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Acute Care and Anaesthetics > Toxicology > Flashcards

Toxicology Flashcards

1
Q

gliclazide overdose

A

high insulin

high C-peptide (T1DM have low)

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2
Q

how to calculate the anion gap in metabolic acidosis?

A

(Na + K) - (Cl + HCO3)

normal is 8-16

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3
Q

what does a negative base excess indicate?

A

metabolic acidosis

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4
Q

what does a positive base excess indicate?

A

metabolic alkalosis

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5
Q

three methods for increasing elimination of toxins?

A

urinary alkalisation
haemodialysis
haemofiltration

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6
Q

what are the five toxidromes?

A
  1. anticholinergic
  2. cholinergic
  3. opioid
  4. sympathomimetic
  5. sedative- hypnotic
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7
Q

anticholinergic toxidrome

A 
hot as a hare
dry as a bone
red as a beet
mad as a hatter
blind as a bat
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8
Q

causes of anticholinergic toxidrome

A

antihistamines
antidepressants
antipsychotics
antiparkinson

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9
Q

management of anticholinergic toxidrome

A

charcoal if within 1 hour

if seizure use BZDs

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10
Q

cause of cholinergic toxidrome

A

organophosphate pesticides

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11
Q

presentation of cholinergic toxidrome

A

SLUDGE - salivation, lacrimation, urination, diarrhoea, GI upset and emesis
can lead to bradycardia
miosis

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12
Q

management of cholinergic toxidrome

A

PPE (absorbed through skin)
atropine
pralidoxie mesylate
BZDs

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13
Q

presentation of opioid toxidrome

A 
sedation
reduced RR
bradycardia
hypotension
pinpoint pupils
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14
Q

management of opioid toxidrome

A

naloxone IM or IV if problem in A or B (dilute to avoid precipitating an acute episode)
need 6 hours observation post dose

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15
Q

what causes the sympathomimetic toxidrome?

A

recreational drugs such as ecstasy, amphetamine, cocaine, cathinones and novel psychoactive substances

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16
Q

presentation of sympathomimetic toxidrome

A

excited state with dilated pupils, tachycardia, hypertension, hyperpyrexia

can progress to seizures and reduced consciousness

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17
Q

what causes the sedative-hypnotic toxidrome?

A

BZDs or zopiclone causing similar opioid symptoms with miosis

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18
Q

management BZDs toxicity with

A

flumazenil (BZD antagonist) - may precipitate withdrawal and lower seizure thresholds

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19
Q

what is the problem with charcoal?

A

patietns have to be willing to drink it as aspiration causes pneumonitis

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20
Q

substances not absorbed by activated charcoal

A 
iron
lithium
K+ 
ethanol
methanol
ethylene
isoprophyl alcohol
hydrocarbons
solvents
cyanide
CO
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21
Q

what makes paracetamol toxic?

A

CP450 metabolise toxic metabolic N-acetyl-p-benzoquinone imine (NAPQI) which causes liver damage

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22
Q

when to check the patients blood level in paracetamol overdose?

A

4 hours after last dose ingestion and plot on nomogram (only if taken all at once - cannot do for staggered)

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23
Q

what additional investigations are needed in paracetamol overdose?

A

LFTs
U&Es
INR
assessing heptorenal toxicity

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24
Q

management of paracetamol overdose

A

N-acetylcysteine IV 12 hours or methionine PO within 8 hours

activated charcoal if within 1 hour

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25
Q

what happens once aspirin is ingested?

A

metabolised to salicylic acid causing respiratory alkalosis (resp centres activated) > metabolic acidosis (raised anion gap due to lactic acidosis)

26
Q

presentation of salicylates overdose

A

tinnitus
N&V
epigastric pain, haematemesis
sweating, pyrexia, tachycardia, tachypnoea

27
Q

management of salicylates overdose

A

give charcoal if within 1 hour
Level <450mg/L give oral hydration
level >450mg/L give IV fluids, urinary alkalisation, check pH hourly and WATCH K+

28
Q

what is the action of cocaine?

A

alkaloid which blocks reuptake of serotonin, dopamine and NA

29
Q

what does repeated use of cocaine risk?

