

A

o Pinpoint pupils (meiosis)
o Reduced respiratory rate
o Bradycardia
o Hypotension
o Reduced conscious level

43
Q

tx of opiate toxicity?

A

IM/IV naloxone
400mcg vial

44
Q

what are features of an acute withdrawal reaction in opiate toxicity?

A

agitation, confusion,
diarrhoea, vomiting, tachycardia, sweating and hypertension

45
Q

features of cocaine toxicity?

A

o Mydriasis (dilated pupils)
o Tachycardia
o Hypertension
o Excitation
o Hyperpyrexia

46
Q

risks of cocaine use?

A

Repeated use of cocaine causes accelerated thrombogenesis and coronary vasospasm
associated with myocardial ischaemia and infarction

47
Q

what should not be used in HTN tx or for chest pain in cocaine use?

A

Beta-blockers - may result in unopposed alpha adrenergic effect with worsening vasospasm, hypertension and myocardial ischaemia.

48
Q

how to tx cocaine toxicity?

A

benzodiazepine such as diazepa

49
Q

tx of Amphetamine, ecstasy and cathinones

A

adequate hydration, benzodiazepines can be
used for treatment of excitation, agitation or convulsions.

50
Q

what may you see in Amphetamine, ecstasy and cathinones toxicity?

A

reduced conscious level, seizures, muscle rigidity, rhabdomyolysis,
jaundice, renal failure and DIC

51
Q

features of methanol toxicity?

A

vertigo, headache, paraesthesia, nausea, vomiting and abdominal pain leading to reduced consciousness and coma.

reduced visual acuity which is said to resemble “driving in a snow storm”.
Damage to the optic nerve can be permanent.

52
Q

how to tx methanol toxicity

A

give ethanol

53
Q

what is ethylene glycol in?

A

commercial products such as coolants and
antifreeze

54
Q

toxic effects of ethylene glycol?

A

Toxic effects of oxalic acid and glycoaldehyde include pulmonary oedema and
tachyarrythmias. Production of calcium oxalate crystals can cause hypocalcaemia and
deposition in the renal tubules may precipitate renal failure.

55
Q

tx of ethylene glycol toxicity?

A

Emergency management initially follows the ABC method, sodium bicarbonate
should be provided to treat profound acidosis, pH should be maintained above 7.2.

give ethanol
haemodialysis

56
Q

features of benzos toxicity?

A

Reduced consciousness
o Bradycardia
o Hypotension
o Reduced respiratory rate and depth
o Meiosis (small pupils)

57
Q

tx of benzo toxicity?

A

flumazenil

58
Q

mechanism of tricycle toxicity?

A

o Anticholinergic effect
o Sodium channel blockade of myocardium
o Alpha adrenoceptor blockade

59
Q

presentation of tricyclic toxicity?

A

o Mydriasis (dilated pupils)
o Dry mouth
o Hot skin
o Urinary retention
o Tachycardia
o Hallucinations

slurred speech,
confusion, reduced consciousness, seizures and coma

60
Q

diagnosis of tricyclic toxicity?

A

ABG’s, U&E’s (hyperkalaemia is a differential
diagnosis of ECG changes), paracetamol and salicylate levels.

61
Q

treatment of tricyclic toxicity?

A

Tachyarrythmias should be managed by treating hypoxia and acidosis = 50-100ml of NaHCO3 8.4% intravenously

Seizures = benzodiazepines such as lorazepam or diazepam but
phenytoin should be avoided as this can worsen any proarrythmic effects.

Hypotension should initially be treated by elevating the foot of the trolley and IV fluids

62
Q

SSRI toxicity features?

A

nausea, vomiting, abdominal pain, diarrhoea, lethargy, tremor, drowsiness, headache,
nystagmus, ataxia, sinus tachycardia, hypotension and hypertension.

More severe toxicity can cause hypoglycaemia, convulsions and tachyarrythmias.
Hypoglycaemia may be a cause of seizures and must be considered.

63
Q

diagnosis of SSRI toxicity?

A

paracetamol and
salicylates and check serum levels

Blood glucose levels
ECG- prolongation of the PR, QRS or QT
intervals.

64
Q

what causes serotonin syndrome?

A

o Decreased reuptake of serotonin i.e. SSRI’s, tricyclics.
o Reduced metabolism of serotonin i.e. MAOI’s.
o Increasing release of serotonin i.e. MDMA, amphetamine, cocaine,
cathinones.
o Direct stimulation of serotonin receptors i.e. tramadol.

65
Q

features of serotonin syndrome?

