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Pharmacology > Poisons and Antidotes > Flashcards

Poisons and Antidotes Flashcards

1
Q

Toxin List with Antidotes

A
  • Paraquat
  • Organophosphates/Carbamates
  • Carbon Monoxide
  • Methemoglobinemia Inducers
  • Cyanide
  • Metals (Iron, Mercury, Lead)
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2
Q

Potential scenarios for poisoning

A

Therapeutic drug toxicity

Exploratory exposure by young children

Environmental exposure

Occupational exposure

Recreational abuse

Medication error

Prescribing error

Dispensing error

Administration error

Purposeful administration for self-harm/harm another

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3
Q

Toxicity

A

Toxicity = Inherent capacity of substance to produce injury

Impacted by:

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4
Q

What is the biggest factor affecting toxicity??

A

DOSE

All substances are poisons; there is none which is not a poison. The right dose differentiates a poison from a remedy. PARACELSUS

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5
Q

Therapeutic index . . . what is most worrisome?

A

Narrow TI

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6
Q

What is the most common route of occupation exposure?

A

Inhalation

(dermal 2nd)

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7
Q

What is the most common route of exposure in POISONINGS?

A

Ingestion

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8
Q

Toxicity can be altered by acuity

A

Example:** Benzene Toxicity**

Acute exposure = CNS depression

Chronic exposure = Leukemia

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9
Q

Mechanisms of antidotes

A

– Complex with Poison

  • NAC/Acetadote/Mucomyst:Acetaminophen
  • Crofab:Rattlesnakes,Copperheads

– Biotransformation to Less Toxic Metabolite
• Pyridoxineandthiamine:EthyleneGlycol
• FolicAcid: Methanol
• NAC/Acetadote/Mucomyst:Acetaminophen

– ** Increases Excretion**
• NormalSaline:LithiumToxicity
• UrineAlkalinization:Salicylates
• Hemodialysis

– Block or Compete for Target Receptors

• Fomepizole:EthyleneGlycol/Methanol

– Bypass Effect of Poison

• Octreotide:Sulfonylurea

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10
Q

Initial Treatment Approach for Acute Poisoning

A

ABCDE

  1. airway
  2. breathing
  3. circulation
  4. disability
  5. exposure
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11
Q

Presentations of common toxins

A
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12
Q

What is bioactivation

A

mechanism of toxicity, may create a more chemically “active” product

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13
Q

Metabolism

A
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14
Q

Acetaminophen Metabolism

A
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15
Q

How Xenobioitics Exert Their Effects

A
  1. REceptor-ligand interactions
  2. Perturbation of membrane function/permeability
  3. Interference with ATP generation
  4. Interaction with macromolecules
  5. Alteration Calcium homesotasis
  6. Generation of oxygen radicals/oxidative stress
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16
Q

Receptor Ligand Interactions

A

TCDD >> aromatic hydrocarbon receptor

PCBS >> estrogen receptor

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17
Q

General Types of Reactions w/Macromolecules

A

Covalent, noncovalent, electron transfer, enzymatic

Hydrogen Abstraction *free radicals often steal hydrogens . . but where it steals it from, then it is a radical *

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18
Q

Oxidative Stress

A

overproduction of prooxidants
or decrease in antioxidants . . .

19
Q

Oxidative Stress

A
20
Q

Oxidative Stress

A
21
Q

can you get reactive oxygen species with normal
p450 reactions?

A

Yes

(major source = hydroxyl radical)

22
Q

Lipid Peroxidation

A

can pull a hydrogen from a fatty acid . . . then the lipid
becomes the radical . . . can become lipid fragments, aldehydes
termination because of antioxidants

*vit E can stop

23
Q

Antioxidants

A

Can donate an electron (charitable to radicals)

24
Q

PARAQUAT

A

HERBICIDE
Ingestion >> fatal pulmonary fibrosis

MOA: hydroxyl radical >> lipid peroxidation >> cell death

*No antidote = supportive care

25
Q

Parathione

A

Metabolized to paraoxon which phosphorylates acetylcholinesterase (inactivates) >> cholinergic crisis SLUDGE!!

– Inhibition of Enzyme Function

26
Q

Parathione Antidote

A
  • Atropine Sulfate: anti-muscarinic
  • Pralidoxime: ACHase activator
27
Q

Carbon monoxide

A

Forms carboxyhemoglobin >> Hb(Fe++)CO
*Binds to HGB better than O2!!!

28
Q

Carbon monoxide

A

Treat until asymptomatic and_ COHb level <10% _

Oxygen at high partial pressure = displaces CO from Hb

29
Q

Indications for Hyperbaric Oxygen

A

– Loss of consciousness, coma, seizure at any time during or after the exposure

– Confusion, cognitive deficits, focal findings, visual symptoms

– MI, dysrhythmias

– Persistent symptoms

**– *Any pregnant patient **

30
Q

How do you get poisoned with Methemoglobin?

A

Results from exposure to nitrates, aromatic amines, nitro compounds, antibiotics, local anesthetics

31
Q

What is Methemaglobin

A

Hb (Fe++) + NO2 = Hb (Fe+++)
(Methemoglobin) (Dark Blue/Brown)

32
Q

What is the antidote to methemaglobin?

A

Methylene blue
Acts as electron donor = reduces Fe+++(ferric) to

**Fe++(ferrous) **

33
Q

Cyanide

A

Interference with ATP generation

34
Q

MOA for cyanide

A

Binding to, and inhibiting, cytochrome oxidase (binds to Fe+++ in cytochrome a3 = _Blocks aerobic respiration) _

35
Q

Toxic amounts of cyanide

A

HCN gas (>50 ppm)

>200 mg cyanide salt = death

36
Q

Cyanide Antidote

A

Two step:

– Amyl/Sodium nitrites: Generate Methemoglobin (binds to the iron)

– Hydroxycobalamin: binds CN forming cyanocobalamin

– Sodium Thiosulfate: Forms SCN

37
Q

What are treatments for metal poisoning?

A

Chelation

Calcium disodium EDTA: Pb

BAL (dimercaprol): As, Hg, Pb

Dimercaptopropane sulfate (DMPS): As, Hg

Deferoxamine: Fe

Penicillamine: **Cu, Pb, Au, As **

38
Q

Mercury Toxicities

A

Mostly inhalation?

– Hg0 and methylmercury HgCl2 are CNS toxicants

– Methylmercury: Low exposure = neurodevelopmental disorders, repro effects

• Minamata disease

– Dimethylmercury: well absorbed topically, lethal (Dr. Karen Wetterhahn), long latent period (~300 days post-exposure)

– Hg0 vapor pulmonary irritant, edema

– Salts corrosive: GI hemorrhage/gastroenteritis and nephrotoxic

39
Q

MOA of mercury poisoning

A

Reactivity with sulfhydryl (SH) groups (cysteine) on proteins (inhibition), interacts with selenium

NOTE: the organic ones cross the BBB!

40
Q

LEAD MOA

A

Lead interacts with proteins!!

– Reactivity with sulfhydryl (SH), phosphate carboxyl groups on proteins

– Mimics calcium, zinc & iron

41
Q

CNS effects of lead toxicity

A

– CNS(many): impaired concentration, headache, encephalopathy, decreased intelligence, altered neurobehavioral development, cognitive decline, stunted growth (children)

42
Q

Lead antidotes

A

Antidotes: EDTA, BAL, Succimer (DMSA)

43
Q
A

Pharmacology (9 decks)

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