cyanide toxiciology
Terms
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- How is Cyanide absorbed?
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1)skin
2)lungs
3)GI - How is cyanide metabolized by the body?
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1)CN is metabolized by rhodanase and thiosulfate to thiocyanate which is excreted
2)CN incorporates into VitB12a/hydroxocobalamin -> cyanocobalamin
3)oxidation to formic acid and oxygen (minor)
4)lung and sweat -> almond odor - What is the mechanism of toxicity for cyanide?
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1)CN binds to heme iron (Fe+3) of cytochrome oxidase and inhibits the final step of oxidative phosphorylation
2)CN paralyzes the ETC and stops cellular use of O2 -> patient suffocates because of inability fo use oxygen -> metabolism shifted to anaerobic metabolism -> lactic acid - What are the symptoms that reflect cellular hypoxia?
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1)the absence of cyanosis despite respiratory depression because CN stops cell's ability to use oxygen therefore the oxygen content of the venous blood remains high so there is no gradient or difference between arterial and venous oxygen concentration
(AO2 - VO2) = 0 - Classic signs of CN toxicity
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1)bright red venous blood
2)profound metabolic acidosis
3)bitter almond breath - Onset of symptoms with inhalation
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fast
1)HA
2)flushing
3)increase RR
4)dizziness w/in 30s
=>coma, death in 10mins - CNS symptoms of CN toxicity
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MOST SENSITIVE ORGAN
-early stimulation followed by CNS depression (opisthotonus, dilated pupils, death) - CV symptoms of CN toxicity
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1)initial HTN and reflex bradycardia followed by hypotension and tachycardia
2)ischemic changes on EKG and arrhythmias - Lung symptoms
- pulmonary edema in severe toxicity
- Skin symptoms
- skin does NOT appear cyanotic until late
- Metobolic symptoms
- lactic acid metabolic acidosis (increase AG)
- How is CN poisoning diagnosis?
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BY SUSPICION
1)pts presenting w/ history of rapid onset of coma and/or metabolic acidosis
2)HTN, bradycardia, tachypnea and LACK of cyanosis
3)Cyanide rapid-spot test - Describe the cyanide rapid-spot test
- ferrous sulfate added to stomach contents -> add NaOH to precipitate iron, boil and cool -> acidify with HCL -> green-blue color = cyanide (purple color = salicylates)
- What is the role of oxygen in CN poisoning?
- 1)use even if PO2 is normal because it INCREASES O2 delivery, MAY REACTIVATE THE INHIBITED OXIDATIVE ENZYMES, and ENHANCES THE EFFECT OF THIOSULFATE
- What is the antidotes used before decontamination?
- LILY KIT = nitrites and thiosulfate
- What is the mechanims of nitrites?
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1)nitrites oxidize iron on hemoglobin to Fe+3 which makes it available for CN to bind and form cyanometHg
2)nitrites induce a methemoglobinemia which removes CN off of the cytochrome oxidase enzyme so that it can be detoxified by thiosulfate - Sequence of administration for CN toxicity
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1)amyl nitrite = crush and inhale for 30s Qmin => 3-5% methemoglobinemia
2)sodium nitrite = 10mLs of a 3% solution IV over 4mins => 20% methemoglobinemia
3)Thiosulfate = 50mLs of 25% IV at a rate of 3-5mL/min
4)Hydroxycobalamin - Mechanism of thiosulfate?
- donates a sulfur to cyanide -> thiocyanate (renally excreted)
- Mechanism of hydroxocobalamin
- binds with CN to form cyanocobalamin (VITB12)-> requires large volumes 4 liters of dilute solution (NOT FDA APPROVED)
- What agent is dangerous to administer because it increases CN release?
- methylene blue
- What if you induce too much methemoglobinemia?
- MetHg decreases the O2 binding capacity of hemoglobin, O2 will only bind to hemoglobin with Fe+2, not methemoglobin with Fe+3
- What are common sources of cyanide?
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1)from VitB12 metabolism
2)electroplating
3)photographic processing
4)plants (bitter almond and apricot)
5)fires (burning of silk, wool, polyurethane acrylics)