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Medicine II: Emergency Medicine > Emergency Toxicology > Flashcards

Emergency Toxicology Flashcards

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1
Q

common physical findings, toxidrome, affect on patients system, laboratory work up and management

A

for each

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2
Q

What is the toxic dose of acetaminophen?

A

Toxic dose of acetaminophen is considered to be over 150 mg/kg in children and 7 g in adults.

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3
Q

How does a patient present with acetaminophen toxicity?

A

Shortly after ingestion of acetaminophen, there may be no symptoms or only anorexia, vomiting, or nausea; hepatic necrosis may not become clinically apparent until 24–48 hours later, when nausea, vomiting, abdominal pain, jaundice, and markedly elevated results on LFTs may appear. Hepatic failure may follow.

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4
Q

How quickly does acetaminophen toxicity become apparent?

A

Causes delayed hepatic injury, 24–72 hours after ingestion

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5
Q

How do we determine the level of acetaminophen toxicity?

A

Nomogram for prediction of acetaminophen hepatotoxicity following acute overdosage.

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6
Q

How do we work up a patient with acetaminophen toxicity?

A

Draw 4-hour postingestion levels, and use nomogram to predict severity following acute ingestion.

Chronic toxicity should be assessed through clinical examination, an acetaminophen level, and liver function tests.

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7
Q

What is the treatment for acetaminophen toxicity?

A

Provide intensive supportive care and GI decontamination as described previously. Administer activated charcoal regardless of possibility that N-acetylcysteine may be administered.

N-Acetylcysteine (NAC) therapy is antidote if indicated

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8
Q

What is the treatment for severe acetaminophen toxicity?

A

For chronic toxicity or for those pts who present after 24 hours postingestion, tx is based on clinical effects, LFTs, and acetaminophen level.

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9
Q

How long do we have to give N-acetylcysteine in acetaminophen toxicity?

A

To be effective, N-acetylcysteine must be given w/in 12–16 hrs of ingestion of acetaminophen and preferably w/in 8 hrs. Do not delay tx if serum acetaminophen level is not readily available and toxic dose may have been taken.

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10
Q

Can N-acetylcysteine be given in pregnancy?

A

Yes

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11
Q

How does a patient present with anticholinergic toxicity?

A

“blind as a bat, hot as Hades, red as a beet, dry as a bone, and mad as a hatter”, can also have other signs and symptoms including tachycardia, gastrointestinal ileus, urinary retention, seizures, delirium, and hallucinations.

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12
Q

What is an example of a drug that presents an anticholinergic toxicity?

A

Atropine and antihistamines

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13
Q

How do we work up a patient with anticholinergic toxicity?

A

ECG monitoring is necessary

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14
Q

What is the treatment for severe anticholinergic toxicity?

A

Treatment is primarily supportive (including sedation with benzodiazepines, cooling, and bladder emptying), although physostigmine can be used in life-threatening situations

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15
Q

Are there any contraindications to anticholinergic toxicity treatment?

A

Physostigmine is contraindicated in patients with an overdose of tricyclic antidepressants.

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16
Q

Why is carbon monoxide toxic?

A

Carbon monoxide binds to hemoglobin with an affinity about 200 times greater than that of oxygen. The resulting carboxyhemoglobin complex cannot transport oxygen, causing tissue hypoxia that can lead to death or permanent neurologic damage if untreated.

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17
Q

How does a patient present with carbon monoxide toxicity?

A

The earliest reliable diagnostic symptom is headache.

LOC and MI are possible symptoms of severe toxicity.

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18
Q

How do we determine the level of carbon monoxide toxicity?

A

Obtain arterial blood for measurement of carboxyhemoglobin content and arterial blood gases.

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19
Q

What is the treatment for carbon monoxide toxicity?

A

Move the patient to fresh air immediately. Administer 100% oxygen by non-rebreathing face mask or endotracheal tube, not by nasal cannula or loose-fitting face mask.

Treatment is with 100% oxygen; hyperbaric oxygen can also be used in certain circumstances,

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20
Q

What is the work up for a patient with carbon monoxide toxicity?

