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Emergency Medicine - BT > Ch 15. Toxicology > Flashcards

Ch 15. Toxicology Flashcards

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1
Q

What are the sympathomimetic drugs of abuse (4)


A
  1. Cocaine

  2. Amphetamines

  3. Cathinone’s (bath salts)

  4. Methcathinone (khat)

  5. Caffeine
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2
Q

How do you differentiate NMS, serotonin syndrome, and anticholinergic toxidromes? (3)

A
  1. All will be agitated, delirious.

  2. NMS and SS have fever, increased HR, increased BP, increased RR, rigidity. NMS has lead pipe cogwheel rigidity. SS has hyperreflexia and clonus.
Serotonin syndrome: agitation, altered LOC, restless, hyperthermia, tachycardia, tachypnea, rigidity, hyper-reflexia, tremor, and MYOCLONUS

  3. Exposure: AntiCh – TCA or an anti drug. Serotonin Syndrome (antidepressants) has a predictable effect of excess serotonin and tends to come on quickly and go away quickly (24-48 hrs). NMS (antipsychotics) has a much more indolent onset (Scott Luckyk Grandma Fever – elderly individual has been acting funny for a few days and now she has a fever). It has a less predictable onset and may not go away for days to weeks. It is rare and a diagnosis of exclusion.

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3
Q

What is your hot and crazy DDx? (6)

A
  1. Sympathomimetics: Cocaine, Meth, Caffeine, Anticholinergics (TCA, plants Jimson weed)

  2. Syndromes: Serotonin Syndrome, Neuroleptic Malignant Sydrome, Malignant Hyperthermia 

  3. Infectious: Sepsis, Meningitis, Encephalitis

  4. Metabolic: Pheochromocytoma, Thyrotoxicosis
    
5. Environmental: Heat stroke

  5. Toxicological: Aspirin, Dinitrophenol (DNP), withdrawal from EtOH, Benzodiazepines, MDMA

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4
Q

What are your anticholinergics (5)


A
  1. Antidepressants

  2. Antipsychotics

  3. Antihistamines (dimenhydrinate)

  4. TCA

  5. Gimsum weed (plants)
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5
Q

Anticholinergic toxidrome (6)


A

“Mad as a hatter, dry as a bone, red as a beet, blind as a bad, hot as Hades, the bowel and bladder lose their tone and the heart runs alone”


  1. Fever

  2. Dry

  3. Altered mental status

  4. Tachycardia

  5. Urinary retention

  6. Decreased bowel sounds

  7. Mydriasis (dilated pupils)

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6
Q

Cholinergic toxidrome (8)


A
  1. Diaphoresis

  2. Vomiting

  3. Diarrhea

  4. Miosis

  5. Salivation
    
6. Urinary incontinence

  6. Bronchorrhea

  7. Bronchospasm

  8. Bradycardia

    Rx. Atropine

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7
Q

Treatment of anticholinergic toxicity (3)


A
  1. Supportive

  2. Physostigmine 1-2mg IV for adults over 5-10mins, start with 0.1mg or 0.2mg and watch the HR closely.
-Beware bradycardia/seizure/cholinergic effects, but probably very safe!

  3. Sodium bicarb for wide complex QRS, QTprolongation (sodium channel blockade, ex TCA)
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8
Q

Cyanide poisoning Sx and antidote (2)


A
  • Consider in all significant smoke inhalations, especially industrial fires, with metabolic acidosis, neuro dysfunction, elevated lactate
    
1. Sx = HA, anxiety, confusion, coma, seizures, tachy or brady dysrhythmia, abdo pain, flushing, renal failure, rhabdo (Basically all of your cells shut down)

    2. Cyanide antidote = cyanokit (hydroxycobalamin, sodium thiosulfate)
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9
Q

How much oxygen does this deliver (3)

  1. Nasal cannula 6L/min = 

  2. Simple oxygen facemask 10L/min = 

  3. Facemask NRB 15L/min = 

A
  1. Nasal cannula 6L/min = 40%

  2. Simple oxygen facemask 10L/min = 50%

  3. Facemask NRB 15L/min = 95%
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10
Q 
Name the antidote:
1. CCB: 
2. BB:  

