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Health 31 > Clinical Toxicology & Antidotes > Flashcards

Clinical Toxicology & Antidotes Flashcards

1
Q

LO
- An “introduction to toxicology”
* Demonstrate an understanding of toxicology, poisons, drugs in
overdose and associated therapeutic interventions.
- Principles of toxicology
- Actions of poisons/drugs in overdose
- Common antidotes
* Understanding of fund

A
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2
Q

what resources can be used for toxicology information? 2

A

TOXBASE and national poisons information services (NPIS)

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3
Q

What are the different categories of poison causes? 4

A
  • acute
  • chronic
  • accidental
  • intentional
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4
Q

intentional poisoning is generally….

A

acute. OD of paracetamol/ other prescribed med

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5
Q

what is the main cause of overdosing?

A

paracetamol
ibuprofen
sertraline
diazepam
durgs of misuse
even caffeine

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6
Q

term given to cluster of clinical features of a poisoned patient?

A

toxidromes

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7
Q

What are examples of toxidromes? 5

A
  • opioid
  • serotonergic
  • anticholinergic
  • cholinergic
  • sympathomimetic
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8
Q

What are the symptoms of opioid toxidrome?

A
  • pinpoint pupils
  • reduced GCS
  • reduced RR
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9
Q

What are the symptoms of serotonergic toxidrome?

A
  • agitation
  • delirium
  • tremor
  • tachycardia
  • labile BP
  • sweating
  • hypertonia
  • brisk reflexes
  • clonus
  • fever
  • serotonin
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10
Q

What is meant by labile BP?

A

blood pressure that easily fluctuates

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11
Q

drug that may -> serotonergic toxidrome?

A

sertraline

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12
Q

What are the symptoms of anticholinergic toxidrome?

A
  • dilated pupils
  • warm, dry pupils
  • confusion, restlessness, hallucinations
  • brisk reflexes, myoclonic jerks
  • tachycardia
  • urine retention
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13
Q

drug that may -> anticholinergic toxidrome?

A

amitriptyline

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14
Q

What are the symptoms of cholinergic toxidrome?

A
  • miosis
  • bradycardia
  • sweating
  • excessive secretions
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15
Q

give 4 sympathomimetic toxidromes that would be seen with ephidrine, amphetamine, ectasy etc overdoses?

A

hypertension, sweating, tachycardia, agitation

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16
Q

Give examples of excessive secretions that occur in cholinergic toxidrome.

A
  • hypersalivation
  • lacrimation
  • rhinorrhoea
  • bronchorrhoea
  • diarrhoea
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17
Q

What laboratory investigations are carried out for poisoned patients?

A
  • routine blood tests
  • ABG: COHb, MetHb
  • anion gap + osmolality gap
  • analytical toxicology: emergency measurements and screening
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18
Q

What are examples emergency measurements taken as laboratory investigations for poisoned patients?

A
  • salicylate
  • iron
  • theophylline
  • methanol
  • ethylene glycol
  • lithium
  • phenytoin
  • carbamazepine
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19
Q

What are drugs screened for as part of laboratory investigations for poisoned patients?

A
  • paracetamol
  • drugs of abuse

(as may have been taken alongside other drugs)

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20
Q

importance of toxidromes?

A

to make decisions quick, as sometimes dont get urine/ blood results back quick from screens etc

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21
Q

What is meant by an anion gap?

A

measures the difference—or gap—between the negatively charged and positively charged electrolytes in your blood.

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22
Q

What is the normal range of values for the anion gap?

A

12-16

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23
Q

How does a raised anion gap affect the blood pH?

A

decreases it (added acid)

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24
Q

What are causes of a raised anion gap?

A
  • ketoacidosis
  • lactic acidosis
  • salicylate overdose
  • alcohols: ethanol, methanol, ethylene glycol
  • renal failure
  • rhabdomyolysis
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25
Q

What is the osmolal gap?

A

measured osmolality - calculated osmolality

calculated osmolality = 2[Na+] + [K+] + urea + glucose

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26
Q

What is the normal reference range for the osmolal gap?

A

<10mOsm/kg

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27
Q

What can cause an increased osmolal gap?

A

alcohols: ethanol, methanol, ethylene glycol, acetone, isopropanol

eg ppl drinking poor quality spirits: may have methanol -> toxic syndorme

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28
Q

What is the general management for poisoned patients? 4

A
  • supportive care
  • prevention of absorption
  • enhancement of elimination
  • specific antidotes
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29
Q

prevention of further absorption of drug form bowel etc is difficult after…

A

about an hour

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30
Q

What techniques are used to prevent absorption?

A
  • whole bowel irrigation
  • activated charcoal
  • gastric lavage (rarely used)
  • emetics (not recommended)
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31
Q

What forms of poison is whole bowel irrigation used for?

A
  • modified release medication
  • body packers
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32
Q

why are emetics not recommended to prevents abs?

