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Emergency Medicine > Lecture 15: Poisonings > Flashcards

Lecture 15: Poisonings Flashcards

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1
Q

The first thing you do with a patient that rolls into the ED with poison on her is..

A

Gross decontamination prior to assessment

do not let it touch you!

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2
Q

T/F: Most toxidromes will respond to IVF.

A

False.

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3
Q

What do you give first, thiamine or dextrose?

A

THIAMINE

GLucose first => worse wernicke’s encephalopathy

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4
Q

A new onset seizure that needs pharm tx should first be managed with IV (), but if it persists, you should () the dose. If it really persists, you should give IV () and intubate.

A
  1. Start with IV ativan
  2. Double ativan
  3. Phenobarbital and intubate
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5
Q

The treatment for isoniazid-induced seizures is…

The I in RIPE therapy for TB tx :)

A

Vit B6 pyridoxine

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6
Q

() is highly ineffective for tx of seizures due to poisonings.

A

Phenytoin

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7
Q

Anticholinergics will cause your pupils to (), whereas cholinergics cause them to ()

A
  • Anticholinergic = mydriasis/dilation
  • Cholinergic = miosis

Cholinergic = Constrict eyes or Anti = your eyes are going AHHHHHH

Also anticholinergics = dry like MY DRY iasis

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8
Q

You suspect your poisoned patient was a drug mule for cocaine. You should order what imaging to confirm your suspicion?

A

Abd XRAY

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9
Q

T/F: A tox screen is indicated in patients with accidental ingestion and are asymptomatic with a consistent history.

A

FALSEEE

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10
Q

Ethlyene glycol poisoning/antifreeze poisoning can present with what kind of crystals in the urine?

A

Calcium oxalate

Cause it makes OXAlic acid!

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11
Q

The preferred method of decontaminating gastric contents is () if the ingestion was less than () hours prior to arrival. It is CONTRAINDICATED if the patient cannot maintain their own ()

A
  • Activated charcoal
  • Ingestion must be within 1 hour prior to arrival
  • Cannot use if airway cannot be protected

Also if the toxin doesn’t have an antidote alrdy. Note the 2 exceptions!

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12
Q

T/F: Activated charcoal can bind tylenol, alcohol, metals, and corrosives.

A

FALSE

Cannot bind alcohol, metals, or corrosives

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13
Q

Gastric lavage is best delivered via (NG/OG) tube.

A

OG tube

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14
Q

Whole bowel irrigation is indicated in:

  • Ingestion of chemicals that () with charcoal
  • Ingestion of () packets
A
  • Poor binding chemicals with charcoal
  • Drug-filled packets
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15
Q

T/F: Gastric irrigation does not require bowel sounds or normal peristalsis.

A

False.

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16
Q

Multi-dose activated charcoal is using at least () doses of oral activated charcoal.

A

At least 2 doses

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17
Q

Urinary alkalinization is primarily indicated in () poisonings

A

Moderate-severe salicylate poisonings

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18
Q
A
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19
Q

You must monitor (electrolyte) levels because hypo() will reduce urine alkalinity in salicylate poisoning tx.

A

Potassium levels, because HypoK will cause more H+ secretion instead

Goal: 4-4.5

Nephrooooo

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20
Q

Hemodialysis can remove highly () bound drugs and highly () soluble drugs.

Hemoperfusion can remove () soluble low molecular wt substances.

A
  • Hemodialysis = protein bound and lipid solubles
  • Hemoperfusion = water-soluble low molecular weight substances

Very invasive, very expensive!

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21
Q

In an inhaled poisoning patient, should you administer oxygen?

A

Yes silly

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22
Q

You can irrigate eyes with either () or ()

A

Water or NS

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23
Q

T/F: You should discard contaminated clothes.

A

Truee

Throw it out

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24
Q

What is the poison control hotline???????

A

1-800-222-1222

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25
Q

There are 3 Questions that must be addressed to determine if an exposure was NON-toxic:

  1. Was the exposure () and is there a clearly identified single substance?
  2. () of the agent was ingested?
  3. Can the () confirm the substance is nontoxic at that dose?
A
  • Unintentional
  • How much was ingested
  • Can the CDC confirm?
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26
Q

Overall, the mainstay of treatment for any poisoning is…

A

Treat the patient, not the poison!

