Toxicology 3: More toxidrome Flashcards

1
Q

TCAs are ___ ___ and ___

A

old, cheap, and toxic

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2
Q

What are chemically and structurally related to TCA?

A
  • Cyclobenzaprine (muscle relaxant)
  • CBZ (anti-epileptic)

Treat like TCA in OD

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3
Q

How do symptoms progress with TCA OD?

A

Rapidly

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4
Q

Clinical presentation of TCA OD?

A
  • Tonic-clonic seizures (decrease seizure threshold)
  • Cardiac (arrhythmia)
  • Anticholinergic (tachycardia, sedating, constipation, urinary retention)
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5
Q

What is therapy for TCA overdose?

A

Supportive

HCO3 may normalize arrhythmia

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6
Q

What is the TCA OD hallmark?

A

QRS prolongation

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7
Q

What is contraindicated with TCA overdose?

A

Physostigmine

An ACHesterase inhibitor and increases ACh

Use it in myasthenia gravis

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8
Q

How do you treat seizures from TCA OD?

A

Adavan and Elavil

Do NOT give flumazenil it will cancel the Benzo and make patient seize

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9
Q

Classic trio of opiod intoxication?

A
  • Miosis
  • Respiratory depression
  • Depressed level of consciousness
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10
Q

Caution with treating opiod intoxication?

A

Withdrawal – irritability, tachycardia, tremor, anxiety, decreased seizure threshold, depression

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11
Q

What is the opiod antidote?

A

Naloxone, reverses respiratory depression

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12
Q

What 3 drugs require higher dose of naloxone?

A
  • Pentazocine
  • Codeine
  • Methadone
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13
Q

Half life of naloxone?

A

Short, so must keep dosing. 2/3 initial dose that was required to reverse respiratory depression per hour

e.g. takes 12mg to reverse RD, start drip 8mg/hr

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14
Q

how does BBlocker toxicity manifest?

A

bradycardia, depression of inotropy

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15
Q

What is the DOC for BBlocker OD? What else may be necessary?

A

Glucagon (increases inotropy)

Atropine or pacing may be required

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16
Q

Side effect of giving glucagon?

A

Hyperglycemia

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17
Q

Hydrocarbon toxicity comes from what?

A

Aspiration and resulting pneumonitis

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18
Q

How do you treat aspiration pneumonia?

A

Clindamycin for anaerobes

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19
Q

When do you treat hydrocarbon toxicity?

A

If patient showing signs of risk of aspiration- burping, coughing, vomitting

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20
Q

Hallmark of PCP toxicity?

A

Violent behavior

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21
Q

What is nerve gas?

A

Organophosphate / pesticide

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22
Q

How do organophosphates work

A

Irreversibly inhibit aceylcholinesterase (causes ACh overload)

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23
Q

What is the characteristic organophosphate OD finding?

A

garlic like odor

24
Q

How does organophosphate effect the body?

A
Parasympathetic activation
Salivation
Lacrimation
Urination
Defecation
GI overload
Excretion
25
Q

Treatment for organophosphate OD?

A

1) Remove everything, decontam with cold water.
2) Atropine (symptomatic treatment)
3) Pralidoxime (use within 24hrs of exposure)

26
Q

How does pralidoxime work?

A

displaces the organophosphate from ACh binding site

27
Q

Barbiturates are used to treat what?

A

Insomnia

28
Q

How do barbiturates work?

A

potentiate GABA mediated neuro-transmission (CNS inhibition)

29
Q

Barbituate OD characteristics?

A
  • Respiratory depression
  • Hypotension
  • Decreased level of consciousness
30
Q

Toxic dose of barbiturates?

A

5-10x the hypnotic dose

31
Q

Clinical presentation of barbituate OD?

A
  • slurred speech
  • lethargy
  • ataxia
  • hypothermia
  • coma
  • death
    patients may appear dead!
32
Q

What type of barbituate do you want if you’re committing suicide?

A

Short acting agent

33
Q

What is significant about phenobarbital?

A

Highly acidic and need to alkalinize the urine

ION TRAPPING

34
Q

Antidote for barbituate OD?

A

Antidote

35
Q

3 steps to lethal injection?

A

1) Thiopental (barb)
2) Neuromuscular blocker
3) Potassium chloride

36
Q

Benzo OD death is rare except whtn

A

combined with alcohol or other CNS depressants

37
Q

How do Benzos work?

A

Enhance GABA-minergic neurotransmission

38
Q

Benzo toxic:therapeutic ratio?

A

HIGH

39
Q

Benzo OD presentation?

A
  • lethargy
  • slurred speech
  • ataxia
  • respiratory depression
  • coma
40
Q

What should you avoid with treating Benzo OD?

A

Emesis due to rapid progression to coma. Use activated charcoal

41
Q

When should you use flumazenil?

A

pure benzo OD only

42
Q

ETOH —> _____ ——> _______

A

Alcohol dehydrogenase

Acetaldehyde

Aldehyde dehydrogenase

CO2 & H2O

43
Q

METOH —> _____ ——> _______

A

Alcohol dehydrogenase

Formaldehyde

Aldehyde dehydrogenase

Formic acid –> optic nerve toxicity

44
Q

Ethylene glycol —> _____ ——> _______

A

Alcohol dehydrogenase

Glycoaldehyde

Aldehyde dehydrogenase

Ca++ oxalate & Glycolic acid

45
Q

How does fomepizol work?

A

inhibits alcohol dehydrogenase, so if mixed with bourbon it makes you drunker

46
Q

Ethylene glycol is ___, ___, ___, ___

A

colorless
odorless
sweet-tasting
water-soluble

47
Q

Isopropyl alcohol is metabolized into what?

A

Alcohol dehydrogenase to acetone, leads to fruity breath (like DKA)

48
Q

Can you use charcoal with ethanol OD?

A

NO

49
Q

APAP normal metabolism?

A

Conjugation to APAP-C (95%)

CP450 to toxic metabolite then by glutathione to something good.

50
Q

APAP antidote?

A

N-acetylcysteine, it replenishes glutathione stores within the liver

51
Q

In APAP OD, what happens?

A

shift to CP450 metabolism, run out of glutathione, toxic metabolites build up and hurt liver tissue

52
Q

Phases of APAP toxicity

A

1) first 24 hours, GI upset, N/V, sweating
2) 24-72 hours, clinically patient feels better and may be asymptomatic, hepatotoxicity develops and LFTs rise and peak around 72 hours
3) >72hours, hepatic dysfunction continues, patient clinically deteriorates. PT/INR elevates, increases NH4 levels
4) 5-14 days either resolves or death

53
Q

Why does PT/INR get messed up with APAP?

A

Liver makes clotting factors and urea

54
Q

how can you test increased ammonia levels?

A

Have patient hold hands up, look for asterexis

55
Q

What is the issue with NAC?

A

gross egg taste and need 18 total doses

56
Q

What is the IV NAC?

A

Acetadote, administer with D5W, but monitor for hyponatremia since it requires a high amount of fluid to give it with