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toxicology Flashcards

1
Q

what are general measures needed in suspected OD/ poisoning?

A
  1. ABCDE assess
  2. History: symptoms, PHMx, why, Risk assess
  3. Basic obs
  4. Specific systems examined
  5. Weight
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2
Q

what general investigations are needed in OD/ poisoning?

A
  • Bloods: FBC, LFT, U&Es, clotting, glucose, CK
  • Blood gas
  • Specific drug plasma conc (4hrs for paracetamol), urine toxicology
  • CXR
  • ECG: cardiac conduction
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3
Q

give some examples of anticholinergics?

A

Atropine
Antihistamines

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4
Q

how would anticholinergic poisoning present?

A

high HR
high BP
high temp
dilated pupils
no bowel sounds
dry

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5
Q

name some cholinergic?

A

Organic phosphorus
Mushrooms
pilocarpine

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6
Q

name some signs of cholinergic excess?

A

pinpoint pupils
loud bowel sounds
moist

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7
Q

name some opioids?

A

Morphine
Codeine
Tramadol
Heroin
Methadone
Hydrocodone
fentanyl

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8
Q

how would opioid OD present?

A

low HR
low BP
resp depression
cold
pinpoint pupils
no bowel sounds
dry

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9
Q

name some sympathomimetic drugs?

A

Caffeine
Cocaine
Amphetamines
MDMA
Theophylline

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10
Q

how would sympathomimetic OD present?

A

tachycardiac
hypertensive
high RR
warm
diklated pupils
loud bowel sounds
dry

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11
Q

name some sedative-hypnotics?

A

Anti-anxiety agents
Muscle relaxants
Benzos
Barbiturates

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12
Q

how would sedative-hypnotic OD present?

A

low HR
low BP
low RR
cold
no bowel sounds
dry

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13
Q

what questions are needed within paracetamol OD?

A
  • Timing
  • Staggered/ non staggered
  • How many tablets  workout mg/kg (500mg a tablet)
  • Other enzyme inducing drugs/ low BMI/ anorexia/ malnutrition  higher risk of hepatoxicity
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14
Q

how would paracetamol OD present within first few hrs?

A

N+V, abdo pain

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15
Q

how would untreated paracetamol OD present?

A

: vomiting continuing for 12hrs, pain/ tender liver from 24hrs, jaundice (2-3days), hepatic encephalopathy (3-5days)
- Loin pain, haematuria, proteinuria  renal failure
- Hepatic failure causes bleeding from coagulation abnormalities , hyperventilation  metabolic acidosis

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16
Q

when would LFTs become deranged within paracetamol OD?

A

> 18hrs after OD

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17
Q

what occurs within paracetamol toxicity?

A

uses the toxic pathway
glutathione can not keep up
causes hepatotoxicity

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18
Q

what can cause glutathione depletion?

A
  • Malnourished: eg dental pain causing to not eat, fasting more than 1 day
  • Eating disorders
  • Failure to thrive or CF in paeds
  • AIDS
  • Cachexia
  • Alcoholism
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19
Q

name some enzyme inhibitors?

A

S- sodium valproate
I – isoniazid
C- cimetidine
K- ketoconazole
F- fluconazole
A - Alcohol binge
C- chloramphenicol
E- erthyromycin
S: sulfonamides
C- ciprofloxin
M- metronidazole

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20
Q

name some enzyme inducers?

A

S: sulphonylureas
C: carbamazepine
R: rifampin
A: alcohol
P: phenytoin
G: grisofulvin
P: Phenybarbital

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21
Q

what is classed as acute paracetamol OD?

A

Excess amount of paracetamol
Ingested all in <1hr
Usually self harm

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22
Q

what is classes after staggered OD

A

Excess paracetamol ingested >1hr
Usually self harm

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23
Q

what is classed as therapeutic excess?

