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ACP Practical Exam Preparation > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Why should SpO2 levels be regarded with suspicion following exposure to burning materials?

A

CO exposure causes falsely high SpO2 readings

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2
Q

What are generally considered to be harmful doses of acetaminophen?

A
  • 250mg/kg single dose
  • 12g in 24h
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3
Q

What is the SLUDGEM/BBB mnemonic, and what does it describe?

A
  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • GI upset
  • Emesis
  • Miosis
  • Bronchorrhea
  • Bronchospasm
  • Bradycardia
    • The three “Bs” – bronchorrhea, bronchospasm, and bradycardia – are the most common causes of death in organophosphate and carbamate poisoning.
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4
Q

What is the primary indication of TCAs, and what is a common example?

A
  • treatment refractory depression
  • Amitryptiline (Elavil)
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5
Q

Describe the toxidrome of TCA overdose

A
  • Sedation
    • may also feature confusion, delirium, and hallucinations.
  • Anticholinergic effects
    • hyperthermia, flushing, and dilated pupils are common.
  • Hypotension
    • most ominous finding; the majority of patients who die from TCA overdose do so as a result of refractory, uncorrectable hypotension.
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6
Q

What are important pieces of information to gather about a chemical at scene if organophosphate/carbamate poisoning is suspected?

A
  • name and amount of the substance the patient was exposed to
  • the pesticide control number
  • WHMIS information
  • photo of the label
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7
Q

What is the role of high-flow O2 therapy in CO poisoning

A
  • Displaces CO from Hemoglobin
  • Reduces half-life of COHb in body (from 4-5 hrs. to 1-2 hrs.)
  • Ensures adequate oxygen of non-poisoned hemoglobin and plasma
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8
Q

Describe pre-hospital management of TCA overdose

A
  • Supportive/ABC care
  • Prompt 12-lead ECG
  • Sodium bicarbonate
    • 1 mEq/kg IV/IO slow push
    • May repeat 0.5 mEq/kg IV/IO slow push every 10-15 minutes as required
    • Tricyclic overdoses may require doses as high as 2-3 mEq/kg IV/IO
    • ​assess for QRS narrowing following administration
  • Consider push-dose EPINEPHrine for hypotension refractory to fluid bolus
  • Magnesium sulfate may be an acceptable antiarrhythmic in the context of cardiac arrest
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9
Q

Briefly describe CO toxicity

A
  • CO competitively binds to hemoglobin 200-250 times more strongly than oxygen
  • Causes a left shift in the oxyhemoglobin dissociation curve and widespread tissue hypoxia
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10
Q

Which beta blockers are associated with significant pro-arrhythmic tendencies?

A

Sotalol and Propranolol

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11
Q

Describe in-hospital management of CO poisoning (single intervention which is not available in pre-hospital setting)

A

Hyperbaric oxygen therapy

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12
Q

Which beta-blocker is more likely to require treatment with magnesium sulfate?

A

sotalol!

causes QTc prolongation, increased risk of TdP

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13
Q

The primary goal of most prehospital management of toxic exposures is:

A

Supportive care and transport

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14
Q

What is a common ECG finding in organophosphate/Carbamate poisoning that is NOT related to bradycardia, and what is the treatment if it is symptomatic?

A
  • QTc prolongation
  • May lead to PMVT or TdP
  • Tx is Magnesium Sulfate
    • 2g IV over 20 minutes
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15
Q

Describe physical properties of Carbon Monoxide

A

colourless, odourless, tasteless, non-irritating gas produced by the incomplete combustion of carbon-containing material such as gasoline, heating fuels, propane, oil, wood, and coal

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16
Q

Describe full management of organophosphate/carbamate poisoning

A
  • Call Clinicall!
  • Thorough decontamination and BSI
  • Supportive/ABC care
  • Manage seizure/arrhythmia
  • Consider Magnesium Sulphate for VT due to QTp
  • ATROPINE
    • ​1-2mg IM/IV
    • Double the dose q.5 minutes until effect is seen
    • Goal is to reverse bradycardia/hypotension (fast) and reduce secretions (slow)
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17
Q

BLS-level interventions for CO poisoning include:

A
  • Removal from source
  • Decontamination as required
  • Keep warm and place in position of comfort
  • 100% FiO2 (NRB + HFNC or BVM)
  • Airway/ventilation support
  • Transport
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18
Q