A

Blood Tests - Obtain arterial blood for measurement of carboxyhemoglobin content and arterial blood gases.

Chest X-Ray - If carbon monoxide poisoning is associated with smoke inhalation, obtain a chest X-ray and consider hospitalization and monitoring for development of noncardiogenic pulmonary edema.

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21
Q

T/F: Carbon monoxide is not a medical emergency and is something we have to make sure to take our time to treat properly.

A

FALSE, Act quickly. Delay in treatment may worsen neurologic damage.

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22
Q

How does a patient present with Ethanol toxicity?

A

Symptoms of alcohol intoxication include ataxia, dysarthria, depressed sensorium, and nystagmus.

Coma and respiratory depression with subsequent pulmonary aspiration due to intoxication are also common causes of illness and death.

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23
Q

How do we determine the level of ethanol toxicity?

A

Laboratory diagnosis may be aided by direct determination of the blood ethanol concentration or by its estimation from the calculated osmolar gap.

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24
Q

How do we work up a patient with ethanol toxicity?

A

Blood Alcohol concentration

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25
Q

What is the treatment for ethanol toxicity?

A

Supportive care is the primary mode of therapy. Special care should be taken to prevent aspiration.

Give thiamine and glucose as needed to prevent Wernicke’s syndrome.

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26
Q

What is the treatment for severe ethanol toxicity?

A

Give thiamine and glucose as needed to prevent Wernicke’s syndrome.

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27
Q

How does a patient present with opiate toxicity?

A

Pin point pupils, Sedation, hypotension, bradycardia, hypothermia, and respiratory depression

28
Q

How long do opiate toxicities last?

A

Depends on the individual opiate half-life. Most opiates have a half-life of 3–6 hours; the major exceptions are methadone (15–20 hours) and propoxyphene (12–15 hours).

29
Q

How do we determine the level of opiate toxicity?

A

if toxic concentrations of opiates are found in blood or urine

30
Q

What is the treatment for opiate toxicity?

A

Provide intensive supportive care and gastrointestinal decontamination. Maintain adequate airway and ventilation.

31
Q

What are examples of opiates?

A

Heroin, Codeine, hydrocodone, dextromethorphan

32
Q

What are examples of substances that can produce ethanol toxicity?

A

Ethanol, methanol, ethylene glycol, and isopropanol are all central nervous system depressants. Levels of all alcohols should be obtained, although the level may not predict the severity of the intoxication

33
Q

How do we diagnose opiate toxicity?

A

The diagnosis is confirmed if toxic concentrations of opiates are found in blood or urine or if the patient regains consciousness after administration of naloxone.

34
Q

How does a patient present with poisonous plants and mushrooms toxicity?

A

gastrointestinal symptoms

35
Q

How quickly does poisonous plants and mushrooms toxicity become apparent?

A

Delayed onset (6–12 hours) of gastrointestinal symptoms suggests amatoxin or monomethylhydrazine poisoning.

36
Q

How do we work up a patient with poisonous plants and mushrooms toxicity?

A

?

37
Q

What is the treatment for poisonous plants and mushrooms toxicity?

A

Provide intensive supportive care and gastrointestinal decontamination. Activated charcoal should be administered every 2–4 hours.

Treat the specific symptoms manifested by the patient, not those thought to be associated with the type of poisonous plant believed to have been ingested.

38
Q

What is the treatment for severe poisonous plants and mushrooms toxicity?

A

If poisoning w/ amatoxin is suspected, hospitalize the patient for observation and obtain baseline hepatic and renal function measurements. Variety of potential antidotes have been recommended, including corticosteroids, penicillin G, thioctic acid, silymarin, and N-Acetylcysteine.

39
Q

What can determine the toxic severity of the plant?

A

the plant’s age, the soil conditions, and other factors influence the severity of toxic symptoms.

40
Q

What are types of potential plant toxins?