3. Cyanide: 

4. Digoxin: 

5. Benzodiazepines: 

6. Local anaesthetic: 

7. Oxidizing toxins (nitrites, benzocaine, sulfonamide): 

8. Isoniazid: 

9. TCA:  

10. Serotonin syndrome: 

11. NMS: 

12. Carbon monoxide: 

13. Cholinergic (pesticides): 
14. Anti-cholinergic
15. Toxic alcohol (methanol, ethylene glycol): 
16. Rattlesnake (Crotiladae envenomation): 

17. Iron:
A
  1. CCB: calcium chloride, high dose insulin, glucagon, Norepi, intralipid, atropine, pacing
  2. BB: calcium chloride, high dose insulin, glucagon, vasopressors, intralipid, atropine, pacing

  3. Cyanide: cyanide antidote kit (amyl nitrite, or sodium nitrite)

  4. Digoxin: digibind

  5. Benzodiazepines: Flumazenil

  6. Local anaesthetic: intralipid
    
7. Oxidizing toxins (nitrites, benzocaine, sulfonamide): methylene blue

  7. Isoniazid: pyridoxine (B12)

  8. TCA: sodium bicarb

  9. Serotonin syndrome: supportive, and cyproheptadine
    
11. NMS: supportive, and bromocriptine/dantrolene
    
12. Carbon monoxide: 100% FiO2, hyperbaric oxygen * Consider in your altered patient, smoke/exhaust exposure, elevated lactate *
    
13. Cholinergic (pesticides): atropine q5min. Repeat indefinetly.
  10. Anti-cholinergic: physostigmine
  11. Toxic alcohol (methanol, ethylene glycol): Fomepizole
  12. Rattlesnake (Crotiladae envenomation): Cro-Fab

  13. Iron: Defuroxamine
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11
Q

Salicylate toxidrome (5)


A
  • ASA, oil of wintergreen (methyl salicylate)
    1. Altered mental status

    2. Tinnitus

    3. Metabolic acidosis, respiratory alkalosis
    
4. Tachycardia, tachypnea, arrhythmias, shock

    5. N+V

    6. Diaphoresis

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12
Q

Activated charcoal does NOT bind these things (6)


A 
* PHAILS *

1. Pesticides

2. Hydrocarbons and heavy metals

3. Alcohol

4. Iron

5. Lithium

6. Solvents
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13
Q

Three options for decontamination (3)


A
  1. Gastric lavage

  2. Charcoal

  3. Whole bowel irrigation
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14
Q

How do you do urinary alkalinisation? (3)


A
  1. Bolus 1-2mEq/kg IV sodium bicarb

  2. 2 amps of sodium bicarb in 800mL D5W, infuse at 200mL/hour

  3. May need 20mEq KCl

  4. Monitor VBG q2hours for K+ and bicarb

  5. Aim for urine pH 7.5-8.5
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15
Q

ECG features of TCA toxicity (3)


A 
*TCA’s block fast sodium channels *

1. Wide QRS, with a slurred S wave

2. Tachycardia

3. Brugada pattern

4. Heart blocks and bradycardia

5. Ventricular tachycardia

6. Prolonged QT

7. Right axis deviation (slurred S wave)
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16
Q

Indication for activated charcoal (example: TCA overdose) (1)


A
  1. Awake, alert, patent airway, bad toxicity, and within 1 hour of ingestion

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17
Q

Bupropion overdose patients are more at risk of __________ (1)


A
  1. Seizures 
(also agitation, tremor, N+V, sinus tachycardia)
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18
Q

Patients taking trazadone are at risk of ________ (1)


A
  1. Priapism
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19
Q

Symptoms of SSRI overdose (1)


A
  1. Nausea, vomiting, sedation, tremor, sinus tachycardia, seizures, serotonin syndrome
ECG: Prolonged QRS and QT
Bad ones: venlafaxine, bupropion

20
Q

Treatment options for toxicology seizures (3)


A
  1. Benzodiazepines

  2. Phenobarbital

  3. Propofol
* Do not use phenytoin (dilantin) for toxicology seizures *

21
Q

What do you worry about in MAOI overdose? (2)

A

Narrow therapeutic window. Can cause toxicity at therapeutic levels. One pill can kill a toddler.


