Toxicology Flashcards

1
Q

What are the 3 primary causes of poisoning?

A
  1. Intentional - [deliberate self poisoning, malicious/3rd party]
  2. Accidental [occupational, domestic, error/misunderstanding, prescribed medications]
  3. Recreational
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2
Q

How are poison’s introduced into the body/4 entry routes?

A
  1. Ingested
  2. Inhaled
  3. Injected
  4. Absorbed
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3
Q

What is the primary approach to the poisoned patient?

A

Priority is to circulation, airway, breathing. Adults CAB, paeds ABC

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4
Q

What are possible concerns regarding a poisoned patient?

A
  • Pt contamination, and toxic environment.
  • Aggressive/agitated Pt
  • Dysrhythmias
  • Loss of airway reflexes/burns to airway
  • Seizures
  • Hypoglycaemia
  • Hyperthermia
  • Consider resuscitation antidotes and other management.
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5
Q

Why would you require CCP back up for a poisoned patient?

A
  • Pacing
  • Dysrhythmia management
  • Inotropic/chronotropic support
  • Atropine in organophosphate poisoning
  • Sodium bicarbonate in tricyclic overdose
  • Calcium in CCB overdose
  • Glucagon in beta blocker OD
  • Management and/or sedation of agitated Pt’s
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6
Q

What is the risk assessment for the poisoned patient?

A
  • Hx
  • Agent(s)
  • Dose(s)
  • Time since ingestion
  • Clinical features and progress
  • Patient factors (weight & co-morbidities)

What did you take? When did you take it? What did you take with it? Have you vomited?

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7
Q

What is the role of poison’s information centre?

A

It’s a handy source of information and guidance. On call toxicologists available in specific cases.

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8
Q

What is a toxidrome?

A

Is a group of examination findings [S&S & Hx], it may suggest the pharmacology behind a person’s clinical presentation.

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9
Q

What are common toxidrome’s?

A
  • Cholinergic
  • Anticholinergic
  • Sympathomimetic
  • Opioid
  • Serotonin
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10
Q

Go through the muscarinic effect acronym SLUDGEM-BBB

A
S = salivation
L = lacrimation
U = urination
D = defecation
G = GI upset
E = emesis
M = miosis
B = bradycardia
B = bronchorrhea
B = bronchospasm
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11
Q

Go through the muscarinic effect acronym DUMBELS

A
D = diarrhoea & Diaphoresis
U = urination
M = miosis [pinpoint pupils]
B = bronchorrhea, Bradycardia & Bronchospasm
E = emesis
L = Lacrimation
S = salivation
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12
Q

What are the 4 primary causative agents of cholinergic toxidrome - muscarinic effecs

A
  1. Organophosphates & carbamate insecticides
  2. Chemical warfare nerve agents
  3. Agents used in alzheimers dementia [donepezil, galantamine, rivastigmine, tacrine]
  4. Agents used in myasthenia gravis [neostigmine, physostigmine, pyridostigmine, endrophonium]
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13
Q

What is the nicotinic effects? [Cholinergic toxidrome] - (MATCH)

A
M = muscle weakness/fasciculation
A = adrenal medulla activity
T = tachycardia
C = cramping
H = hypertension
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14
Q

What are some signs & symptoms of anticholinergic toxidrome? [Catch phrase]

A

“Red as a beet, dry as a bone, blind as a bat, mad as a hatter and hot as a hare”

  • Dry skin
  • Hyperthermia
  • Thirst
  • Dry mouth
  • Dilated pupils
  • Tachycardia
  • Urinary retention
  • Slowed gastric emptying
  • Decreased bowel sounds
  • Delirium
  • Hallucinations
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15
Q

What are (up to) 10 examples of causative agents for anticholinergic toxidrome? [drugs/agents]

A
  1. Antiparkinsonian drugs [benxtropine, amantadine]
  2. Antitussives [dextromethorphan]
  3. Antihistamines [promethazine, doxylamine]
  4. Motion sickness agents [mecilizine, hyoscine-scopolamine]
  5. Bronchodilators [ipratropium]
  6. Antimuscarinic agents [atropine, hyoscyamine]
  7. Antidepressants [Tricyclic]
  8. Anticonvulsants
  9. Atypical antipsychotic agents
  10. Antipsychotic agents
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16
Q

What are the examples of sympathomimetic toxidrome?

A
  • CNS excitation
  • Seizures
  • Tremor
  • Hyperreflexia
  • Hyper/hypotension
  • Tachycardia
  • Low potassium, raised blood glucose, acidosis
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17
Q

What are some causative agents for sympathomimetic toxidrome?

A
  • Amphetamines
  • Cocaine
  • LSD
  • Caffeine
  • Theophylline [related to caffeine]
  • Phencyclidine [amphetamine derivative]
  • Methylphenidate [ritalin]
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18
Q

What is serotonin toxidrome [syndrome] ? (Factors related to it)

A
  • Mental status [agitation/restlessness/ confusion/hypomania]
  • Fever
  • Motor system [clonus/myoclonus, tremor/shivering, hyperreflexia/rigidity]
  • Autonomic nervous system [diaphoresis/tachycardia/flushing]
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19
Q

What are some causative agents for serotonin syndrome?