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27
Q

In a poisoned pt who is HTN and agitated, the drug of choice is…

A

BZDs

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28
Q

Bicarb can be useful for ()-QRS tachyarrhythmias

A

Wide-QRS

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29
Q

Naloxone can be administered 3 ways

A
  • IV
  • IM
  • IN
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30
Q

The supportive care tx for cardiac arrhythmias is just correction of (), (), and administration of an antidote

A
  • Correct hypoxia
  • Correct any acid-base abnormalities
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31
Q

You should consider aggressive cooling in a poisoned patient once their temperature reaches…

A

39C or 102.2F

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32
Q

Re-warming is indicated once core temperature reaches…

A

< 32C or 90F

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33
Q

AG is calculated from:

A

Na - (Cl + HCO3)

Normal AG is 10-15

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34
Q

AG Metabolic acidosis causes is memorized by the mnemonic CAT MUDPILES.

A
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35
Q

In AG Metabolic acidosis, the first management step involves addressing any lack of () first.

A

Any lack of respiratory compromise is the first thing to check!!!!!

You’re acidotic! You better be tryna blow off some CO2

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36
Q

The presentation of narcotic/opioid toxidrome is memorized with the mnemonic CPR-3H

A
  • Coma
  • Pinpoint Pupils
  • Respiratory Depression
  • HypoTN
  • Hypothermia
  • Hyporeflexia
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37
Q

MATHS is the mnemonic for sympathomimetic

A
  • Mydriasis/muscle cell death
  • Agitation/Arrhythmia/Angina
  • Tachycardia
  • HTN/hyperthermia/Hyperactive bowel sounds
  • Seizure/sweating

Everything is just firing off

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38
Q

The drug of choice for sympathomimetics toxicity is (). () is CONTRAINDICATED.

A
  • BZDs for sympathomimetic toxicity.
  • DO NOT USE BBs
39
Q

The two drugs that cause CHOLINERGIC toxicity are:

A
  • Organophosphate insectides
  • Carbamate insecticides

AKA insecticides

40
Q

The presentation of Cholinergic toxicity can be summed up in 3 words. () all over.

A

Crying all over

41
Q

There are two drugs given for cholinergic toxicity.

A
  • Atropine (Blocks muscaric receptors)
  • Pralidoxime (reactivates acetylcholinesterase)
42
Q

What very common medication used for motion sickness is also an anticholinergic like atropine :)

A

Scopolamine!

43
Q
  • Dry as a bone
  • Mad as a hatter
  • Full as a tick
  • Blind as a bat
  • Red as a beet
A

ANTIcholinergic toxicity

44
Q

You can differ anticholinergic toxicity from sympathomimetic toxicity via (skin) and (bowel sounds)

A
  • Dry skin
  • Decreased bowel sounds

This is anticholinergic

45
Q

The antidote for anticholinergic poisoning is…

A

Physostigmine

Cholinesterase inhibitor to increase Ach concentration

Used once conventional fails.
Anticholinergic poisoning slows GI so activated charcoal 1 hr window doesn’t apply

46
Q

You can discharge someone home with anticholinergic toxicity after they have been asymptomatic for () hours

A

6 hours

47
Q

() and () are the MC drug classes + non-BZDs that can cause sedation/hypnosis

A
  • BZDs
  • Barbiturates
48
Q

For barbiturate poisoning that does NOT respond to supportive care, you should use enhanced excretion methods, such as () or ()

A
  • Repeated charcoal
  • Extracorporal removal (hemodialysis/perfusion)
49
Q

BZD ODs can be confirmed by the presence of (), and the reversal agent is (), but it can precipitate seizures!!

A
  • Respiratory depression
  • Flumazenil
50
Q

Same as for anticholinergic toxicity, you can discharge after () hours of no symptoms for sedative/hypnotic OD.

A

6 hours later

51
Q

Some of the biggest drugs that can cause serotonin syndrome are:

  • () inhibitors
  • () reuptake inhibitors
  • () in cough syrup
  • () antidepressants
  • L-(amino acid)
A
  • MAO inhibitors
  • SSRIs
  • DXM
  • TCAs
  • L-tryptophan
52
Q

The mnemonic for serotonin syndrome is HATS or SHAT which stands for

A
  • Hyperthermia, HTN
  • AMS, agitation
  • Tremor, tone (rhabdo), Tachycardia/pnea
  • Seizures
53
Q

Initially, you should treat serotonin syndrome with (), but if that + supportive care fails, you should use a serotonin receptor antagonist called ()

A
  • BZDs for agitation, tremors, and seizures
  • Cyproheptadine is a serotonin receptor antagonist
54
Q

T/F: All patients with serotonin syndrome get admitted.