  1. Serotonin syndrome 

  2. Tyramine reaction (headache with dietary indiscretion)
22
Q

Symptoms of anti-psychotic overdose (4)


A
  • Basically the same Sx the drug cause but more of it *
    
1. CNS depression, lethargy, ataxia, confusion
2. Respiratory depression in severe cases
    
3. Some can have antimuscarinic (tachy, dry skin, urinary retention, delirium, fever)

    4. Sinus tachy (prolonged PR, QRS, QT)
23
Q

Worrisome side-effect of clozapine? (1)

A
  1. Agranulocytosis
24
Q

Treatment options for Torsade de pointe (2)


A
  1. Shock (200J)

  2. Magnesium 2g bolus

  3. Overdrive pacing
25
Q

Movement disorders associated with antipsychotics (4)

A
  1. Akathisia (early, reversible) Rx. Diphenhydramine or benztropine or benzo
    
2. Acute dystonia (early, reversible) Rx. Diphenhydramine or benztropine or benzo

  2. Parkinsonism (delayed, reversible) Rx. Diphenhydramine or benztropine or benzo
  3. Tardive dyskinesia/peri-oral tremor (delayed, irreversible)
26
Q

Symptoms of lithium toxicity (3), and treatment (2)


A

Often a result of acute overdose, or chronic lithium with a decrese in GFR (lithium is excreted unchanged by the kidney)

1. GI (N+V+D+bloating+general abdo pain) – GI Sx more common with acute OD

2. Cardiac (bradycardia + hypotension + ventricular dysrhythmia) 

3. Neuro: confusion, decreased LOC, seizures
ECG: prolonged QT, ST depression
Therapeutic range 0.6-1.2mmol/L. Toxic range >2mmol/L
Lithium can induce severe hypothyroidism
Treatment: 2L IV NS, then 200mL/hour. Dialysis if severe Sx, chronic level >4, acute level >8


27
Q

How do these drugs affect the GABA channel?

  1. Benzodiazepines 

  2. Phenobarbital
A
  1. Benzodiazepines: (lowers the stimulation threshold of GABA, leading to more frequent activation)
    
2. Phenobarbital: (activates GABA and keeps the channel open longer)
28
Q

Describe the metabolism of ethanol (1)


A
  1. Ethanol via ADH to Acetaldehyde,

Acetaldehyde via Acetyl CoA to Acetic acid

29
Q

Normal rate of alcohol metabolism in normal and chronic drinkers (2)


A
  1. Normally 4mmol/L


2. Up to 6mmol/L in chronic drinkers
* 17mmol/L is the legal driving limit *


30
Q

Isopropyl alcohol presents with two laboratory findings (2)


A
  1. Ketones


2. Osmolar gap (no acidosis)

31
Q

Clinical features of isopropyl alcohol ingestion (2)


A
  1. Intoxication (twice as potent as ethanol)


2. Severe gastric irritation: N+V+abdo pain+pancreatitis+UGIB

32
Q

What product contains methanol? (1) Ethylene glycol (1)?


A
  1. Windshield washer fluid (also in solvents and Solid fuel for stoves)
    
1. Ethylene glycol is primarily a coolant (antifreeze)

33
Q

What is the toxic dose of methanol (1). What is the major toxic effect? (1)


A
  1. Toxicity occurs after 1 mouthful (30mL) - same with ethanol

  2. The major toxic effect: blindness, severe metabolic lactic acidosis

34
Q

Explain the metabolism of methanol (1), ethylene glycol (1)


A
  1. Methanol is metabolized by ADH into formaldehyde and then to formic acid * Super toxic *
  2. Ethylene glycol is metabolized into glycolic acid, and can precipitate into calcium oxalate crystals
35
Q

Triad of methanol poisoning (3), triad of ethylene glycol poisoning (3)


A
  1. Methanol: CNS depression, metabolic acidosis, visual changes “snow storm vision”
2. Ethylene glycol: CNS depression, metabolic acidosis, renal failure
    - Both will initially present with tachypnea while compensating for the acidosis. Can get tachycardia and hypotension as well
36
Q

What is Takotsubo syndrome? (1)


A
  1. Transient apical ballooning of the left ventricle, often after a catecholamine surge
37
Q

Treatment of cocaine associated ACS (5)

A
  1. ASA

  2. Benzo’s

  3. CCB (NO BB)
    
4. Nitro

  4. Heparin

  5. Cath lab if ST elevation
38
Q

Complications of hallucinogens (ex MDMA/ecstasy, LSD, psilocybin) (5)


A
  1. Hyponatremia

  2. HTN

  3. Hyperthermia
    
4. Arrhythmias

  4. Rhabdo

  5. Seizures
    
7. Psychosis
39
Q

Describe acetaminophen metabolism (1)


A
  1. Acetaminophen (CP450) NAPQI (TOXIC) Glutathione detoxifies to APAP
    
In overdose, acetaminophen overwhelms glutathione stores, and toxic NAPQI accumulates and causes hepatic necrosis.
    
