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Spring Pharm Block 2 > Toxidromes Part III > Flashcards

Toxidromes Part III Flashcards

1
Q

What drug control schedule are benzodiazepines in?

A

C-4

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2
Q

T/F: Death from benzodiazepines overdose is common.

A

False: death from benzos is rare

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3
Q

What is the greatest concern in a benzodiazepine overdose?

A

They are synergistic with other CNS depressants –> especially alcohol

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4
Q

Describe the mechanism of action of benzodiazepines and compare them to barbiturates.

A

They enhance GABA transmission. They are not as potent as barbiturates because GABA must be present for them to work

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5
Q

Describe the clinical presentation associated with a benzodiazepine overdose.

A

Lethargy, slurred speech, ataxia, respiratory depression

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6
Q

What is the antidote to benzodiazepines and what is its contraindication?

A

Flumazenil –> contraindicated in patients that ingested TCAs or any patient that is at risk for seizures

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7
Q

What non-TCA drugs in overdose are treated like a TCA overdose?

A

Carbamazepine (anti-epileptic) and Cyclobenzaprine (muscle relaxant)

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8
Q

Describe the mechanism by which ethyl alcohol (ETOH) is broken down into its metabolites after ingestion.

A

ETOH (alcohol dehydrogenase) –> acetyl aldehyde (aldehyde dehydrogenase) –> acetyl CoA and CO2

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9
Q

What population under-express alcohol dehydrogenase?

A

Asians –> results in faster inebriation

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10
Q

What drug previously discussed in class inhibits aldehyde dehydrogenase?

A

Metronidazole –> causes a disulfiram reaction –> acetyl aldehyde builds up cause severe N/V.

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11
Q

Describe the mechanism by which methanol is broken down into its metabolites after ingestion.

A

Methanol (alcohol dehydrogenase) –> formaldehyde (aldehyde dehydrogenase) –> formic acid

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12
Q

What is the result of formic acid accumulating in the body?

A

Metabolic acidosis and it is toxic to the optic nerve (causes blindness)

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13
Q

What common substances contain methanol?

A

Paint thinner, windshield wiper fluid, and bad moonshine

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14
Q

Describe the mechanism by which ethylene glycol is broken down into its metabolites after ingestion.

A

Ethylene glycol (alcohol dehydrogenase) –> glycolaldehyde (aldehyde dehydrogenase) –> glycolic acid and calcium oxalate crystals

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15
Q

What pathophysiology results from the accumulation of glycolic acid and calcium oxalate crystals in the body?

A

Glycolic acid = metabolic acidosis

Ca oxalate = crystalizes in kidneys and causes real failure

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16
Q

What common substance contains ethylene glycol?

A

Anti-freeze

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17
Q

What is the least toxic and most toxic alcohol?

A

Least: ETOH
Most: Ethylene Glycol

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18
Q

Name two substances that can be used as an antidote to ethylene glycol or methanol and describe the mechanism of each.

A
  • ETOH: alcohol dehydrogenase prefers to bind ETOH resulting in fewer metabolites from ethylene glycol
  • Fomepizole: alcohol dehydrogenase inhibitor that inhibits formation of toxic metabolites without causing inebriation.
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19
Q

Is dialysis effective in treatment of methanol or ethylene glycol overdose?

A

Yes, dialysis removes ethylene glycol and methanol. But it also removes the antidotes –> must redose antidotes when dialysis is complete.

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20
Q

What is isopropyl alcohol used for?

A

Rubbing alcohol

21
Q

What is the clinical result of isopropyl alcohol ingestion?

A

It is relatively non-toxic but causes bad gastritis.

22
Q

What type of patients might present with isopropyl alcohol ingestion?

A

Severe alcohol use disorder

23
Q

Describe the metabolic pathway of acetaminophen (APAP).

A

90% conjugated in the liver to glucuronide and sulfate metabolites
5% metabolized by CP-450 into a hepatotoxic metabolite which is then further metabolized and inactivated by glutathione

24
Q

Describe the mechanism by which APAP overdose causes toxicity.

A

The conjugation pathway is overwhelmed and more APAP goes down the toxic CP-450 pathway and there is not enough glutathione to inactivate the excess hepatotoxic metabolites

25
Q

Describe the 4 phases of APAP toxicity.