Describe the toxidrome of organophosphate/carbamate poisoning

A
  • Symptoms can be divided into muscarinic and nicotinic effects
  • Muscarinic
    • miosis, excessive sweating and bronchial secretions, bradycardia, hypotension
  • Nicotinic
    • mydriasis, tachycardia, fasciculations, muscle weakness, paralysis
  • May use the SLUDGEM/BBB mnemonic
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19
Q

Describe management of opioid overdose pre-hospitally

A
  • Emphasize airway, ventilation, and oxygenation support
  • Consider alternative DDx
  • Naloxone IM/IV
    • 0.4mg-0.4mg-0.8mg-2.0mg
    • 4.0mg then 10.0mg (Clinicall consult required) for ACP
    • Target return of spontaneous respirations, not increased LOC
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20
Q

Describe ACP-Level management of cyanide poisoning, not including BLS measures

A
  • Fluid + Pressors as needed
  • Manage seizures
    • Midazolam, 2-5mg IV/IO or 5-10mg IM
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21
Q

Describe how management of CCB overdose is different from standard bradycardia care

A
  • BGl testing is routine to aid in diagnosis
  • CaCl2 administration occurs early (prior to epi administration)
    • 1-2g IV over 10 minutes
  • Atropine less likely to be successful
  • TC pacing not included in CPGs (likely still appropriate)
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22
Q

What popoulation will have chronically elevated carboxyhemoglobin levels?

A

smokers

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23
Q

Describe the pathophysiology and toxidrome of cyanide poisoning

A
  • Cyanide inhibits the activity of cytochrome oxidase A3 in the mitochondria, preventing aerobic respiration
    • Poisons the electron transport chain
  • For toxidrome: First fast, then slow! (i.e. elevated vitals, followed by depressed)
    • Tachycardia, mild transient hypertension progressing to hypotension, bradycardia, and cardiovascular collapse
    • Tachypnea is common initially with progression to respiratory depression and respiratory arrest; pulmonary edema may develop
    • Headaches, anxiety, dizziness, agitation and confusion are common in early stages; patients may become obtunded or seize
    • Nausea and vomiting may develop; ingestion of caustic, alkaline cyanide salts may cause gastrointestinal bleeding
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24
Q

What is the goal of naloxone administration in opioid overdose?

A

the restoration of adequate respirations – a return of full consciousness is not necessary

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25
Q

Describe physical properties of hydrogen cyanide

A
  • colourless gas with a faint, bitter, almond-like odor
26
Q

Prior to treating anyone with suspected cyanide poisoning, what must be done first?

A

DECONTAMINATION!!!!

Decontaminate or die, you ding-dong

27
Q

Describe pathophysiology of Beta-Blocker overdose

A
  • Bradycardia
  • Hypotension
  • Myocardial depression and cardiogenic shock can develop in severe cases
  • Mental status changes, such as confusion, delirium, seizures, and unconsciousness, can occur at virtually any point.
  • Respiratory depression has been reported. Bronchospasm and hypoglycemia, produced by the beta blockade, can complicate management.
  • Ventricular dysrhythmias are more common with propranolol and sotalol
28
Q

Describe ACP-level management of Beta-Blocker Overdose

A
  • Always obtain a 12-lead ECG
  • Manage bradycardia
    • Atropine (may have limited success)
    • Transutaneous Pacing (may have limited success)
    • Epinephrine infusion (clinicall consultation, high doses likely required!)
  • Manage seizures
    • Midazolam
  • Glucagon
    • 5mg IV push (that’s a lot!)
  • Arrhythmia management
    • CaCl2
    • NaHCO3
    • MgSO4 - especially with sotalol ingestion
29
Q

Describe the mechanism of action of naloxone in reversal of opioid OD

A
  • Competitive opioid receptor antagonist
30
Q

Is decontamination required for patients with CO exposure?

A

No. Not in isolation. But may still be warranted if Cyanide exposure co-exists

31
Q

Define a “dry decontamination”

A

removal of clothing prior to placing in ambulance

32
Q

What are risk factors for unintentional acetaminophen overdose?