A
  • Selective serotonin re-uptake
  • SNRIs
  • Antidepressants
  • Monoamine oxidase inhibitors
  • Lithium
  • Antiemetics
  • Analgesic agents and antitussives
  • Anticonvulsants
  • Drugs of abuse
  • Ginseng
  • St Johns Wort
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20
Q

How would you manage serotonin syndrome?

A

Manage ABC’s, hyperthermia, dehydration, hyperreflexia/rigidity (CCP’s)

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21
Q

What are some conditions that result from opioid toxidrome?

A
  • CNS depression
  • Hypoventilation
  • Hypotension
  • Miosis
  • Rapid response to naloxone
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22
Q

What are 3 other opioids/medications that have special cases for risk assessment?

A
  1. Destropropoxyphene
  2. Tramadol
  3. Pethidine
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23
Q

What are some clinical features of opioids?

A
  • Opioid toxidrome [CNS depression, hypoventilation, hypotension]
  • Tachycardia
  • Bradycardia
  • Pulmonary oedema
  • N & V
  • Prolonged non-lethal intoxication can lead to hypothermia, compartment syndrome, skin necrosis, hypoxic brain injury.
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24
Q

What are some opioid management principles? (4)

A
  1. Dangers [drug paraphernalia]
  2. Maintenance of airway and breathing
  3. Use of naloxone
  4. Manage other presentations [seizures, pulmonary oedema, hypothermia]
25
Q

What occurs after benzodiazepines consumption/overdose?

A
  • They are sedative-hypnotics
  • Involved in up to 1/3 of deliberate self-poisonings
  • Potential for airway obstruction and aspiration
  • Patient may present with hypothermia, hypotension and bradycardia.
  • Increased risk of complications if co-ingestion of CNS depressants [alcohol, opioids, antidepressants]
26
Q

What are some clinical features of benzodiazepines?

A
  • Onset usually within 1-2hrs [more rapid if IV]
  • Lethargy
  • Ataxia
  • Slurred speech
  • Drowsiness
  • Reduced responsiveness
  • Profound coma is rare [more common in elderly]
27
Q

How would you manage benzodiazepine overdose?

A
  • Manage ABC’s [positioning, respiratory support]

- May need more aggressive treatment if co-ingestion occurred

28
Q

What are some concerns with corrosive ingestion?

A
  • Can cause injury to upper airway & GI tract
  • Upper airway injury is potentially life threatening
  • Significant GI tract injury is indicated by stridor, drooling & vomiting
  • The absence of lip or oral burns does exclude GI injury
29
Q

What is your corrosive management?

A
  • DRABC’s
  • mouth may be washed
  • small amount of water may be administered orally [1/2 cup] but avoid copious amounts of oral fluids.
  • Transport without delay
  • Do not induce vomiting*
30
Q

What is paraquat poisoning?

A
  • It is a widely used herbicide
  • Potentially lethal following ingestion as little as a mouthful
  • Usually results in fulminating multi-organ failure - death
  • May present with signs of oral burns and/or GI S&S
31
Q

How do you treat paraquat poisoning?

A
  • Do NOT induce vomiting
  • Consider giving foods or other solids
  • Withhold oxygen
  • Urgent transport
32
Q

What is glyphosate and what can it cause?

A

A common herbicide.

  • GI corrosive symptoms
  • Upper airway complications from oropharyngeal corrosive injury
  • Aspiration pneumonitis and non-cardiogenic pulmonary oedema
  • Myocardial depression and hypotension
  • Can lead to multi-organ failure and metabolic acidosis
33
Q

What does hydrocarbons include?

A
  • Petroleum distillates
  • Kerosene
  • Turpentine
  • Essential oils
  • Beneze
  • Toluene
  • Xylene
    [deliberate misuse of the above]
34
Q

What are some clinical features of hydrocarbon poisoning?

A
  • Immediate coughing or gagging [aspiration]
  • Wheeze, tachypnoea, hypoxia, haemoptysis and pulmonary oedema
  • Dysrhythmias
  • Profound CNS depression & coma
  • Seizures
  • Ataxia
  • N & V
35
Q

What is your management plan for hydrocarbon poisoning?

A
  • Remove Pt from source
  • De-escalation strategy if agitated
  • Do NOT induce vomiting [if ingested]
  • Provide oxygen and bronchodilators, if bronchospasm presents
  • Manage seizures as per guidelines
  • CCP backup for dysrhythmia management.
36
Q

What is carbon monoxide poisoning?

A

CO is a common cause of fatal and disabling poisoning in most developed countries.
Haemoglobin - carboxyhaemoglobin
[innacurate pulse oximetry]

37
Q

What are the effects of carbon monoxide poisoning?

