Iron toxicity Flashcards

1
Q

Describe the 5 stages of iron toxicity

A

I

GI (abdo pain, N/V/D, hematemesis, melena, lethargy, shock, met acidosis)

30m-6hrs

II

Quiescent phase (stop vomiting but developing acidosis)

6-24hrs

III

Met acidosis, renal failure, hepatotoxicity, GI symptoms, CNS dysfxnhypovolemic/distributive/cardiogenic shock

6-72hrs

IV

Fulminant hepatic failure: coma, coagulopathy, jaundice

12-96 days

V

GI strictures, gastric outlet obstruction, bowel obstruction

2-8wks

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2
Q

What are the toxic levels of Fe

A

20-60 mg/kg toxic

more than 60 mg/kg serious toxicity

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3
Q

what is the pathophys of iron toxicity

A

disrupts oxidative phosphorylation, decr ionotropy of myocardium, tnhibits thrombin

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4
Q

what symptom indicates serious fe toxicity

A

vomiting, do not give antiemetics until they vomit

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5
Q

indications for defuroxime

A
serum level 60-90umol/L and symptomatic
serum level more than 90
shock
metabolic acidosis
coma
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6
Q

what can iron toxicity be treated with

A

defuroxime until the urine is rose coloured

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7
Q

List common Fe preparations and their elemental Fe content

A

fummarate: 33%
sulfate20%
gluconate12%

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8
Q

What causes the coagulation defects seen in iron poisoning?

A
  • Early: Direct effects of vitamin K dependent clotting factors
    Late: Hepatic failure and decreased production of clotting factors
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9
Q

List 5 occupations that increase risk of lead exposure.

A
  • Lead smelting
  • Battery manufacture
  • Radiator repair
  • Bridge and ship construction or demolition
  • Smoldering or welding
  • Cable or tin can production
  • Stained glass manufacture
  • Lead-crystal or crystal pottery making
  • Glass production
  • Firing range operation
  • Lead based pain abatement
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10
Q

Describe the anemia that is characteristic of lead poisoning?

A
  • Inhibits heme synthesis
    • Normochromic or hypochromic
    • Severity of anemia correlates with lead BLL
    • smear shows basophilic stippling
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11
Q

What diagnostic clue to chronic lead poisoning may be apparent of skeletal x-rays?

A
  • “Lead band/lines” – Increased metaphyseal brightness seen with chronic exposures
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12
Q

What are the indications for chelation therapy in lead poisoning?

A
  • BLL >70 mcg/dL (3.38umol/L)
    • Protracted GI symptoms
      CNS symptoms from acute exposure
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13
Q

In seriously lead poisoned patients what chelating agents are used?

A
  • Dimercaptol (British antilewisite; BAL) first chelator

Calcium Disodium ethylenediaminetetraacetic acid (CaNa2-EDTA) given with second dose of BAL

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14
Q

What is the pathophysiology of arsenic poisoning?

A
  • Binds sulfhydryl groups, inhibiting critical enzymes in glycolysis
    • Disrupts oxidative phosphorylation by replacing phospohorous (arsenolysis)
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15
Q

What strategies can limit or remove arsene?

A
  • Exchange transfusions

- Urinary alkalinization

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16
Q

List chronic effects of arsenic poisoning.

A
  • Mees’ line on the nails
  • Painful sensorimotor neuropathy
  • Hyperkeratosis of the soled and palms
    Anemia (basophilic stippling), leukocytosis or penia, abn u/a, renal or lfts
17
Q

Which chelators are used in arsenic poisoning?

A
  • Dimercaptol (IM)
    • DMSA orally
      D-penicillamine
18
Q

Which chelating agents are indicated for clinically significant inorganic mercury toxicity?

A
  • BAL (dimercaptol) used for clinically significant inorganic mercury intox but contraindicated in pts with organomercurial poisoning (increases brain merc levels in pts with mentyl merc poisoning)
    • DMSA
    • D-penicillamine
    • Chelation therapy binds the sulfhydryl group that bind mercury after its absorption
19
Q

Outline your basic approach to heavy metal toxicities:

A
  1. In acute exposures of large amounts:
    a. Draw levels, AXR à Fe, Pd, As, Hg are ALL radio-opaque
    b. AC not indicated, none bind adequately
    c. WBI in acute ingestion
    d. Manage ABCs
    e. Anticipate and manage CNX, renal, hepatic, toxicities
    f. Find the antidote à chelation