A
  • more common among individuals who have low levels of health literacy and who do not recognize its prevalence in multiple products.
  • Individuals with pre-existing liver disease are at increased risk of acetaminophen toxicity and can experience significant liver dysfunction, even with doses of acetaminophen that are generally considered safe
33
Q

Describe normal and abnormal COHb levels in adults

A
  • 0-3% normal or sub-normal (no treatment required)
  • 3-10%
    • Potentially pathological
    • If symptomatic, treat and transport
    • If asymptomatic, non-conveyance appropriate if patient is otehrwise healthy, non-pregant, is a responsible adult, and has no risk factors
  • >10%
    • Always requires tratment and transport
34
Q

Describe the pathophysiology of organophosphate and carbamate poisoning

A
  • Acetylcholinesterase inhibitors
  • Cause accumulation of ACh at nicotinic and muscarinic receptor synapses
  • Combination of parasympathetic signs AND muscle paralysis
  • Death is usually due to diaphragmatic paralysis and respiratory failure
35
Q

A patient was found with CO poisoning from automobile exhaust in an apparent suicide attempt. Will they likely require decontamination?

A

No!

CO exposure in isolation does not require decontamination.

36
Q

Describe common changes in BGl with BB and CCB overdose

A
  • BB overdose associated with hypoglycemia
    • should be treated in field
  • CCB overdose associated with hyperglycemia
    • aids in DDx, but does not require in-field management
37
Q

What are the dihydropyridines and non-dihydropyridines, and how are they different?

A
  • Calcium channel blockers
  • dihydropyridines (vasodilation)
    • amlodipine, nifedipine, felodipine
    • block L-type calcium channels in the vasculature
  • non-dihydropyridines (negative inotropy)
    • verapamil, diltizaem
    • act on calcium channels in the myocardium
    • more likely to directly cause decreased cardiac output
38
Q

Why is cyanide poisoning suspected in patients exposed to structure or vehicle fires?

A

Fires involving modern building materials, plastics, and furnishings can produce large amounts of cyanide

39
Q

Desribe the mechanism of acute pulmonary edema in CCB overdose and identify the class of CCB more closely associated with this presentation

A
  • non-dihydropyridines (Diltizaem and Verapamil) cause negative inotropy
  • leads to acute heart failure, resulting in pulmonary congestion
40
Q

Describe pre-hospital and definitive management for acetaminophen overdose

A
  • Pre-hospital
    • prompt recognition and documentation
    • Supportive care
    • Rapid transport or meet with CCP
  • Definitive
    • NAC (N-acetyl-cysteine)
    • Generally most effective within 8 hours
    • Pre-notify hospital, consult with clinicall
41
Q

A patient was found with CO poisoning from a house fire. Will they likely require decontamination?

A

Yes!

If the source of contamination is a fire, CN exposure should be suspected

42
Q

What are common ECG findings in TCA overdose?

A
  • Wide QRS
    • >100 ms
  • Deep S waves in leads I, aVL
    • Likely associated right axis deviation
  • Tall R waves in lead aVR
    • Dominant R wave often demonstrates Brugada-esque morphology
  • Tachycardias, including sinus tachycardia
43
Q

Describe BLS management of Beta-Blocker overdose

A
  • Supportive (ABC) care
  • Correct hypoglycemia
  • Transport
44
Q

Describe ways in which management of Beta-blocker poisoning is different from normal management of bradycardia

A
  • atropine and TC pacing are less likely to be effective
    • but should still be attempted!
  • Epinephrine infusion may require unusually high dosing to be effective
    • consult clinicall!
  • High-dose IV glucagon may be indicated
    • 5mg IV push!
  • Hypoglycemia may also be present
45
Q

Describe the Mechanism of Action of sodium bicarbonate in management of TCA overdose

A
  • Serum alkalinization
    • Favors neutral, non-ionized form of the drug, preventing sodium-channel binding
    • Promotes renal clearance/diuresis
  • Increased extracellular sodium
    • Increases the electrochemical gradient across cardiac cell membranes, potentially attenuating the TCA-induced blockade of rapid sodium channels
46
Q

Describe the toxidrome for actetaminophen overdose

A
  • Early
    • no specific signs or symptoms
  • Late
    • nausea and vomiting
    • malaise
    • lethargy
    • pallor and diaphoresis
    • right upper quadrant abdominal pain
47
Q

What are the three primary mechanisms by which TCAs exert cardiotoxic effects in OD?