A

thrombogenesis

coronary vasospasms

30
Q

management of cocaine overdose

A

BZDs
check CK for agitation
ECGs for vasospasms (give BZDs)

31
Q

management of sympathmimometic toxidrome (amphetamines, ecstasy)

A

hydration
BZDs
ecstasy can cause SIADH effect (hyponatraemia) due to thirst

32
Q

management of hallucinogens (LSD, magic mushrooms, ketamine)

A

supportive

BZDs for acute psychosis

33
Q

what is methanol present in?

A

de-icer

moonshine

34
Q

presentation of methanol

A

ethanol toxicity

driving in a snowstorm (damage to the optic nerve risks permanence)

35
Q

management of methanol poisoning

A

raised anion gap metabolic acidosis - sodium bicarbonate
ethanol
dialysis

36
Q

what is ethylene glycol

A

also present in antifreeze. give sodium bicarbonate and ethanol and fomepizole

37
Q

TCA toxicity triad

A
  1. anticholinergic effect
  2. sodium channel blockade of myocardium
  3. alpha adrenoceptor blockade
38
Q

what is the toxidrome in tricyclics?

A

anticholinergic

39
Q

management of tricyclic overdose

A

ECG (narrow complexes > broad > VT/VF)
charcoal within 1 hour
NaHCO3 8.4% sodium bicarbonate
BZDs for seizures

40
Q

which SSRI is dangerous?

A

paroxetine

41
Q

which drugs increase the risk of serotonin syndrome?

A 
SSRIs
TCAs
MAOIs
MDMA, amphetamines, cocaine, cathinones
tramadol
42
Q

presentation of serotonin syndrome

A 
agitation
tremor
hypertonia
diaphoresis
tachycardia
hyperpyrexia
43
Q

beta blocker overdose presentation

A

bronchospasm, glucose tolerance
bradycardia
hypotenison
cardiogenic shock

44
Q

management of serotonin syndrome

A

chlorpromazine

cyproheptadine

45
Q

maangement of beta blocker overdise

A

IV glucagon 5-10mg
atropine 3mg IV
fluids

46
Q

what does CCB overdose cause?

A 
myocardial depression
bradycardia
peripheral vasodilation
metabolic acidosis
hyperglycaemia
hyperkalaemia
47
Q

management of CCB overdose

A 
atropine 3mg IV
fluids
IV calcium chloride 10% 0.2ml/kg up to 10ml over 5 minutes
insulin and dextrose
glucagon if severe hypotension
arrhythmias= intralipid
48
Q

how does CO poisoning impair oxygen availability?

A
  1. oxygen carrying capacity of blood is reduced
  2. oxygen curve shifts to the left so less is delivered to tissues
  3. mitochondrial function is impaired
49
Q

presentation of CO poisoning

A 
headache
malaise
lethargy
nausea
cherry red discolouration is a late sign
50
Q

what is the COHb level in smokers?

A

<10%

51
Q

why is pulse oximetry of no use in CO poisoning?

A

cannot differentiate between CO and oxyHb

52
Q

management of CO poisoning

A

oxygen

neurological sequelae can happen

53
Q

substances that cause metHB

A
  • Local anaesthetics= prilocaine, lidocaine, benzocaine
  • Antibiotics= dapsone, sulphonamides, trimethoprim
  • Nitrites and nitrates
  • Others= metoclopramide, aniline dyes
54
Q

presentation of metHB

A

slate grey

ABG will be chocolate brown

55
Q

management of metHB

A

methylthioninium chloride or methylene blue IV

if fails consider G6PD deficiency

56
Q

management of acute dystonias?

A

procyclidine 5-10mg IV/IM (risks euphoria and abuse) or benztropine 1-2mg IV/IM

57
Q

management of neuroleptic malignant syndrome

A

dantrolene 1mg/kg IV

58
Q

what does myoglobin cause?

A

renal injury due to free radicals, renal tubules damage and vasoconstriction

59
Q

what is elevated in rhabdomyolysis

A

creatinine
potassium
CK
phosphate

dark urine is positive for Hb

60
Q

management of myoglobin

A

urine output 200-300ml/hr
urinary alkalisation with 1L sodium bicarbonate
treat hyperkalaemia

Acute Care and Anaesthetics (10 decks)

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