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PATH 407 > Cyanide, Carbon Monoxide and Insecticide > Flashcards

Cyanide, Carbon Monoxide and Insecticide Flashcards

1
Q

What are the two methods used to manufacture HCN industrially?

A

Andrussow process
NH3 + CH4 + 1.5O2 ➔ HCN + 3H2O
@1200 C with Pt/Rh catalyst, exothermic at -115.2 kcal/mol

BMA process
NH3 + CH4 ➔ HCN + 3H2
@1300 C with Pt/Rh catalyst, endothermic at 60 kcal/mol

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2
Q

What is a method used to manufacture HCN in the laboratory?

A

H + NaCN ➔ HCN + Na

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3
Q

What are the ways you can be exposed to cyanide? Give one example for each.

A
  1. Natural - Almonds, apple seeds
  2. Commercial Industrial - Insecticide
  3. Smoke inhalation - Cigarette smoking
  4. Pharmaceutical - long term use of nitropusside vasodilator
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4
Q

How is cyanide metabolized?

A

Main method ➔ Metabolized to thiocyanate by hepatic mitchondrial enzyme rhodanase (80%)

Other methods ➔
1. Expiration of HCN
2. Reaction with hydroxocobalamin to form cyanocobalamin (Vitamin B12)
- CN is inserted in the place of OH to form Vit B12
3. Oxidation to formic acid and CO2
4. Reaction with cystine

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5
Q

How does cyanide cause toxicity?

A

Cyanide reacts with cytochrome c oxidase (complex 4) of the ETC which prevents complex 4 from delivering electrons for the reduction of oxygen and results in no aerobic ATP production.

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6
Q

What are the symptoms of cyanide toxicity? (5)

A
  1. Dizziness, weakness, headache, confusion
  2. Perceived shortness of breath
  3. Coma
  4. Tachypnea
  5. Pinkening of skin
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7
Q

What is the treatment for cyanide toxicity?

A
  1. Airway control and 100% O2
  2. Volume support
  3. Bicarbonate to combat metabolic acidosis
  4. Specific Therapies
    - Amyl nitrate
    - Sodium nitrite
    - Sodium thiosulphate
    - Hydroxocobalamin
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8
Q

How does amyl nitrate work to treat cyanide toxicity?

A
  1. It is a potent vasodilator by delivery of NO
  2. It also causes oxidation of Fe(2+) to Fe(3+) which converts it to “methemoglobin”. CN will then bind to methemoglobin instead of cytochrome c oxidase because Fe(3+) has a higher affinity for CN than cytochrome c oxidase.
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9
Q

How does sodium nitrate treat cyanide toxicity?

A

It oxidizes Fe(2+) to Fe(3+) - induce methemoglobinemia

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10
Q

How does sodium thiosulphate work to treat cyanide toxicity?

A

It is a substrate for hepatic rhodanase, hence it will compete with CN as the substrate, lowering down the metabolism of CN.

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11
Q

How does hydroxocobalamin work to treat cyanide toxicity?

A

CN will react with hydroxocobalamin to form Vit B12

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12
Q

How do we analyze/measure CN in the body?

A

Colorimetric

  1. CN is liberated from the blood by addition of strong acid & HCN is trapped in a basic solution as CN again
  2. CN is converted to cyanogen chloride (CNCl) by reaction with chloramine-T
  3. After the rxn is complete, color is formed after the addition of pyridine-barbituric acid reagent
  4. The absorbance is read at 578 nm
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13
Q

When do we determine CN exposure by SCN determination?

A

When patients are on sodium nitroprusside for an extended period of time

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14
Q

Why is thiocyanate (SCN) determination not useful in the investigation of acute cyanide toxicity?

A

Testing is not indicated until day 7-14 because SCN will not be present in appreciable amounts

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15
Q

How is CO manufactured?

A
  1. Industrial
    O2 + 2C ➔ 2CO
    @ 800 C, exothermic at -221 kJ/mol
  2. Water-gas rxn
    H2O + C ➔ H2 + CO
    Endothermic at 131 kJ/mol
  3. Dehydration of formic acid with sulphuric acid
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16
Q

What are the ways you can be exposed to carbon monoxide? Give examples for each.

A
  1. Anywhere there is incomplete combustion
    - Housefires
    - Cooking with gas indoors or in a tent, igloo, snowcave
  2. Heme metabolism
    - Normal HbCO is 0.4-0.7%
    • 1-2% in urban non-smokes
    • 5-6% in urban smokers
      • Heme oxygenase catalyzes the degradation of heme to biliverdin, Fe(2+) and CO
17
Q

How is CO eliminated? What are factors that affect the elimination of CO?

A

Eliminated through the lungs with a half life of about 3-4 h in room air
- Breathing 100% O2 reduces half life to 30-90 min
- Hyperbaric O2 therapy reduces half life to 15-25 min

18
Q

How does CO cause toxicity?

A

CO’s affinity for hemoglobin is about 250x that of O2. Consequently, O2 gets bumped from Hb and there is no oxygen transport to peripheral tissues. Additionally, once CO is bound to Hb, the O2 at the 3 other binding sites are more tightly bound

CO also binds even more avidly to cardiac myoglobin which may cause myocardial depression, hypotension and worsening tissue hypoxia.