A
  • Sodium channel blockade (QRS prolongation, tall R wave in aVR)
  • inhibition of potassium channels (QTc prolongation)
  • direct myocardial depression
48
Q

Describe the mechanism of action of Glucagon in Beta-Blocker OD management

A
  • Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction.
  • These effects are unchanged by the presence of beta-receptor blocking drugs.
  • This suggests that glucagon’s mechanism of action may bypass the beta-adrenergic receptor site.

i.e. glucagon acts on an independent receptor to stimulat chronotropic, inotropic, and dromotropic effects.

49
Q

Factors which determine the severity of CO exposure are:

A
  • Concentration of atmospheric CO
  • Duration of exposure
  • Individual physiology
    • Toxic levels vary widely between individuals
50
Q

Describe Prehospital managment of CCB overdose

A
  • Supportive care (ABCs)
  • Obtain BGl
    • may assist in DDx, hyperglycemia is often seen in CCB OD
  • Atropine
    • may not be successful
  • CaCl2
    • 1-2g IV slow IVP over 10 MINUTES
  • Epinephrine
    • IV push dose or infusion
    • only if bradycardia is refractory to CaCl2
51
Q

Describe the toxidrome and supportive findings of carbon monoxide poisoning

A
  • Follows exposure to combustion
  • headache, weakness, dizziness, and nausea along with tachycardia and tachypnea
  • “Cherry Red” skin
  • Paradoxically high SpO2 readings
  • High COHb readings
    • 3-10% may be normal for Pt or pathological. Always transport if high risk or symptomatic
    • >10% is always pathological
52
Q

Describe BLS Tx of cyanide poisoning

A
  • Decontaminate thoroughly
    • Remove clothing
    • Flush exposed skin and mucosal membranes with soap and water
    • If eyes are involved, flush with a gentle stream of water for at least 15 minutes
  • Supportive care (ABCs)
  • Mandatory Clinicall consultation
    • Arrange prompt access to Hydroxocobalamin
53
Q

Describe ACP-level interventions for CO exposure (Not including BLS interventions)

A
  • Prophylactic glucose administration
  • Alkalosis avoidance (do not hyperventilate!)
  • Obtain COHb (rainbow probe)
  • IV Fluids and vasopressors to manage hypotension
  • Manage sizures with benzodiazepenes
54
Q

Describe common ECG changes in Beta-Blocker overdose

A
  • PR prlongation
  • QRS prolongation
  • any bradydysrhythmia
55
Q

Briefly list drugs which have unique applications in the following toxicological emergencies:

  1. Cyanide
  2. Calcium Channel Blockers
  3. Beta Blockers
  4. Acetaminophen
  5. TriCyclic Antidepressants
  6. Organophosphates/carbamates
A
  1. Cyanide
    • Hydroxocobalamin
  2. Calcium Channel Blockers
    • CaCl2 (1-2g IV over 10 minutes)
    • Given PRIOR to IV epinephrine
  3. Beta Blockers
    • Glucagon (5mg IV push)
  4. Acetaminophen
    • N-acetyl cysteine
  5. TriCyclic Antidepressants
    • Sodium Bicarbonate
    • 1mEq/kg IV slow push (consult clinicall, may require up to 2-3 mEq/kg), repeat 1/2 dose q. 10-15 minutes
  6. Organophosphates/carbamates
    • Atropine (1-2mg, double dose every 5 minutes to effect)
56
Q

Describe pathophysiology of beta-blocker overdose

A
  • The primary mechanism for beta blocker toxicity is through the adrenergic blocking action of these medications.
57
Q

What is the importance of an organosphosphate being labelled “contact” or “systemic” to human physiology?

A

None!

refers to MOA in pests and plants

58
Q

What are priorities of care in CO poisoning?

A
  • Removal from source
  • High flow O2 administration
  • Transport
59
Q

Why is glucose administration indicated in CO exposure?

A
  • intracellular glucose may be decreased even in presence of normal or elevated blood glucose
  • Inadequate intracellular oxygen supply leads to globally inefficient anerobic respiration and rapid depletion of intracellular glucose stores
60
Q

Which toxidrome is suggested by the following ECG?

A

TCA overdose, as evidenced by

  • Wide QRS
  • tall R wave in aVR
  • deep S waves in I and aVL
  • Tachycardia

ACP Practical Exam Preparation (10 decks)

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