A

TRUE

55
Q

A common ingredient found in cough syrup can be used as a hallucinogenic and it is ()

A

DXM

Dextromethorphan

Other hallucinogenics are like LSD, PCP, psilocybin/shrooms, ecstasy, ketamine

56
Q

For the agitation, hyperthermia, seizures, tachycardia and HTN in hallucinogenic OD, you should use ()

A

BZDs

57
Q

In refractory hallucinogenic OD, once BZDs fail, you should consider () or () for refractory HTN. Otherwise, you should consider inducing a ()

A
  • Nitroprusside or phentolamine for refractory HTN in hallucinogenic OD.
  • Induce a medical coma if refractory.
58
Q

Summary of all the toxidromes

A

BZD OD doesn’t affect pupils like an opioid OD!!!!

Brendans mnemonic is CHAOSSS

59
Q

About 1/4 of the 450 deaths due to tylenol/APAP toxicity are unintentional, because in children, () occurs

A

Supratherapeutic dosing

AKA too much tylenol by accident :(

60
Q

There are 4 demographics that are at an increased risk for APAP toxicity:

  • Chronic () use
  • AIDS
  • () use
  • anti-() therapy users
A
  • Chronic alcohol use
  • AIDS
  • Anticonvulsant use
  • anti-TB therapy user
61
Q

In a patient 6 years or Older, > 10g of tylenol or 200mg/kg as a single ingestion in a () time period is a toxic exposure. BUT IF you are younger than 6, the time period changes to over ().

A
  • Older is 24 hours
  • Younger is 8 hours
62
Q

Tylenol toxicity presents with 4 stages of toxicity.

  • Stage 1 is characterized by: (symptoms) and (lab change)
  • Stage 2 is characterized by improvement, but (lab changes)
  • Stage 3 is characterized by ()itis and recurrent GI symptoms.
  • Stage 4 is characterized by either () or ()
A
  • Stage 1 = N/V + hypoK
  • Stage 2 = ELEVATED LFTs
  • Stage 3 = Pancreatitis + coagulopathy
  • Stage 4 = improvement or multi-organ failure/death.

Every day is about 1 stage.

63
Q

T/F: Even in an asymptomatic APAP OD patient, you should get serum APAP levels.

A

True

Can take 30-120 minutes to reach peak concentration!

64
Q

A rumack-matthew monogram is used in () toxicity. It is for clinical outcome determination and can only be used after acute ingestion between () to () hours

A
  • APAP toxicity
  • 4-24 hours

Just know tx above the line!

65
Q

The main drug of choice to counter APAP toxicity is.., and its MOA is to prevent metabolites from binding to () cells and diminishing hepatic ()

usuall Within 8 hours of exposure.

A
  • Acetylcysteine PO/IV
  • Hepatic cell binding inhibitor
  • Diminishes hepatic necrosis
66
Q

Past the 8 hour window to use acetylcysteine for APAP toxicity, your last resort is (), and it is also used in patient demonstrating signs of ()pathy

A
  • Last resort: Extra-corporal excretion
  • Used in signs of hepatic encephalopathy, such as AMS/neuro deficits.

altho i feel like the algo says give AC

67
Q

You should request an serum APAP level as your immediate next step if APAP ingestion occurred after more than () hours.

A

4

Less or unknown = consider GI decontamination!

Gastric lavage/activated charcoal

68
Q

T/F: All patients undergoing acetylcysteine therapy for APAP toxicity must be admitted.

A

TRUEEE

69
Q

You should not expect LFTs to be elevated in APAP toxicity until how long?

A

Give it like a day or 2 at least

2-3 days is stage 2!

70
Q

The MC lab finding you would prob see in ETOH toxicity is…

A

Hypoglycemia

ETOH inhibits gluconeogenesis

71
Q

You only really need a BAC if you don’t know…

A

How much they ingested!

72
Q

Generally, a BAC of () or more is when you see reflexes/gross motor control start to take a hit in ETOH toxicity.

A

0.1 or higher

73
Q

At a BAC of (), you would probably see noticeable changes in breathing and pulse.