A

Excess paracetamol
Intent to treat pain/ fever
No intent of self harm
Elderly – misreading labels
Dental pain- couldn’t manage pain and took extra

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24
Q

how do you manage acute paracetamol OD that presents <8hrs?

A

Wait 4hrs from ingestion  take blood sample
Start acetylcysteine if 4hr plasma above line
Start acetylcysteine if evidence of hepatoxicity

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25
Q

what is management of acute OD -para presenting 8.12hrs?

A

Blood samples immediately
If ≥150mg/kg: start acetylcysteine or symptomatic and waiting blood samples
If <150mg/kg: wait results and then decide

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26
Q

how do you manage acute OD -para, pres more than 24hrs

A

Blood samples immediately
If ≥150mg/kg: start acetylcysteine or symptomatic and waiting blood samples
If <150mg/kg: wait results and then decide – check INR

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27
Q

how would you manage staggered para OD?

A

Start acetylcysteine immediately
Take blood samples 4hrs after last ingestion
Stop acetylcysteine if low risk of hepatotoxicity

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28
Q

how would you manage therapeutic excess OD?

A

If symptomatic: start acetylcysteine
Manage therapeutic excess depending on pt weight, quantity consumed

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29
Q

how would you manage a super acute - all ingested and presented within 1hr?

A

Activated charcoal
Check blood samples after 4hrs of last ingesting and decide

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30
Q

how does acetylcysteine work?

A
  • Can help with repair of damaged tissues
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31
Q

what can occur within acetylcysteine infusion?

A
  • Infusion reaction: anaphylaxis risk, itchy, syncope, drop in BP
32
Q

what is the SNAP protocol?

A
  • Parvolex given IV with 5% glucose
  • SNAP protocol: 100mg/kg in 200ml over 2hrs and then 200mg in 1000ml over 10hrs (12hrs in total)
33
Q

what are signs would indicate benzo OD?

A

low GCS, ataxia, dysarthria, resp depression

34
Q

how do you manage a Benzo OD?

A

Flumazenil – 0.5mg IV  indicated in resp depression, caution if dependent due to withdrawal and seizures

35
Q

why should you be cautious with flumazenil?

A

lots of side effects

36
Q

what cardiac signs indicate beta blocker OD?

A

QRS widening, hypotension, sinus bradycardia, 1st-3rd AV block, VF/VT

37
Q

what CNS signs can be seen with beta blocker OD?

A

drowsiness, confusion, convulsions, coma, absence of pupil reactivity

38
Q

apart from cns and cardiac effects, what else can be seen with beta blocker OD?

A

: bronchospasm, pulmonary oedema and hyperkalaemia

39
Q

how do you manage beta blocker OD?

A

Glucagon: severe hypotension, HF, cardiogenic shock unresponsive to atropine
- Bolus of 5-10mg IV injection administered in glucose %% over 1-3mins then reduce down

40
Q

what side effects can glucagon do when managing BB OD?

A
  • Side effects: N+V, hyperglycaemia, hypokalaemia, hypocalcaemia
41
Q

if glucagon fails when managing BB OD, what can be used as next lines?

A

Use atropine and pacing if needed

42
Q

what mmol/L is classes as lithium poisoning?

A

> 1.5

43
Q

what can cause lithium toxicity?

A
  • Causes of dehydration/ renal impairment make it more likely
  • NSAIDs, diuretics, ACE-I can make worse
44
Q

what are signs of lithium toxicity?

A
  • Nephrogenic diabetes insipidus  polyuria and polydipsia
  • Hypothyroidism
  • N+V
  • Fine tremor, dysarthria and ataxia
  • Sweating
  • Seizures and coma
  • Weight gain – increases appetite
45
Q

how can you manage lithium toxicity?

A
  • Forced diuresis: N.saline to enhance elimination
  • Omit drugs: monitor levels  caution to not go to low as can cause bipolar relapse
  • Haemodialysis: severe features of toxicity  neuro symptoms, seizures and coma
46
Q

which drugs have narrow therapeutic ranges?

