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Pharm2 1 > Toxicology 3: More toxidrome > Flashcards

Toxicology 3: More toxidrome Flashcards

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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?

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A

garlic like odor

24
Q

How does organophosphate effect the body?

Study These Flashcards
A 
Parasympathetic activation
Salivation
Lacrimation
Urination
Defecation
GI overload
Excretion
25
Treatment for organophosphate OD?
1) Remove everything, decontam with cold water. 2) Atropine (symptomatic treatment) 3) Pralidoxime (use within 24hrs of exposure)
26
How does pralidoxime work?
displaces the organophosphate from ACh binding site
27
Barbiturates are used to treat what?
Insomnia
28
How do barbiturates work?
potentiate GABA mediated neuro-transmission (CNS inhibition)
29
Barbituate OD characteristics?
- Respiratory depression - Hypotension - Decreased level of consciousness
30
Toxic dose of barbiturates?
5-10x the hypnotic dose
31
Clinical presentation of barbituate OD?
- slurred speech - lethargy - ataxia - hypothermia - coma - death patients may appear dead!
32
What type of barbituate do you want if you're committing suicide?
Short acting agent
33
What is significant about phenobarbital?
Highly acidic and need to alkalinize the urine ION TRAPPING
34
Antidote for barbituate OD?
Antidote
35
3 steps to lethal injection?
1) Thiopental (barb) 2) Neuromuscular blocker 3) Potassium chloride
36
Benzo OD death is rare except whtn
combined with alcohol or other CNS depressants
37
How do Benzos work?
Enhance GABA-minergic neurotransmission
38
Benzo toxic:therapeutic ratio?
HIGH
39
Benzo OD presentation?
- lethargy - slurred speech - ataxia - respiratory depression - coma
40
What should you avoid with treating Benzo OD?
Emesis due to rapid progression to coma. Use activated charcoal
41
When should you use flumazenil?
pure benzo OD only
42
ETOH ---> _____ ------> _______
Alcohol dehydrogenase Acetaldehyde Aldehyde dehydrogenase CO2 & H2O
43
METOH ---> _____ ------> _______
Alcohol dehydrogenase Formaldehyde Aldehyde dehydrogenase Formic acid --> optic nerve toxicity
44
Ethylene glycol ---> _____ ------> _______
Alcohol dehydrogenase Glycoaldehyde Aldehyde dehydrogenase Ca++ oxalate & Glycolic acid
45
How does fomepizol work?
inhibits alcohol dehydrogenase, so if mixed with bourbon it makes you drunker
46
Ethylene glycol is ___, ___, ___, ___
colorless odorless sweet-tasting water-soluble
47
Isopropyl alcohol is metabolized into what?
Alcohol dehydrogenase to acetone, leads to fruity breath (like DKA)
48
Can you use charcoal with ethanol OD?
NO
49
APAP normal metabolism?
Conjugation to APAP-C (95%) | CP450 to toxic metabolite then by glutathione to something good.
50
APAP antidote?
N-acetylcysteine, it replenishes glutathione stores within the liver
51
In APAP OD, what happens?
shift to CP450 metabolism, run out of glutathione, toxic metabolites build up and hurt liver tissue
52
Phases of APAP toxicity
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
Why does PT/INR get messed up with APAP?
Liver makes clotting factors and urea
54
how can you test increased ammonia levels?
Have patient hold hands up, look for asterexis
55
What is the issue with NAC?
gross egg taste and need 18 total doses
56
What is the IV NAC?
Acetadote, administer with D5W, but monitor for hyponatremia since it requires a high amount of fluid to give it with

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