There is probably some impairment of cellular respiration due to the binding of CO to cytochrome c because HbCO levels do not correlate well with clinical symptomatology.

19
Q

What are the symptoms of carbon monoxide toxicity and different stages?

A

5-10%
- May aggravate preexisting heart disease
- Headache

15-25%
- Dizziness and nausea

50-70%
- Hallucination, confabulation, seizure, memory & gait disturbance, coma, death

20
Q

What are the physical findings of carbon monoxide toxicity? (5)

A
  1. Tachycardia
  2. Hyper/hypotension
  3. Hyperthermia
  4. Tachypnea, non-cardiogenic pulmonary edema
  5. Cherry red skin - frequently seen post-mortem in patients who died from CO poisoning
21
Q

What is the treatment for carbon monoxide toxicity?

A
  1. 100% O2 by ET tube or nonrebreather mark depending on situation
  2. Heart monitor and evaluation for myocardial damage
  3. Manage metabolic disturbances as per usual
  4. Pulse oximeter does not work
  5. Make sure to consider CN exposure
  6. Hyperbaric O2 if symptoms after 4 hrs of 100% O2
22
Q

What are the different forms of Hb?

A
  1. Deoxy form
  2. Oxy form
  3. Meth form
  4. Carboxy form
23
Q

What kinds of Hb can’t the co-oximeter distinguish?

A

Co-oximeter cannot distinguish glycosylated Hb from non-glycosylated forms

24
Q

How do we determine level of CO?

A

CO is not directly quantified - rather carboxyhemoglobin is quantified as a percent
- Accomplished by different absorbance spectra that various Hb have

  1. By measuring total absorbance at a number of frequencies, one can set up a series of linear equations
    - # absorbance measurements = # types of Hb you wish to quantify (usually HbA, HbA2 and HbF)
25
Q

What are the two classes of insect “nerve poisons”?

A

Organophosphates
Carbamates

26
Q

Give 4 examples of organophosphates.

A

Malathion
Diazinon
Parathion
Sarin

27
Q

What is the mechanism of toxicity of organophosphates?

A

Acetylcholine esterase (AChE) is an enzyme that is located in the synaptic cleft of peripheral and central nerves. Its function is to hydrolyze the neurotransmitter acetylcholine (ACh) into choline and acetic acid so as to prevent protracted activation of the post-synaptic membrane. Active site of AChE is dependent on Ser 200, His 400 and Glu 327.

  1. Organophosphate agents irreversibly phosphorylate Ser 200
    - Ser nucleophilically attacks P, leading to a tetrahedral intermediate and the ejection of a leaving group
  2. Consequently ACh floods
    - Parasympathetic synapses
    - Neuromuscular junctions
    - Sympathetic preganglionic synapses
28
Q

Peripheral Parasympathetic Muscarinic stimulation leads to what kind of symptoms?

A

DUMBELS
D - Diarrhea
U - Urination
M - Miosis
B - Bronchospasm, Bronchorrhea, Bradycardi
E - Emesis
L - Lacrimation
S - Salivation

29
Q

Stimulation of nicotinic receptors neuromuscular junction lead to what kind of symptoms? (4)

A
  1. Fasciculation
  2. Cramping
  3. Weakness
  4. Diaphragmatic paralysis
30
Q

Stimulation of nicotinic receptors of the postganglionic sympathetic neuron lead to what kind of symptoms? (4)

A
  1. Tachycardia
  2. Hypertension
  3. Pallor
  4. Mydriasis
31
Q

What does the clinical presentation of organophosphate toxicity depend on?

A

Relative amounts of muscarinic and nicotinic stimulation. Generally the muscarinic (DUMBELS) symptoms will dominate.

32
Q

What is the mechanism of toxicity of carbamates?

A

Alkylating agents that lead to reversible carbamylation of Ser residue of AchE

Toxicity of carbamates is mediated in an identical fashion as organophosphates. But because carbamylation is reversible, administration of pralidoxime is unnecessary.

33
Q

What are the general treatments of insecticide exposure?

A

A - Airway
B - Breathing
C - Circulation

Pt may need to be paralyzed with a non-depolarizing agent such as pancuronium

Decontamination of patient - soap and water

34
Q

What are the specific therapies for insecticide exposure?

A
  1. Atropine
    - Antimuscarinic antichlolinergic: 2-5 mg IV with redosing every 5-10 min until secretions stop
  2. Pralidoxime (2-PAM)
    - Dephosphorylates Ser residue
    - Decreases Atropine requirements
    - Decreases Nicotinic symptoms
35
Q

What is the pralidoxime mode of action?

A
  1. 2-PAM approaches carbamylated AChE
  2. Oxime attacks the carbonyl
  3. Carbamylated oxime is formed and enzyme is free
36
Q

What are long term symptoms associated with insecticide poisoning?

A
  1. Intermediate syndrome
    - 24-96 h after initial exposure
    - Redistribution of lipophilic organophosphate from adipose tissue and inadequate oxime therapy
  2. Organophophate-induced Delayed Neuropathy
    - 1-3 weeks after sever exposure
    - Weakness, ataxia, paralysis with no respiratory symptoms

PATH 407 (7 decks)

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