A

Oxalates

Amygdalin and Cyanogenic Glycosides

Cardiac Glycosides

Anticholinergics

Nicotine-Like Toxins

Solanine

Toxalbumins

41
Q

Amygdalin and Cyanogenic Glycosides Plant Toxin

A

Cyanide is produced by the gastrointestinal hydrolysis of chewed-up fruit pits or seeds (Prunus species: cherry, apricot, peach) or leaves and stems (Hydrangea, elderberry). Severe poisoning is uncommon.

42
Q

Cardiac Glycoside Plant Toxin

A

Digitalis and similar compounds are present in varying amounts in certain plants. Serious clinically effects after consumption of only one oleander leaf, or oleander tea, have been reported

43
Q

Oxalate Plant Toxin

A

Insoluble calcium oxalate crystals in the leaves and stems of some plants irritate the mucous membranes and can cause edema of the mouth, throat, and tongue. In rare severe reactions, drooling, dysphagia, and airway obstruction may occur. Renal failure may occur if sufficient amounts of oxalates are absorbed.

44
Q

Anticholinergic Plant Toxin

A

The typical anticholinergic syndrome of dry mouth, tachycardia, delirium, urinary retention, and mydriasis is seen. Most poisonings are mild, and supportive treatment is sufficient

45
Q

Nicotine-Like Toxins

A

These toxins include nicotine and aconitine. Symptoms include nausea and vomiting, salivation, diarrhea, restlessness, and seizures. Mydriasis may also occur. Following an initial phase of excitement, respiratory depression and hypotension may occur.

46
Q

Solanine Plant Toxin

A

produces gastrointestinal symptoms similar to those of nicotine. In addition, plants containing solanine often have significant amounts of atropinic alkaloids, so that the net effect is unpredictable. Onset of symptoms may be delayed several hours.

47
Q

Toxalbumins Plant Toxin

A

These highly toxic compounds (e.g., abrin, ricin, phallin) can cause acute gastroenteritis, dehydration, and shock. Convulsions, hemolysis, and renal and hepatic injury can also occur. Oral and esophageal irritation or burns may be seen.

48
Q

What is the toxic dose of serotonin?

A

?

49
Q

How does a patient present with serotonin toxicity?

A

Altered mental status, Fever, Increased muscle rigidity/clonus, Tremor, Hyperreflexia

50
Q

How quickly does serotonin toxicity become apparent?

A

xx

51
Q

How do we determine the level of serotonin toxicity?

A

xx

52
Q

How do we work up a patient with serotonin toxicity?

A

xx

53
Q

What is the treatment for serotonin toxicity?

A
  • Discontinue all serotonergic agents
  • Provide sedation with benzodiazepines
  • Active cooling; Neuromuscular blocking agents if unable to cool
  • Consider use of cyproheptadine
54
Q

What is the treatment for severe serotonin toxicity?

A

xx

55
Q

Are there contraindications for the treatment of serotonin toxicity?

A

xx

56
Q

What is the toxic dose of sedative hypnotics?

A

xx

57
Q

How does a patient present with sedative hypnotics toxicity?

A

xx

58
Q

How do we determine the level of sedative hypnotics toxicity?

A

xx

59
Q

How do we determine the level of sedative hypnotics toxicity?

A

xx

60
Q

How do we work up a patient with sedative hypnotics toxicity?

A

xx

61
Q

What is the treatment for sedative hypnotics toxicity?

A

xx

62
Q

What is the treatment for severe sedative hypnotics toxicity?

A

xx

63
Q

Are there contraindications for the treatment of sedative hypnotics toxicity?

A

xx

64
Q

What is the average toxic does of TCA?

A

5mg

65
Q

What are the symptoms of TCA toxicity?

A

Anticholinergic symptoms range from mydriasis, agitation, and tachycardia to seizures and coma

Cardiovascular manifestations are often life-threatening and include QRS widening, profound hypotension, atrioventricular blocks, and ventricular arrhythmias

66
Q

What is the best predictor of TCA toxicity?

A

Prolongation of QRS

67
Q

In treating TCA toxicity what do you not do?

A

make them vomit

Medicine II: Emergency Medicine (11 decks)

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