A
  • Digoxin
  • Theophylline
  • Lithium
  • Phenytoin
  • Gentamicin
  • Vancomycin
  • Tobramycin
47
Q

what drugs interact with warfarin and increase INR?

A

Amiodarone
Ciprofloxacin
Fluconazole
Macrolides
Isoniazid
Ethanol (acute)
Cimetidine
Omeprazole
Cranberry juice
diarrhoea

48
Q

what interacts with warfarin and can lower INR?

A

Rifampcin
Carbamazepine
Phenytoin
Phenobarbital
St Johns wort
Cigarette smoking
Ethanol – chronic
Food high in vitK

49
Q

what are mild signs of CO poisoning?

A

slight headache, N+V, fatigue

50
Q

what are signs of moderate CO poisonings?

A

severe headache, confusion, drowsiness, tachycardiac

51
Q

what are signs of severe CO poisoning?

A

: unconsciousness, convulsions, cardio-resp failure, death

52
Q

how do you manage CO poisoning?

A
  • Remove source of CO
  • High flow O2 with tight fitting mask – 15L non-breather
  • Intubation
  • Hyperbaric Oxygen  unconscious or >40%COhb or 20% and pregnant
  • Other supportive therapy
53
Q

what are CNS signs of amitriptyline OD?

A

: extreme drowsiness, confusion, sensation of being hot then very cold, muscle stiffness, seizures, fainting, coma

54
Q

what are eye and mouth signs of amitriptyline OD?

A

blurred vision, dilated pupils, eye pain, dry mouth

55
Q

what happens to RR in amitriptyline OD?

A

slow RR

56
Q

what happens to renal/ urinary system in amitriptyline OD?

A

difficulty to urinate, not proper flow of urine

57
Q

what happens to cardiac system in amitriptyline OD?

A

irregular pulse, slow pulse, low BP, shock

58
Q

what are general signs of TCA OD?

A

TCA OD: can cause hyperreflexia, metabolic acidosis
- cardio-resp depression

59
Q

how do you manage amitriptyline OD?

A

sodium bicarb if at risk of arrhythmia and seizure

60
Q

what are signs of SSRI OD?

A

serotonin syndrome
SHIVERS
: Shivers, Hyperreflexia and myoclonus, Increased temp, Vital sign abnormalities, Encephalopathy, Restlessness, Sweating

61
Q

what is the warfarin antidote?

A

VitK - situ dependent

62
Q

what is digoxin antidote?

A

Digoxin specific AB if cardiac output is impaired
digifab

63
Q

what is apixaban/ rivaroxaban antidote?

A

Andexanet alfa
Specific reversal for factor Xa inhib
Usually for life threatening/ uncontrolled GI bleed and on apixaban

64
Q

what is nitrous oxide antidote?

A

Hydroxocabalamin 1mg IM STAT

65
Q

what is antifreeze?

A

ethylene glycol

66
Q

how would someone who drank antifreeze - ethylene glycol present?

A

May seem drunk with occasional haematemsis

67
Q

what is the management of antifreeze/ ethylene glycol OD?

A

Fomepizole

68
Q

what is the moa of fomepizole?

A

Competitive inhib of alcohol dehydrogenase
Used to reduce production of toxic metabolites

69
Q

how do you manage mild-moder cyanide poisoning?

A

hydroxocobalamin

70
Q

how do you manage severe cyanide OD?

A

thiopental sodium
Oxygen, dicobalt edetate, sodium nitrate

71
Q

what is the medical platform for posoining guidance?

A

toxbase

72
Q

how do you manage iron OD?

A

desferrioaxamine

73
Q

how do you manage organophosphorus OD?

A

Atropine
Pralidoxime

74
Q

how might iron poisoning present?

A

N+V and abdo pain initially
- can improve and then deteriorate again
- diarrhoea and haematemesis
- GI disorder

75
Q
A

Mental Health (4 decks)

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