A

often too late and other risks involved (for v drowsy px.. resp danger of aspiration

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33
Q

name one compound that may be used to prevent abs of a toxic/ poisonous compound? rare

A

activated charcoal

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34
Q

What techniques are used to enhance elimination? 3

A
  • multiple dose activated charcoal
  • urine alkalinisation
  • extracorporeal: haemofiltration, haemodialysis
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35
Q

What drugs can multiple dose activated charcoal be used to enhance elimination of?

A
  • carbamazepine
  • colchicine
  • quinine
  • theophylline
  • phenobarbital
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36
Q

What drug can urine alkalinisation be used to enhance the elimination of?

A

aspirin

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37
Q

What drugs can extracorporeal techniques be used to enhance the elimination of?

A

haemodialysis
- lithium

  • salicylates
  • ethylene glycol
  • methanol
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38
Q

What is an antidote?

A

A therapeutic substance administered to counteract the adverse effects of a xenobiotic

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39
Q

What are the limitations to antidotes?

A

may be rarely used, can be expensive and limited shelf life

  • May need to be sourced from another hospital
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40
Q

Where can guidance on the availability of antidotes be found?

A

the joint RCEM/NPIS guideline

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41
Q

name some drugs that should be available immediately in A&E

A

acetylcysteine (as paracetamol OD common)
glucagon
naloxone

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42
Q

What are the possible mechanisms of antidotes? 7

A
  • forms inert complex w poison
  • accelerates detoxification of metabolite/poison
  • reduces rate of conversion to toxic compound
  • competes w toxic substances for essential receptor sites
  • blocks essential receptors through which toxic effects are mediated
  • bypasses effect of poison
  • intralipid
43
Q

What is the antidote to iron? (forms inert complex w poison)

A

desferrioxamine

44
Q

What is the antidote to cyanide? (forms inert complex w poison - chellates)

A

dicobalt edeate

45
Q

What is the antidote to digoxin? (forms inert complex w poison - chellates)

A

digoxin-specific antibody fragments

46
Q

What is the antidote to heparin? (forms inert complex w poison - chellates)

A

protamine

47
Q

What is the antidote to paracetamol?

A

acetylcysteine

48
Q

How does acetylcysteine work?

A

accelerates the detoxification of paracetamol

49
Q

What is methaemoglobinaemia? How does this compare to normal O2 transport?

A
  • Hb w oxidised haem iron (Fe3+)
  • O2 transport however depends on reduced haem iron (Fe2+)
  • haem iron maintained as reduced by NADH-dependent MetHb reductase
  • in this condition, excess metHb in place of normal Hb
50
Q

How does methylene blue work?

A

accelerates detoxification of MetHb by acting as electron donor in reduction of metHb
to reverse effects

51
Q

What is the antidote to methaemoglobinaemia?

A

methylene blue

52
Q

How do the symptoms of methaemoglobinaemia worsen with increasing concentrations?

A

slide 29 table

53
Q

What is the antidote to ethylene glycol and methanol poisoning?

stops production of toxic metabolites

A

fomepizole (4-methylpyrazole)

54
Q

What is the antidote to benzodiazepines (anaesthetic use)? +midazolam

A

flumazenil

55
Q

What is the antidote to opioids?

A

naloxone

56
Q

What is the antidote to warfarin?

A

vitamin k (Phytomenadione)

57
Q

How does flumazenil work?

A

competes w benzodiazepines by binding to receptor site

58
Q

How does naloxone work?

A

competes w opioids for the opioid receptors

59
Q

How does vitamin K work?

A

competes w warfarin for same receptor site

60
Q

How does atropine work?

A

blocks receptors through which toxic effects are mediated

61
Q

What is atropine the antidote to? 4

A
  • nerve agents
  • organophosphate insecticides
  • drugs for myasthenia gravis e.g. pyridostigmine
  • clitocybe mushrooms (muscarine)
62
Q

What is the antidote to beta blockers?

A

glucagon

63
Q

How does glucagon work against beta blockers?

A

bypasses the beta-receptor site
BB block cAMP -> dec HR
slide 34!!

64
Q

why is it hard ot give glucagon high doses by syringe?

A

as it crystallises

65
Q

why is intralipid an important antidote for many drugs? - How does intralipid work?

A

forms a lipid sink for lipophilic drugs to drop into and be removed

66
Q

name one issue with naloxone?

A

short half life so it may seem like patient has been treated but might not be

67
Q

name 3 antidotes that work by competing with toxic substances for essential receptor sites?

A

flumenazil, naloxone and vitamin K

68
Q

ethylene glycol is used in anti freeze and screenwash, what is it metabolised in the liver by to form toxic metabolites?

A

alcohol dehydrogenase

69
Q

what does tox from ethylene glycol result from?

A

metabolic acidosis and inhibition of oxidative phosphorylation and protein synthesis

70
Q

what does oxalic acid precipiate with to cause end organ damage in patients that have been poisoned with ethylene glycol?