A

0.3 or higher

74
Q

IV thiamine is primarily used in ETOH toxicity if there is a ()

A

Hx of chronic ETOH use.

75
Q

Pt presents to the ED. Was binge drinking and vomited a little. No hx of chronic ETOH abuse. No SI/HI. Pretty solid health history. His glucose is about 40. Your dispo for this patient is to….

A

Give some IV dextrose and observe in ED until sober and then d/c

76
Q

Ingestion of () is ethylene glycol poisoning.

A

Antifreeze

100 mL or a 1/2 cup is a LETHAL DOSE

77
Q

Ethylene glycol is processed in the liver and makes a (acid/base), eventually leading to metabolic (acid/base) and end-organ damage.

A

Oxalic acid, leading to metabolic acidosis

78
Q

Generally, the first set of symptoms you would see in a patient presenting with antifreeze/ethylene glycol toxicity is…

A

CNS depression after 1 hr (like they drunk)

In just 12 hours, you will show end-organ signs

79
Q

ABG for ethylene glycol toxicity should show a wide AG metabolic () and a UA can be fluoresced to show () crystals.

A
  • High AG metabolic acidosis
  • Calcium oxalate crystals

Oxalic acid

80
Q

BEcause serum ethlyene glycol levels take 2 days to come back, we prefer to determine exposure amount based on serum (). A () > 50 is highly suggestive of ethylene glycol poisoning.

A

Serum Osmolality gap

81
Q

You should only use Bicarb for alcohol toxicity if the pH is less than …

A

7.2

82
Q

Specifically in ethylene glycol, you use one of two drugs for the metabolic blockade.

The first drug is (), which inhibits alcohol dehydrogenase and prevents breakdown of EG into its toxic metabolites.

The alternate/2nd drug is (), which is used because it has a higher affinity for alcohol dehydrogenase than EG.

A
  1. Fomepizole IV
  2. Ethanol

Foamy piss O (cause oxalic acid and oxalate crystals)

83
Q

Besides metabolic blockade for ethylene glycol toxicity, you can do () in more severe symptoms.

A

Hemodialysis

84
Q

T/F: B vitamin therapy for EG toxicity is very helpful.

A

False

85
Q

If you are uncertain about if someone actually ingested EG, you shoudl watch them for () hours, making sure they have a negative ethanol, no symptoms, no osmolar gap, and no presence of metabolic acidosis

A

6 hours

I think its 6 hours for everything =

86
Q

Besides aspirin, a common OTC drug that contains salicylate is…

A

Pepto Bismol

87
Q

Salicylate is converted to (), which can impair gastric emptying, leading to () formation

A

Salicylic acid, leading to bezoar formation

88
Q

Acute salicylate poisoning is DOSE Dependent:

  • < 150mg/kg = (ear) + N/V
  • 150-300 mg/kg = Tachy(), Hyperpyrexia, sweating, ataxia, anxiety
  • 300mg/kg + = (neuro) + ()failure

Note: these are not salicylate serum levels

A
  • < 150 = tinnitus, hearing loss
  • 150-300 = tachypnea
  • 300+ = AMS, seizures, heart/lung/renal failure
89
Q

A salicylate level measured greater than () mg/dL is considered toxic.

A

30 mg/dL or more

Note that it takes 4-6 hours to peak and you check hourly until peak.

90
Q

The first acid-base disorder in salicylate poisoning is (), but then it becomes ()

A

Respiratory alkalosis, followed by metabolic acidosis

I think of it as you start hyperventilating first, but as you convert it to salicylic acid, you get metabolic acidosis.

91
Q

You need to get () imaging if you suspect bezoar formation in salicylate poisoning.

A

Abdominal imaging

You would suspect if level rises despite gastric lavage/charcoal

92
Q

Your patient’s salicylate level is rising steadily every hour despite adequate gastric lavage and activated charcoal. Your next step in management should be…

A

Order abdominal imaging to check for bezoar formation

93
Q

The two ways to reduce salicylate burden in salicylate toxicity is by () urine with (), or in more severe cases, doing ()

A
  • Mod-severe: Urinary alkalinization via bicarb (FIRST-LINE)
  • Severe: hemodialysis (also if renally impaired)
94
Q

Bezoars can be removed…

A

Surgically

Emergency Medicine (29 decks)

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