Group 9 Flashcards

(32 cards)

1
Q

What is flumazenil used for?

A
  • Reversing benzodiazepine sedation post-surgery.
  • Treating benzodiazepine overdose (e.g., midazolam, diazepam).
  • Diagnostic tool for benzodiazepine-induced altered mental status.
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2
Q

What is the adult dosing regimen for reversing benzodiazepine sedation?

A
  • Initial dose: 0.2 mg IV over 15 seconds.
  • Repeat: 0.2 mg every minute.
  • Max total dose: 1 mg.
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3
Q

Why is flumazenil contraindicated in patients with tricyclic antidepressant (TCA) overdose?

A

Risk of seizures due to lowered seizure threshold.

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4
Q

What are relative contraindications for flumazenil?

A

Chronic benzodiazepine use, epilepsy, hepatic impairment, and pregnancy (Category C).

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5
Q

What is dimercaprol’s mechanism of action?

A

Binds heavy metals (e.g., arsenic, mercury) via sulfhydryl (-SH) groups, forming non-toxic complexes excreted in urine.

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6
Q

What is the standard dosing regimen for arsenic poisoning?

A

3–5 mg/kg IM every 4 hours until urinary arsenic <50 mcg/24 hrs (duration: 7–10 days).

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7
Q

What is the standard dosing regimen for arsenic poisoning?

A

3–5 mg/kg IM every 4 hours until urinary arsenic <50 mcg/24 hrs (duration: 7–10 days).

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8
Q

How long does flumazenil’s effect last, and what risk does this pose?

A

30–60 minutes; risk of re-sedation requiring repeat doses.

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9
Q

Why is dimercaprol stored in amber-colored ampoules?

A

To prevent oxidation of the drug.

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10
Q

What are contraindications for dimercaprol?

A

Peanut allergy (due to peanut oil solvent), iron/cadmium poisoning, pregnancy (Category C).

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11
Q

How is dimercaprol administered, and why not intravenously?

A

Deep IM only; IV administration risks toxicity due to the oily formulation.

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12
Q

Classify herbicides by chemical structure and provide examples.

A
  1. Phenoxy acids: 2,4-D.
  2. Bipyridyls: Paraquat.
  3. Triazines: Atrazine.
  4. Glycine derivatives: Glyphosate.
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13
Q

What is Paraquat’s mechanism of toxicity?

A

Induces oxidative stress via redox cycling → pulmonary fibrosis.

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14
Q

How does Glyphosate toxicity primarily occur in humans?

A

Due to surfactants in formulations causing mitochondrial dysfunction and cardiotoxicity.

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15
Q

How is Paraquat poisoning managed?

A
  • Avoid supplemental oxygen (unless hypoxic).
  • Consider hemoperfusion in severe cases.
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16
Q

What is the primary route of absorption for herbicides?

A

Ingestion, though dermal and inhalational exposure are also significant

17
Q

What herbicide acts as a mitochondrial uncoupler?

A

2,4-D, causing neuromuscular and gastrointestinal disturbances.

18
Q

Why is urinary alkalinization used in 2,4-D poisoning?

A

Enhances renal excretion of the herbicide.

19
Q

What is a key diagnostic tool for herbicide-induced pulmonary toxicity?

A

Chest radiography to assess lung damage (e.g., Paraquat fibrosis).

20
Q

What is a major risk of chronic herbicide exposure?

A

Carcinogenesis, endocrine disruption, and neurodegenerative disorders.

21
Q

What is the max single pediatric dose of flumazenil?

A

0.2 mg IV, with a max total dose of 1 mg.

22
Q

What is the peak effect time of flumazenil after administration?

A

6–10 minutes, with effects lasting 30–60 minutes.

23
Q

Why is flumazenil stored in airtight containers?

A

To maintain stability and prevent degradation.

24
Q

What is the alternative dosing regimen for dimercaprol after the first two days of arsenic poisoning?

A
  • Days 3–4: 2.5–3 mg/kg IM every 6 hours.
  • Week 2: 2.5–3 mg/kg IM every 12 hours.
25
Why is dimercaprol **ineffective for cobalt-induced cardiomyopathy**?
It does not address cardiac-specific toxicity from cobalt; limited evidence for efficacy.
26
What precaution is needed for dimercaprol in patients with **hypertension or G6PD deficiency**?
May exacerbate hypertension or trigger hemolysis in G6PD-deficient individuals.
27
Classify herbicides by **mode of action** with examples.
- **Photosynthesis inhibitors:** Atrazine (blocks photosystem II). - **Growth regulators:** 2,4-D (mimics plant hormones). - **Cell membrane disruptors:** Paraquat (generates free radicals).
28
How does **enterohepatic recirculation** affect herbicide excretion?
Prolongs toxicity by reabsorbing unmetabolized compounds (e.g., some phenoxy acids).
29
What **chronic effects** are linked to herbicide exposure?
**Carcinogenesis** (e.g., non-Hodgkin lymphoma), **endocrine disruption**, and **neurodegenerative disorders**.
30
What **lab tests** are critical for herbicide poisoning diagnosis?
CBC, renal/liver function tests, and **urinary arsenic levels** (for dimercaprol monitoring).
31
What **imaging** is used for suspected paraquat toxicity?
**Chest radiography** to detect pulmonary fibrosis or edema.
32
What is the role of **activated charcoal** in acute herbicide ingestion?
Limits absorption if administered within **1–2 hours post-ingestion**.