A
  • Hypoxia

- Endovascular oxidative injury and inflammation

38
Q

What are some guiding principles to organophosphorous agents?

A
  • Protection of self and others from contamination
  • Remove Pt from contamination
  • If Pt contaminated will need to be decontaminated
  • Maintenance of ABC’s
  • Management of hypotension
  • CCP backup & prenotify
39
Q

What happens in paracetamol poisoning?

A

Paracetamol overdose leads to a depletion of glutathione stores → body then unable to convert intermediate toxic metabolites into non-toxic metabolites .

Easy to access in bulk.

40
Q

What are the clinical features of iron overdose?

A
  • N & V, may be haematemesis
  • Diarrhoea
  • Abdominal pain
  • Can be potentially fatal
41
Q

What are some things to consider with iron overdose; regarding treatment plan?

A

Manage hypovolaemia and transport to hospital.

42
Q

What are 3 examples of hypoglycaemic agents?

A
  1. Insulin
  2. Sulphonylureas
  3. Biguanides
43
Q

How will you manage hypoglycaemic patients?

A

Manage ABC’s, and per the QAS guideline.

44
Q

What are 3 examples of cardiovascular drugs?

A
  1. Beta blockers
  2. Calcium channel blockers
  3. Digitalis [digoxin]
45
Q

Why are beta blockers potentially fatal?

A

Due to their cardiovascular effects. [Sotalol and propranalol are considered more toxic]

46
Q

What are the clinical features of beta blockers?

A
  • PR prolongation
  • Bradycardia
  • Hypotension
  • Delirium
  • Coma
  • Seizures
  • Bronchospasm
  • Hyperkalaemia
  • Hypo/hyperglycaemia
47
Q

Why do verapamil and diltiazem cause cardiovascular collapse?

A

Due to the central cardiac effects and peripheral vasodilation.

48
Q

What are some clinical features of calcium channel blockers?

A
  • Bradycardia [1st deg heart block]
  • Hypotension
  • CNS depression
  • Seizures
  • Sinus of myocardial ischaemia and stroke may occur
  • N & V
  • Hyperglycaemia
49
Q

What is your management plan for calcium channel blockers?

A
  • Manage ABC’s
  • Manage hypotension
  • Urgent transport to hospital
  • Call CCP’s for: calcium, pacing, chronotropic support and arrhythmia management.
50
Q

What are the clinical features of Digoxin overdose?

A
  • N & V
  • Hypotension
  • Abdominal pain
  • Bradycardia
  • Increasing automaticity
  • Lethargy
  • Delirium
  • Confusion
  • Visual disturbances
51
Q

What drugs are included in the Selective Serotonin Reuptake Inhibitors (SSRI) group?

A
  • Fluoxetine
  • Sertraline
  • Paroxetine
  • Fluvoxamine
  • Citalopram

*Seizure management

52
Q

What is the major brand encountered in the Serotonin Noradrenaline Reuptake Inhibitors (SNRI) class?

A

Venlafaxine [effexor].

*14% or Pt’s have seizures but is dose related

53
Q

TCA overdose is the leading cause of morbidity & mortality, and the ingestion of 10-20mg/kg is potentially life threatening. T/F

A

True

54
Q

What is the 3 major effects of TCA overdose?

A
  1. CNS [sedation & coma]
  2. Anticholinergic effects [agitation, delirium & restlessness, mydriasis, dry/warm/flushed skin, tachycardia, myoclonic jerks]
  3. CVS [initially sinus tach, hypotension, broad complex tachy/bradyarythmias]
55
Q

Fantasy is a street name for Gamma Hydroxybutyrate [GHB] and is a colourless & odourless liquid. T/F

A

T

56
Q

What are the clinical features for GHB?

A
  • Miosis
  • Myoclonic movements
  • Possible airway obstruction
  • Cheyne-Stokes breathing
  • Vomiting
  • Sometimes mimicking generalised seizures
  • Agitation and delirium
  • Coma
  • Respiratory depression
  • Bradycardia
  • Sweating
57
Q

What are the clinical features for psychostimulant toxicity?

A
  • Dilated pupils that react sluggishly to light
  • Clenched jaw
  • Restlessness, agitation,
    repetitive movements
  • Rapid speech
  • Motor agitation or pacing
  • Hypertension
  • Tachycardia
  • Sweaty palms, flushed diaphoretic facial skin
  • Hypervigilance, • Paranoia
  • Hyperthermia
58
Q

What will you need to manage in regards to psychostimulant toxicity?

A
  • Manage CABs/ABCs.
  • Verbal de-escalation strategy if agitated
  • May need restraint
  • Manage hyperthermia
  • Manage seizures as per guidelines
  • Manage poor perfusion/dehydration
  • Manage chest pain
    [Aspirin is not recommended for chest pain if the patient is hypertensive due to increased risk of cerebral haemorrhage.]