NAC

40
Q

Four stages of acetaminophen toxicity (4)


A
  1. Stage 1 (0-24hrs) – anorexia, NV, malaise, hypokalemia and metabolic acidosis portend big ingestion

  2. Stage 2 (day 2-3) – RUQ pain, elevated LFTs
  3. Stage 3 (day 3-4) – fulminant hepatic failure. Metabolic acidosis, coagulopathy, renal failure
    
4. Stage 4 (2 weeks) – patients that survive hepatic failure begin to recover


41
Q

What is a toxic acetaminophen ingestion – (single ingestion or chronic) (2). Dosing of NAC (1)


A
  1. > 10g or 200mg/kg as a single ingestion

  2. > 6g or 150mg/kg over 2 days

    Beware extended release acetaminophen. Check two levels 4 hours apart

    *Use the Rumack-Matthew Nomogram (4 hour acetaminophen level)

  • NAC: 150mg/kg IV over 1 hour, then 50mg/kg over 4 hours, then 100mg/kg over 16 hours
NAC: beware anaphylactoid reactions. Treat with gravol.
42
Q

Clinical features of digoxin toxicity (4)


A
  1. GI – NV, abdo pain, anorexia

  2. CNS – HA, dizzy, confusion, fatigue, weakness, coma

  3. Cardiac – Almost any arrhythmia. Bidirectional VTach = digoxin

  4. Lytes – hyperkalemia (correlates with degree of acute OD!)

    Digoxin level will be mildly elevated or normal in chronic toxicity, and markedly elevated in acute toxicity. 

    In chronic tox – neuro Sx predominate (weak, fatigue, confused)

    In acute tox – GI Sx predominate (NV abdo pain)

    ** If the patient is hyperkalemic = indication for digibind **

43
Q

Medications to treat angioedema (6)

A

-Control airway PRN.

1. Epinephrine

2. Antihistamines – unlikely to be beneficial

3. Corticosteroids

4. Icatibant – bradykinin 2 antagonist

5. C1 esterase inhibitor

6. FFP – contains ACE

Angioedema is from bradykinin excess. Hereditary angioedema is C1 esterase inhibitor deficiency
 Isolated angioedema face or lips: discharge after 4 hours obs. Edema of uvula, tongue, airway: admit.

44
Q

What is the toxicity of phenytoin (1)?

A
  1. Cardiovascular – bradycardia, AVblocks, hypotension. Related to the IV administration because of the propylene glycol diluent. Infuse SLOWLY. 

45
Q

Clinical feature of valproate overdose? (1)


A
  1. CNS depression – drowsiness to coma.
46
Q

What is methemoglobinemia (1)

Clinical features of methemoglobinemia (1)

Which drug classes cause methemoglobinemia (3)

Diagnosis and treatment of methemoglobinemia (2)


A
  1. Oxidized iron in the hemoglobin molecule: converts it from ferrous (2+) to ferric (3+) state
Ferric (3+) iron cannot bind oxygen

    Clinical features of methemoglobinemia (1)

  2. Normal is 1-2%. At 10-20% you get a greyish cyanosis. At 20% you get HA, weakness, anxiety.
    At 50% cardiac arrhythmias, ischemia, seizures, coma.

Which drug classes cause methemoglobinemia (3)

1. Anti-malarials

2. Local anaesthetics (esp benzocaine)

3. Nitrates/nitrites (amyl nitrite, sodium nitrite, silver nitrate, nitroglycerin)


Diagnosis and treatment of methemoglobinemia (2)

1. Diagnosis: co-oximetry on venous or arterial sample

2. Treatment: methylene blue if >25% or symptomatic

47
Q

When do alcohol withdrawal seizures occur after cessation of alcohol? (1)


A
  1. 6-48 hours
*

33% of those that seize will go on to delirium tremens


Emergency Medicine - BT (16 decks)

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