A

1: (0-24h): severe GI upset
2: (24-72h): Pt feels better –> LFTs rise and peak at around 72 hours
3: (72h +): liver dysfunction continues –> PT/INR increase s/p decreased production of clotting factors, ammonia increases and may lead to hepatic encephalopathy
4: (5-14 days): death or resolution of hepatic impairment

26
Q

Describe what is indicated by a rise in LFT enzymes.

A

They tell you that liver damage has occurred (enzymes released from damaged cells) but they give no true indication of liver function.

27
Q

What is the antidote for APAP overdose and how does it work?

A

N-acetylcysteine (NAC): replenishes glutathione stores

28
Q

At what point after ingestion is the antidote for APAP overdose most effective?

A

Best when used acutely –> NAC does not reverse liver damage, it only stimulates breakdown of toxic metabolites with glutathione.

29
Q

Describe the two routes by which NAC may be administered and list the name for each form.

A

PO: aka mucomyst
IV: aka acetadote

30
Q

Other than APAP overdose, what can mucomyst be used for?

A

Used in nebulized form to thin and mobilize mucus that accumulates in CF patients

31
Q

What are the disadvantages of each form by which NAC can be administered for APAP overdose?

A

PO: Has a noxious smell, is hard to take and keep down, and requires large volumes to be effective
IV: must be administered in D5W at high volumes (fluid overload and hyperglycemia) and has high risk of allergic reaction

32
Q

What is used to combat the nausea associated with PO NAC administration?

A

Ondansetron, Aprepitant (anti-emetic), metoclopramide (prokinetic)

33
Q

How many doses of PO NAC should the APAP OD patient receive?

A

17 full doses –> must repeat dose if one is vomited back up

34
Q

Name and describe the graph used to predict the level of toxicity expected from an APAP overdose.

A

Rheumac Nomogram –> can only be used 4 hours or more after ingestion.

35
Q

What two substances should always be tested for in any overdose and why?

A

APAP and ASA –> because they are readily available

36
Q

What is the clinical result of ASA (or any NSAID) toxicity?

A

Metabolic Acidosis

37
Q

Name the graph used to predict the level of toxicity expected from an ASA overdose.

A

Dunn Nomogram

38
Q

Describe the clinical result of cyanide toxicity.

A

Rapid metabolic acidosis caused by anaerobic metabolism in the cells

39
Q

What is the mechanism by which cyanide causes anaerobic metabolism?

A

It binds to Hgb with much higher affinity than oxygen and significantly decreases oxygen carrying capacity of blood.

40
Q

T/F: Cyanide is a good drug to use for someone that wants to commit suicide.

A

True: it is quickly lethal

41
Q

What is a key clinical sign associated with cyanide toxicity?

A

Skin changes: cherry red early (especially noted in the lips) and cyanotic late

42
Q

What smell is commonly associated with cyanide in the air?

A

Smell of bitter almonds

43
Q

How is a diagnosis of cyanide toxicity commonly made?

A

Based on clinical presentation –> cyanide blood levels require long turn-around time

44
Q

What presentations (5) should lead the provider to suspect cyanide toxicity?

A
  • Sudden collapse of a lab or industry worker
  • Fire victim with coma and acidosis
  • Suicide attempt with acidosis and unexplained coma
  • Ingestion of nail polish remover
  • ICU patient on sodium nitroprusside with mental status change or unexplained acidemia
45
Q

What patient population in the ICU is at particular risk for cyanide toxicity from sodium nitroprusside?

A

Elderly patients with hepatic and renal issues

46
Q

What three drugs are contained in the Lilly Cyanide Antidote Kit?

A
  1. Amyl Nitrite Pearls - forms methemoglobin
  2. Sodium Nitrite (Nitroglycerine) - forms methemoglobin
  3. Sodium Thiosulfate - donates sulfa groups to rhodanase
47
Q

What is the mechanism by which methemoglobin treats cyanide toxicity?

A

It has half the O2 carrying capacity as regular Hgb but cannot be bound by cyanide

48
Q

What is the mechanism by which rhodanase treats cyanide toxicity?

A

Rhodanase detoxifies cyanide but it relies on sulfa groups, which are depleted in cyanide overdose

Spring Pharm Block 2 (7 decks)

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