Herbal Supplement and Vitamin Toxicity

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Reinaker

Last updated 9:45 PM on 3/24/26
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18 Terms

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Dietary Supplements Definiton and general info

= nutrients with non-drug status

Not subject to rigorous safety + quality standards

  • Loosely regulated by FDA

Weak regulations rely on post-marketing surveillance to identify

  • good reporting to system or poison centers

Dangerous ingredients

Contaminated products (e.g. adulterants)

After marketing, FDA can

-  Notify public if supplement is unsafe or in violation of regulations

-  Suggest changes to make the supplement safer

-  Recall the product

- Ban the product

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Vitamin A

+clinical manifestations: acute, chronic, treatment for acute manifestations

*will not expect elevated levels (can have hepatotoxicity before elevated levels show*

clinical manifestations

Acute: headache, seizures, N/V, hepatotoxicity, IIH

Chronic: hair thinning/loss, hypercalcemia, osteoporosis

Treatment

  • Seizures: benzodiazepine

  • Hepatotoxicity: n-acetylcysteine

  • IIH: acetazolamide (furosemide if unable to tolerate), high-dose steroids

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Vitamin D

+clinical manifestations, treatment

Hypercalcemia

(weakness, headaches, nausea, vomiting, diarrhea, polyuria, polydipsia, ataxia, seizures)

Treatment

Start with IV fluids

IF Moderate + euvolemic→ + Loop Diuretics

Calcitonin + bisphosphonates

Severe Cases: corticosteroids

hydrocortisone daily OR prednisone daily x5 days

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Vitamin E

+clinical manifestations, treatment

N/V/D, fatigue, coagulopathy (in vitamin K deficient and patients on warfarin)

clinical manifestations

treatment: Symptomatic and supportive care

  • avoid triggers: exessive work, dental treatments

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Vitamin B6

+clinical manifestations, treatment

clinical manifestations

  • Incoordination, ataxia, seizures

treatment

  • Seizures: benzodiazepines

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Niacin

+clinical manifestations, treatment

clinical manifestations

  • N/V/D, hepatotoxicity, hypertension

treatment

  • Symptomatic and supportive care

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caffeine effects

Decreases feelings of fatigue: increased striated muscle contractility

Increases endurance: release endogenous catecholamines → stimulation of beta receptors

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Caffeine Mechanism of Toxicity

o   Release endogenous catecholamines → positive inotropy + chronotropy

o   Presence of methyl group leads to greater CNS penetration (vs. other methylxanthines)

o   Antagonist at adenosine receptors (cant give adenosine like with theophylline)

o   Inhibits phosphodiesterase (responsible for breakdown of cAMP) → increased cAMP

—Results in: increased intracellular calcium

— Clinically:

·      Smooth muscle relaxation, peripheral vasodilation (hypotensive and tachycardia)

·       Myocardial stimulation, contraction of skeletal muscles

·       CNS excitation

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