A

calcium

71
Q

Schematic of ethylene glycol metabolism
slide 38

A
72
Q

How do osmolar and anion gaps change over time post-toxic alcohol ingestion?
sldie 39

A

osmolar gap cna be normal w late presentation
but anion gap grows over time

useful to see where u are and Hx of when poisoning occurred

73
Q

What are the 3 treatment options for ethylene glycol poisoning?

A
  • ethanol
  • fomepizole (4-methylpyrazole)
  • haemodialysis
74
Q

what is the rationale behind treating those with ethylene glycol tox with ethanol?

A

both metabolised by ADH

ADH has greater affinity for ethanol, decreased formation of toxic metabolites

75
Q

lethal dose of ethylene glycol

A

aorund 100ml

76
Q

treating those with ethylene glycol tox with ethanol, what serum conc should be acheived?

A

> 100mg/dl

need doses that cause drowsiness

77
Q

what is the rationale behind treating ethylene glycol poisoning with fomepizole?

A

potent inhibitor of ADH

78
Q

cons of fomepizole?

A

expensive and not readily available

79
Q

pros of fomepizole?

A

easier to administer, predictable PK

80
Q

why is haemodialysis a good treatment for ethylene glycol poisoning?

A

removes parent compound and its metabolite

81
Q

When is haemodialysis indicated for ethylene glycol poisoning?

A

when there’s:

  • renal failure
  • severe metabolic acidosis refractory to bicarbonate
  • ethylene glycol conc. >50mg/dl
82
Q

slide 41

A
83
Q

What are some sources of cyanide poisoning?

A

fired smoke from burning of:

  • natural substances: wool, silk, cotton
  • synthetic: plastics, nylon, polyurethane foam
84
Q

How is cyanide toxic?

A

poisons the mitochondrial electron transport chain within cells so no ATP can be produced

kills resp in cells, rapid

85
Q

What are the antidotes to cyanide? 4

A
  • O2
  • methaemoglobin inducers (sodium nitrite)
  • dicobalt edetate
  • hydroxocobalamin (cyanokit)
86
Q

sodium nitrate (methaemoglobin inducers) used as cyanide antodotes to get what instead of what?

A

Fe3+ instead of Fe2+
3: less efficient at transporting, cant be affected by cyanide -> net benefit

87
Q

What is Kelocyanor?

A

commercially available prep of dicobalt ededate containing dicobalt edetate 300mg + free cobalt

88
Q

How effective is dicobalt edetate?

A
  • rapidly after IV injection
  • superior to combined sodium thiosulphate + sodium nitrate
89
Q

dicobalt is effective after iv injection and superior to other treatments and is cheap. In the absence of cyanide it may lead to cobalt tox. list SEs

A
  • facial + laryngeal oedema
  • Vomiting

– Urticaria, anaphylactic shock

– Hypotension, cardiac arrhythmias

– Convulsions

90
Q

What is the disadvantage of hydroxocobalamin?

A
  • large doses (5-10g) required
  • expensive
91
Q

hydroxycobalamin used for?

A

cyanide poisoning

92
Q

What are the 2 categories of sources of lead poisoning in the UK?

A
  • occupational
  • non-occupational
93
Q

What are occupational sources of lead poisoning?

A
  • Inhalation of lead dust/ fumes in lead-using industries (lead acid battery manufacturing and recycling; mining, smelting and refining of lead and other ores)
  • During demolition/renovation of old properties
94
Q

What are non-occupational sources of lead poisoning?

A

House renovation, lead paint, imported toys or cookware, pica,

old lead pipes, contaminated traditional remedies or cosmetics

95
Q

What are possible lead poisoning symptoms?

A
  • asymptomatic
  • non-specific: abdominal pains, raised BP, etc.
96
Q

lead poisoning may be asymptomatic . what are some of the non specific symptoms?

A

abdominal pains, headache, raised BP, poor concentration, anaemia, constipation

97
Q

What can occur in severe lead poisoning? In what age group is it most common?

A
  • encephalopathy
  • children
98
Q

What are the renal effects of lead poisoning?

A
  • proximal tubular dysfunction
  • irreversible interstitial fibrosis
  • progressive renal insufficiency
99
Q

What therapy is used for lead poisoning?

A

chelation therapy

100
Q

At what blood lead concentrations should chelation therapy be considered?

A

> 50mcg/dl

101
Q

What are the 2 main chelation therapy options?

A
  • oral DMSA (succimer)
  • IV sodium calcium edetate
102
Q

What is the issue w chelation therapy?

A
  • it only removes lead from blood
  • therefore repeated courses are usually required with adequate intervals of at least 1 week to allow the lead to re-distribute from the bones
103
Q

true or false: chelation therapy only removes lead from the blood?

A

true

104
Q

repeated courses of chelation therapy for lead tox are usually required with adequate intervals of at least 1 week between, why is this?

A

allow lead to redistribute from the bones

Health 31 (16 decks)

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