A

agitation, tremor, hypertonia,
diaphoresis, tachycardia and hyperpyrexia. Severe cases may be complicated with
severe hyperthermia, rhabdomyolysis, renal failure and coagulopathies

66
Q

management of serotonin syndrome?

A

intubation and mechanical ventilation
treatment of dehydration, active cooling measures and benzodiazepines for agitation
or seizures. Cyproheptadine and chlorpromazine are both serotonin antagonists

67
Q

features of organophosphate poisoning?

A

SLUDGE
o Salivation
o Lacrimation
o Urination
o Diarrhoea
o Gastrointestinal upset
o Emesis

headache, anxiety, nausea, vomiting,
diarrhoea and meiosis
pulmonary oedema, bronchospasm,
respiratory failure, muscular weakness or paralysis, convulsions and coma.

68
Q

tx of organophosphate poisoning?

A

AVOID CONTAMINATION OF YOURSELF
o If there is significant bronchospasm or bronchial secretions / oedema then
atropine should be administered IV until the patient shows signs of
atropinisation, i.e. tachycardia, mydriasis, dry mouth.
o Pralidoxime mesylate can be given in moderate to severe poisoning to
competitively bind the cholinesterase receptors and dislodge the
organophosphate without inhibiting it. It must be given early, before “aging”
occurs to be effective.

69
Q

toxic effects of carbon monoxide?

A
70
Q

features of CO poisoning?

A

hortness of
breath, tachycardia, chest pain, neurological signs, reduced consciousness, seizures
may all be presenting symptoms however common features include headache,
malaise, lethargy and nausea.
The cherry red discolouration of lips and mucous membranes that is described appears
at with a carboxyhaemoblobin concentration of approximately 80% and is therefore
only really a feature of terminal carbon monoxide poisoning.

71
Q

hx of CO poisoning?

A

Multiple symptomatic patients from a single area where a heating device is
being used i.e. gas fire.
o Recurrent symptoms when heating appliance is used.
o Patients being found in enclosed areas where a motor has been running i.e. car
workshop, garage or room with petrol generator.
o Patients being found in enclosed areas where solvents have been used i.e.
spray painting in enclosed room.
o Episodes of self harm where a cars exhaust has been redirected back into the
vehicle using a conduit.

72
Q

what indicates CO poisoning?

A

Carboxyhaemoglobin

73
Q

how to treat CO poisoning?

A

OXYGEN

74
Q

BB toxicity features?

A

Beta blockers antagonise the beta-adrenoceptors in the heart and peripheral
vasculature, causing a bradycardia and subsequent reduced blood pressure. They can
also cause bronchospasm, sleep disturbance, tiredness and some deterioration in
glucose tolerance by blocking beta adrenoceptors in the bronchi, pancreas and liver.

75
Q

treatment of BB toxicity?

A

charcoal in 1 hr
Bradycardia can be treated with atropine and up to 3mg should be given intravenously
hypotension with fluids
intravenous glucagon 5-10mg

76
Q

features of CCB toxicity?

A

myocardial depression, bradycardia
and peripheral vasodilation producing profound hypotension and cardiogenic shock
confusion, nausea and vomiting may occur and metabolic
acidosis, hyperglycaemia and hyperkalaemia

77
Q

tx of CCB toxicity?

A

ensure a patent airway and
adequate ventilation
charcoal within 1 hr
Bradycardia - atropine and up to 3mg IV
hypotension - IV fluid
Intravenous calcium chloride 10% 0.2ml/kg up to 10ml
insulin and dextrose infusion
Glucagon may help to correct myocardial depression and hypotension.

78
Q

what can occur after ingestion of antipsychotic or antiemetic drugs?

A

acute dystonia eg
o Oculogyric crises
o Torticollis
o Trismus
o Tremor, dyskinesia and rigidity

79
Q

features of acute dystonia?

A

The patient may present with grimacing, facial twitching, masseter spasm, deviation
of gaze, limb rigidity and behavioural disturbance with a history of antipsychotic or
antiemetic drug ingestion, this may have been up to a week previously.

80
Q

tx of acute dystonia?

A

Procyclidine 5-10mg IV/IM or benztropine 1-2mg IV/IM

81
Q

Neuroleptic malignant syndrome fetaures?

A

confusion, rigidity, tremor,
autonomic instability, sweating, hyperpyrexia and the patient is at risk of developing
rhabdomyolysis and renal injury

82
Q

tx of Neuroleptic malignant syndrome?

A

Dantroline 1mg/kg IV can be given and repeated up to cumulative maximum
dose of 10mg/kg.

acute care (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions